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Intravascular large B-cell lymphoma (IVLBCL) is a rare form of extra-nodal large B-cell lymphoma with an estimated annual incidence of about 0.5-1 in 1,000,000 people . It is characterized by the growth of lymphoma cells within the lumina of blood vessels, especially capillaries, manifesting as disseminated ischemic lesions . In Caucasians, it predominantly involves the central nervous system (CNS) and the skin, with the cutaneous variant carrying a better prognosis. Whereas in Asians it preferentially involves the bone marrow, liver, and spleen and is associated with hemophagocytic syndrome. As IVLBCL has a non-specific clinicoradiological presentation and carries a poor prognosis due to its aggressive nature and rarity, we report this case to raise its awareness among physicians. We describe a Southeast Asian patient presenting with recurrent strokes, chronic cough, and weight loss. His clinical presentation was unique. Although his computed tomography (CT) scan showed multiple ground glass opacities, his chest radiographs (CXRs) remained clear. The diagnosis was promptly achieved via endobronchial ultrasound-guided biopsy of mediastinal lymph nodes and transbronchial lung biopsy with subsequent successful treatment.
| 4.144531 | 0.927734 |
sec[0]/p[0]
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en
| 0.999997 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
A CT scan of the brain showed a right parietal hyperdensity of indeterminate etiology. A subsequent brain magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) revealed acute multifocal infarcts in the left splenium of the corpus callosum and right parietal subcortical white matter with no intra- or extra-cranial stenosis . The laboratory results on admission are shown in Table 1 . An extensive young stroke workup was normal. This included immunological studies (anti-nuclear antibody, anti-double stranded DNA antibody, anti-neutrophil cytoplasmic antibodies), thrombophilia screen (anti-cardiolipin and lupus anticoagulant antibodies, anti-thrombin antibody, proteins C and S), serum flow cytometry, microbiological studies (human immunodeficiency virus, hepatitis B and C), serum homocysteine level, urine and serum drug screen, transthoracic echocardiography with bubble contrast, and 24-hour holter. Chest radiographs and electrocardiograms on admission were normal.
| 3.949219 | 0.849121 |
sec[1]/p[2]
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en
| 0.999996 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
Five days later, the patient developed a worsening headache. Repeated brain MRI and MRA showed new multi-territorial infarcts. Cerebral spinal fluid analysis revealed a normal protein level, cell count, and microbiological studies; there were no malignant cells, and flow cytometry was negative. A CT scan of the thorax, abdomen, and pelvis performed three days later revealed bilateral peri-bronchovascular ground glass opacities (GGOs) seen predominantly in the upper lobes and superior segment of the lower lobes and enlarged right lower paratracheal lymph nodes . There was no hepatosplenomegaly or adrenal involvement. A CXR performed one week later for a fever spike remained clear .
| 3.849609 | 0.981445 |
sec[1]/p[3]
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en
| 0.999997 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
The patient underwent bronchoscopy with endobronchial ultrasound-guided biopsy of the right paratracheal lymph nodes, transbronchial lung biopsy, and bronchoalveolar lavage of the right upper lobe GGOs. Histology of lung biopsy revealed increased cellularity in the alveolar septa due to intravascular infiltrates of atypical medium to large cells (H&E, 400x magnification) . Intravascular infiltrates of atypical medium-to-large cells were found to be CD20-positive lymphomatous large B-cells, occurring in rows and elongated aggregates (H&E, 600x magnification) . Lymph node biopsy showed diffuse infiltrates of large lymphoid cells with variably irregular nuclei (H&E, 600x magnification) and was CD20 positive (CD20, 600x magnification) . A cytogenetics study by fluorescence in situ hybridization (FISH) showed BCL6 rearrangements without MYC or BCL2 rearrangements. Bronchoalveolar lavage showed no malignant cells, and microbiological studies including Mycobacterium tuberculosis were unyielding. A diagnosis of IVLBCL was made. Subsequent positron emission tomography-computed tomography (PET-CT) scans showed fluorodeoxyglucose (FDG) avidity in the corresponding areas of pulmonary abnormalities noted on CT and in the adrenal glands, spleen, and bone marrow . However, bone marrow trephine and aspirate showed no lymphomatous involvement.
| 4.160156 | 0.939453 |
sec[1]/p[4]
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en
| 0.999997 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
The patient completed six cycles of MR-CHOP (methotrexate, rituximab, cyclophosphamide, adriamycin, vincristine, and prednisolone) with a dose of intrathecal cytarabine during the first cycle. Serum lactate dehydrogenase (LDH) normalized by the end of the second cycle. A PET-CT after the third cycle showed complete resolution of the FDG-avid pulmonary GGOs and adrenal and splenic involvement . The patient subsequently underwent autologous hematopoietic stem cell transplant. At this time of writing, the patient is still in complete remission for three years after the initial diagnosis.
| 3.679688 | 0.980957 |
sec[1]/p[5]
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en
| 0.999997 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
Intravascular large B-cell lymphoma manifests in two variants: the 'Western' type primarily affects the central nervous system and skin, while the 'Asian' variant mainly targets the liver, spleen, and bone marrow, often linked with hemophagocytic syndrome . Despite our patient being Asian, his presentation was unusual, involving neurological and pulmonary symptoms. From a literature review, symptoms are non-specific and vary depending on organ involvement.
| 3.53125 | 0.434082 |
sec[2]/p[0]
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en
| 0.999996 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
Diagnosing IVLBCL can be challenging due to its rarity and aggressive nature. When evaluating a patient presenting with young-onset stroke alongside constitutional symptoms and elevated serum LDH, it is crucial to consider IVLBCL among other potential diagnoses. In cases where a chest X-ray is normal, performing a CT scan of the thorax is advisable as it can reveal findings that might be missed on the X-ray, thus preventing diagnostic delays. Notably, our case and several reported cases have shown a similar pattern of upper lobe predominant GGOs on CT scans of the thorax, which can aid in narrowing down the diagnosis. In our case, it remains important to rule out pulmonary tuberculosis, particularly in Southeast Asia. While core biopsy is usually the preferred method for suspected lymphoma, bronchoscopy with transbronchial lung biopsy and endobronchial ultrasound-guided fine needle aspiration of lymph nodes can be considered if other safer biopsy sites are not available, as demonstrated in our case report.
| 4.089844 | 0.684082 |
sec[3]/p[0]
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| 0.999996 |
39100808
|
https://doi.org/10.7759/cureus.66112
|
A 30-year-old female who is an active cigarette smoker presented to the emergency department with acute left lower extremity pain and swelling. A duplex ultrasound demonstrated acute occlusive deep venous thrombosis of the left common iliac through the left popliteal veins. A CT scan demonstrated a severe stenosis of the left common iliac vein. Five days after symptom onset, she was taken to the office-based lab (OBL), and access was performed via the left femoral vein.
| 3.472656 | 0.98877 |
sec[1]/p[0]
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en
| 0.999998 |
39099949
|
https://doi.org/10.7759/cureus.63903
|
The initial venography and intravascular ultrasonography demonstrated occlusion and acute thrombosis . Subsequently, venous thrombectomy was performed using a Philips Quickclear 10-french thrombectomy device. Balloon angioplasty demonstrated significant compression of the left common iliac vein at the site of arterial compression . Following thrombectomy and balloon angioplasty, Medtronic Abre stents were placed from the distal IVC to the left common femoral vein . The patient was discharged home on therapeutic apixaban after the procedure. The following day, the patient reported complete resolution of her left leg edema with no residual symptoms and no reported adverse reaction to the procedure.
| 3.708984 | 0.97998 |
sec[1]/p[1]
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en
| 0.999998 |
39099949
|
https://doi.org/10.7759/cureus.63903
|
This case demonstrates that a patient with an acute occlusive DVT can be safely and comprehensively treated in an OBL. In the case of MTS, endovascular treatment is highly preferred over surgical thrombectomy. In fact, surgical thrombectomy treatment has only accounted for roughly 4% of MTS cases since 2000 . In order to increase awareness of what OBLs can safely and cost-effectively offer, it is important to identify procedures that can be performed in OBLs and ensure that patients are made aware. It provides those who are hesitant to undergo a minimally invasive procedure due to hospital stays and associated costs with a procedural option.
| 3.806641 | 0.90625 |
sec[2]/p[2]
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en
| 0.999997 |
39099949
|
https://doi.org/10.7759/cureus.63903
|
Our case report demonstrates the safety and efficacy of office-based angioplasty and stenting for acute occlusive DVT secondary to MTS. After the patient presented to the emergency department and was appropriately managed, her occlusion was successfully treated with endovascular standard of care in an OBL. The increase in the prevalence of ambulatory care settings for mild to moderately complex procedures highlights a trend in the shift of these procedures away from inpatient hospital settings. While the decision to perform procedures in an outpatient setting will vary based on patient complexity, provider comfort, and the condition itself, there is a clear potential benefit to expanding the settings in which patients may have a procedure performed. These benefits include increased scheduling flexibility, reduced healthcare costs, decreased hospital burden, and a decreased risk of in-hospital infections.
| 4.023438 | 0.946289 |
sec[3]/p[0]
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en
| 0.999997 |
39099949
|
https://doi.org/10.7759/cureus.63903
|
Neonatal pulmonary alveolar proteinosis (PAP) is a rare and potentially life-threatening condition that affects newborns. It is distinguished by the collection of a periodic acid-Schiff (PAS)-positive diastase-resistant amorphous proteinaceous material in the alveoli leading to respiratory insufficiency . Two types of PAP have been described; congenital PAP which has a fulminant course and is usually fatal, and other one is late-onset PAP which is less severe and mimics the adult form . The clinical presentation at birth is nonspecific ranging from asymptomatic to progressive respiratory failure. The diagnosis is confirmed by lung biopsy and bronchoalveolar lavage . Treatment options are limited with poor success rates including whole-lung lavage, lung transplantation, administration of granulocyte-macrophage colony-stimulating factor (GM-CSF), and gene therapy . Here, we present a case of a severe form of congenital PAP presenting at birth as respiratory distress refractory to standard treatment.
| 4.207031 | 0.918945 |
sec[0]/p[0]
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en
| 0.999997 |
39105019
|
https://doi.org/10.7759/cureus.63866
|
A 1.3 kg female child was born to a 28-year-old multigravida mother with a bad obstetric history at 28 weeks of gestation by cesarean section in view of fetal distress. Antenatal history revealed four previous neonatal deaths out of which one was stillbirth and the rest all succumbed within 24 hours of life. All previous pregnancies were preterm births, and the babies had respiratory distress at birth. The mother had a unicornuate uterus which was hypothesized to be the cause for premature deliveries. There was a history of third-degree consanguinity present. The antenatal period was uneventful till 28 weeks when the patient started experiencing preterm labor for which she was admitted, antenatal steroid coverage with intravenous (IV) dexamethasone was given, and owing to fetal compromise, she was taken up for emergency cesarean.
| 3.574219 | 0.988281 |
sec[1]/p[0]
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en
| 0.999997 |
39105019
|
https://doi.org/10.7759/cureus.63866
|
The baby had severe respiratory distress at birth requiring delivery room continuous positive airway pressure (CPAP). In the neonatal intensive care unit (NICU), the baby was kept on CPAP support with a fraction of inspired oxygen (FiO2) requirement of 30% and a positive end-expiratory pressure (PEEP) of 5. Total parenteral nutrition and first-line antibiotics were initiated. The baby had a Silverman Anderson score of 5 with a chest x-ray suggestive of low lung volume and bilateral homogenous ground glass appearance suggestive of respiratory distress syndrome (RDS) as seen in Figure 1 .
| 3.714844 | 0.978027 |
sec[1]/p[1]
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en
| 0.999998 |
39105019
|
https://doi.org/10.7759/cureus.63866
|
In view of the increasing Fio2 requirement of >30%, Neosurf was administered within two hours of life as standard treatment protocol for RDS. In view of persistent respiratory distress, the baby was intubated by the fourth hour of life on a conventional ventilator. A second dose of surfactant, i.e., Neosurf, was administered. After 24 hours, the respiratory distress settled, and the baby was weaned off to CPAP by 36 hours of life.
| 3.466797 | 0.931641 |
sec[1]/p[2]
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en
| 0.999994 |
39105019
|
https://doi.org/10.7759/cureus.63866
|
After 12 hours of extubation, the respiratory distress increased mandating re-intubation. Septic screen came out negative. There was persistent desaturation with blood gas suggestive of respiratory acidosis for which the conventional ventilation setting was increased gradually to a maximum of Fio2 of 100%, PEEP of 6, and peak inspiratory pressure (PIP) of 24. The baby was shifted to high-frequency ventilation thereafter. The baby failed to show improvement despite adequate ventilation and succumbed due to refractory respiratory failure.
| 3.443359 | 0.984375 |
sec[1]/p[3]
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en
| 0.999996 |
39105019
|
https://doi.org/10.7759/cureus.63866
|
Postmortem lung biopsy was done suspecting surfactant deficiency due to previous neonatal deaths and nonresponse to conventional treatment with maximum ventilatory support. The biopsy was suggestive of diffuse alveolar damage with PAS-positive hyaline proteinaceous material lining the alveoli and preserved lung architecture suggestive of congenital alveolar proteinosis as depicted in Figure 2 .
| 3.828125 | 0.653809 |
sec[1]/p[4]
|
en
| 0.999996 |
39105019
|
https://doi.org/10.7759/cureus.63866
|
A 66-year-old man presented with neck pain and numbness in his left arm. He had a history of humerus chondrosarcoma that was resected and replaced with a prosthesis 24 years ago. He had also undergone surgery for lung and hip metastases from the chondrosarcoma 10 years ago, respectively. On examination, the patient had limited shoulder movement and arm atrophy in his left arm due to the humerus prosthesis. He also had partial restriction of forearm movements, but normal wrist movements and muscle strength. He had no neurological deficits. Magnetic resonance imaging (MRI) scan revealed a large, expansile lesion involving the C3 vertebra. The lesion was invading the surrounding soft tissues and causing spinal cord compression. The patient underwent an anterior cervical approach for resection of the tumor. The tumor was successfully removed, and the patient's symptoms improved. He was then given radiation therapy. One year later, the patient developed a recurrence of the tumor. The tumor was resected again, and the C2–C5 vertebrae were fused with iliac crest autograft and an anterior screw-plate system. The patient received post-operative radiation therapy and remained disease-free for 5 years. Five years after the second surgery, the patient developed another recurrence of the tumor. The tumor was resected again, and the C2–C4 vertebrae were corpectomized and reconstructed with iliac crest autograft. The patient then underwent posterior occipitocervical fusion.
| 3.765625 | 0.98584 |
sec[2]/sec[1]/p[0]
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en
| 0.999997 |
39104713
|
https://doi.org/10.3389/fsurg.2024.1397729
|
In our case, the lesion involved the C2 vertebral body, odontoid process, and extended into the C3 and C4 vertebral bodies. Although a transoral approach could access the C2 vertebral body and odontoid process, it was deemed unsuitable due to the lesion's extension to the C3 and C4 vertebrae and the higher complication rate associated with the transoral approach. Therefore, the high cervical anterolateral retropharyngeal approach was chosen in this case for tumor resection and anterior spinal cord decompression .
| 3.785156 | 0.917969 |
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| 0.999998 |
39104713
|
https://doi.org/10.3389/fsurg.2024.1397729
|
Chlamydia , as an obligate intracellular Gram-negative bacterium, is known to be responsible for several serious global healthcare challenges. Among these bacteria, Chlamydia abortus is an especially important zoonotic pathogen; it mainly causes infections in ruminants but, less frequently, may cause pneumonia in humans. Even more rarely, it can initiate an extremely severe pneumonia ( 1 ). Thus far, only six cases of pneumonia due to C. abortus have been reported worldwide; of these, five were not severe ( 2 – 6 ) and only one was severe ( 7 ). To further raise awareness of this rare disease, we here describe a case of severe pneumonia caused by C. abortus .
| 3.851563 | 0.730469 |
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en
| 0.999998 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
A 72-year-old woman was admitted to our emergency department on December 1, 2023, with complaints of fever as well as cough, phlegm in the throat, and shortness of breath, all of which had been present for 10 days. She had had a cerebral infarction a year earlier as well as an aneurysm of the left internal carotid artery but did not take medication regularly. Nevertheless, she said that she was able to take care of herself. Ten days earlier, she had developed a cold and a fever with a temperature of about 38.0°C along with a cough, phlegm in her throat, dyspnea, generalized muscle aches and pains, and intermittent diarrhea. Her symptoms were not relieved by cold medicine. Thus, after 5 days of illness, she went to her local hospital. There, after computed tomography (CT) of the chest, she was diagnosed with community-acquired pneumonia. The CT pointed to an infection in the upper lobe of the left lung , and she was given piperacillin–tazobactam (4.5 g q8h as an intravenous infusion) for 4 days. However, her condition did not improve. She was then admitted to the emergency department of our hospital.
| 3.5 | 0.986816 |
sec[1]/p[0]
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en
| 0.999998 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
On the patient’s arrival at our emergency department, physical examination showed the following: temperature, 38.9°C; respirations, 26/min; pulse, 102/min; blood pressure, 130/75 mmHg; oxygen saturation, 72% (under mask oxygen of 4 L/min); clear consciousness; tachypnea; rhythmic dry and wet rales audible in both lungs; abdominal tenderness; and no swelling of the limbs. Laboratory tests showed the following: calcitonin, 9.0 ng/mL; C-reactive protein, 299 mg/L; leukocyte count, 11.12 × 10 9 /L; neutrophil ratio, 96.4% (which was significantly higher than normal). Arterial blood gas analysis showed type I respiratory failure and an oxygenation index of 108 mmHg. Blood biochemistry suggested hyponatremia and hypochlorhydria. Blood creatinine, liver enzymes, and lactate dehydrogenase were significantly higher than normal. The levels of plasma pro-brain natriuretic peptide (pro-BNP) were 1150 pg/mL ( Table 1 ). A repeat CT scan of the chest suggested infectious lesions in both lungs and a small pleural effusion on each side . Color Doppler ultrasound of the vasculature of both lower extremities revealed atherosclerosis and intermuscular venous thrombosis of both lower legs. Color Doppler ultrasound of the heart showed aortic arteriosclerosis. Tricuspid valve regurgitation was mild; the ejection fraction was 65%. The patient was diagnosed with severe community-acquired pneumonia and was ventilated by a high-flow nasal cannula (oxygen concentration, 80%; flow rate, 55 L/min) with the oxygen saturation maintained at about 95%; she was also medicated with meropenem (0.5 g q8h by intravenous infusion) and methylprednisolone (40 mg q12h by intravenous infusion). At one point during this procedure, her blood pressure dropped to 90/52 mmHg; however, it returned to the normal level after active fluid replacement.
| 3.884766 | 0.978027 |
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en
| 0.999997 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
The next day the patient was admitted to the respiratory ward, and ventilation by high-flow nasal cannula (oxygen concentration 75%, flow rate 50 L/min) was continued to maintain oxygen saturation at about 95%. The retest of her blood inflammation index was still significantly higher than normal ( Table 1 ), and it was felt that the atypical pathogen infection had to be covered. The treatment was therefore adjusted to omadacycline (0.1 g qd by intravenous infusion with 0.2 g being given on the first day), methylprednisolone (40 mg q12h by intravenous infusion), ambroxol hydrochloride (30 mg bid by intravenous infusion) for phlegm, and nadroparin calcium for anticoagulant and symptom-supportive therapy.
| 3.412109 | 0.97998 |
sec[1]/p[2]
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en
| 0.999997 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
To detect the etiology of her pneumonia, the patient underwent a series of microbiologic diagnostic tests for bacteria, fungi, and viruses, and including staining and culture, serologic testing, and others. However, all of the tests were negative ( Table 2 ). Thus the patient’s clinical symptoms continued to deteriorate, with oxygen saturation maintained between 89 and 95%. She experienced shortness of breath and—after being given an emergency tracheal intubation for mechanical ventilation 24 h after admission—was transferred to the ICU.
| 3.566406 | 0.98291 |
sec[1]/p[3]
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en
| 0.999998 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
At the ICU, her treatment was adjusted to meropenem (1.0 g q8h by intravenous infusion) with continuing methylprednisolone, ambroxol hydrochloride, and nadroparin calcium plus the addition of thymopeptide (1.6 mg qd by hypodermic injection) and immunoglobulin (10 g qd by intravenous infusion) to improve the immunity. On the next day, bedside bronchoscopy showed that there was more white mucous sputum in both bronchi, and the lumen was clear after aspiration. The bronchoalveolar lavage fluid was then sent for mNGS examination. Two days later, the result suggested C. abortus , with 5072 sequence numbers and a relative abundance of 95.03%. A repeat bedside radiograph of the chest showed infection in both lungs, with greater infection in the right lung and partial absorption of infection in the left lung by comparison with the previous CT localization film of the chest . Therefore the patient was given moxifloxacin (0.4 g qd by intravenous infusion) combined with doxycycline (0.1 g bid PO), and the meropenem was stopped. The patient’s condition gradually stabilized under these treatments; methylprednisolone was reduced; and eventually—after 8 days of mechanical ventilation—the tracheal tube was removed to be replaced by a nasal cannula for the administration of oxygen. The bedside chest radiograph was then reviewed again; it pointed to infections in both lungs, similar to the previous one , with a small pleural effusion on the left side . After extubation, the patient appeared to have blood in her sputum. A review of the color Doppler ultrasound of her lower extremity vessels suggested that there was no increase in thrombus, so the nadroparin calcium was stopped. Three days after extubation, the patient was stable and transferred back to respiratory medicine.
| 3.783203 | 0.977539 |
sec[1]/p[4]
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en
| 0.999998 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
In the respiratory medicine department, moxifloxacin and doxycycline were continued up to 14 days. During this period, CT pulmonary angiography did not indicate a thrombus. A repeat CT scan of the chest suggested partial resorption of the lesions whereas others had increased, as had the bilateral pleural effusions . After 14 days of antichlamydial treatment, the patient’s blood inflammatory index had returned to normal; therefore, the antibiotics were stopped. Because the serum D-dimer level increased to 12.79 μg/mL, after communicating with the patient’s family members, the patient was discharged with a prescription for rivaroxaban 10 mg qd PO. A month after discharge, the patient was reexamined by CT of the chest, indicating significant absorption of both lung lesions and pleural effusions . The full timeline of hospitalization and clinical treatment is shown in Figure 2 .
| 3.667969 | 0.980469 |
sec[1]/p[5]
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en
| 0.999996 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
C. abortus infection initially presents with flulike symptoms, causing fever, headache, and weakness in the limbs. Due to the lack of specificity of the clinical symptoms and clinicians’ low level of knowledge of the disease, it is easy to miss or misdiagnose this disease. Chlamydial infection can also cause serious visceral complications; therefore, clinicians need to be alert to this possibility ( 12 , 13 ). In this case, the patient presented with typical influenza-like symptoms (such as fever and generalized muscle pain) at the beginning of the disease, followed by respiratory symptoms (such as cough, phlegm, and dyspnea). These were accompanied by extrapulmonary manifestations such as diarrhea as well as laboratory tests suggesting hyponatremia and hypochlorhydria, impaired hepatic and renal function, and elevated lactate dehydrogenase. These are similar to the clinical features of Legionella pneumonitis ( 14 ) and C. psittaci pneumonia ( 15 ).
| 3.992188 | 0.631348 |
sec[2]/p[1]
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en
| 0.999995 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
This patient’s lung imaging showed rapid progression from a solid lesion in the upper lobe of the left lung to solid lesions in multiple lobes, with air bronchial signs at the site of the solid lesion accompanied by bilateral pleural effusions. These imaging features are nonspecific and are also seen in streptococcal and other atypical infections, making early diagnosis of the pathogen critical.
| 3.669922 | 0.949707 |
sec[2]/p[2]
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| 0.999997 |
39104862
|
https://doi.org/10.3389/fmed.2024.1426577
|
The female patient had previously experienced one miscarriage after two years of marriage after having sexual intercourse. The prior incidence of fertilization and implantation indicated that the couple has a case of secondary infertility. With an unsuccessful pregnancy, the couple underwent three unsuccessful intrauterine insemination (IUI) attempts, two failed cycles of in vitro fertilization (IVF), and two failed attempts at frozen embryo transfer (FET). This medical history highlights the complexity of their infertility struggles and the need for specialized treatments to enhance their chances of conceiving.
| 3.359375 | 0.984375 |
sec[1]/p[3]
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en
| 0.999995 |
39105032
|
https://doi.org/10.7759/cureus.63926
|
Gonadotropin-releasing hormone (GnRH) antagonist protocol was opted to regulate the timing of ovulation and promote the development of multiple follicles in the ovaries. After 14 days of ovarian stimulation, we proceeded with the ovum pick-up (OPU). A GnRH agonist trigger was administered, and ovarian aspiration was scheduled 36 hours post-trigger. During the OPU, we retrieved five high-quality metaphase II oocytes and four metaphase I oocytes. On the same day, intracytoplasmic sperm injection (ICSI) was performed, resulting in the formation of four high-quality cleavage-stage embryos. PRP treatment was administered on day eight before ET to enhance the endometrium. Following the PRP treatment, a significant increase in endometrial thickness was observed, from 6.5 mm to 8.7 mm, on day 10 of the menstrual cycle. Before ET, a laser-assisted hatching procedure was performed to improve implantation outcomes. The decision to proceed with FET was made after thorough consultation with the female partner and obtaining detailed informed consent. On the day of ET, two high-grade laser-hatched embryos were transferred. PRP treatments and laser-assisted hatching were integral to this treatment plan, aimed at enhancing endometrial receptivity and improving implantation success. Figure 1 shows a blastocyst hatched by LAH.
| 4.050781 | 0.91748 |
sec[1]/p[9]
|
en
| 0.999996 |
39105032
|
https://doi.org/10.7759/cureus.63926
|
This case study provides one example of evidence that using PRP in conjunction with tempol medicine may be a ground-breaking method for improving thin endometrium and raising the chances of succeeding in clinical pregnancy through ART.
| 3.121094 | 0.97168 |
sec[2]/p[4]
|
en
| 0.999997 |
39105032
|
https://doi.org/10.7759/cureus.63926
|
The effective application of LAH on the embryo prior to ET is described for a patient who had secondary infertility, a history of miscarriage, and multiple implantation failures. The case further highlights how PRP and LAH may benefit individuals who have experienced repeated implantation failure. The results imply that certain ART difficulties may be addressed by procedures like PRP and LAH and the importance of individualized approaches in evolving reproductive technologies.
| 3.701172 | 0.875488 |
sec[3]/p[0]
|
en
| 0.999998 |
39105032
|
https://doi.org/10.7759/cureus.63926
|
Although a ‘treat-and-repair’ strategy in which pulmonary vasodilator is administered initially and subsequent defect closure is postulated to be effective in the cases of atrial septal defect with pulmonary arterial hypertension (PAH), 1 , 2 this strategy has not been applied to large patent ductus arteriosus (PDA) with PAH because of excessive pulmonary blood flow due to pulmonary vasodilator therapy. Herein, we report a proof-of-concept case of catheter closure for large PDA with PAH in a patient who underwent palliative surgical duct banding initially followed by a treat and repair approach.
| 4.101563 | 0.861328 |
sec[0]/p[0]
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en
| 0.999998 |
39104511
|
https://doi.org/10.1093/ehjcr/ytae354
|
A 10-year-old girl with trisomy 21 was referred to our hospital for the treatment for large PDA with severe pulmonary hypertension. Although she was diagnosed with a large PDA with severe pulmonary hypertension in infancy, she was followed up conservatively with diuretics and angiotensin-converting enzyme inhibitors because of her family’s refusal of the surgery. Physical examination revealed no cyanosis (percutaneous oxygen saturation of 98% in the upper and lower extremities), continuous murmur (Levine 2/6 at the upper left sternal border), or no tachypnoea. Chest radiogram revealed an enlarged pulmonary artery with moderately increased pulmonary vascularity and cardiothoracic ratio of 58%. Electrocardiogram revealed no left or right ventricular hypertrophy . Echocardiogram showed well-balanced right ventricle and left ventricle with small pericardial effusion , moderate tricuspid valve regurgitation of 3.9 m/s, and large PDA with bidirectional shunt . Angiographic image revealed a 13.6 mm long tubular arterial duct 3 (type C in Krichenko classification), measuring ϕ9.2 mm on the pulmonary artery side, ϕ8.1 mm in the middle, and ϕ12.7 mm on the aortic side, which was regarded as having a high risk of device embolization during the transcatheter occlusion in the setting of pulmonary hypertension 4 . Cardiac catheterization revealed an increase in mPAP, the ratio of pulmonary to systemic blood flow (Qp/Qs), pulmonary vascular resistance (Rp), and Rp/systemic vascular resistance (Rs) ( Table 1 ). The occlusion test and the acute pulmonary vasodilator test (AVT) with inhaled 20 ppm nitric oxide plus 100% O 2 showed a decrease in mPAP and an increase in descending aortic pressure (dAoP) and the cardiac index (CI), with a minimal change in the Rp or Rp/Rs. She was diagnosed with large PDA associated with PAH, which is categorized in the grey zone for operability. 1 , 2 , 5 , 6 We therefore adopted the ‘treat-and-repair’ strategy, in which palliative surgical arterial duct banding was performed before pulmonary vasodilator therapy for several months and was followed by transcatheter closure of the PDA. In the banding of the arterial duct, the duct was exposed through a left thoracotomy and banded at 10 mm from the aorta with a circumference of 15 mm (outer diameter ϕ4.8 mm) using a 0.6 mm thick and 5 mm wide polytetrafluoroethylene tape (W. L. Gore & Associates, Flagstaff, AZ, USA). The final diameter and the site of the duct banding were determined by considering the diameter of the device used for catheter closure. In the cardiac catheterization and angiography 10 days after the duct banding procedure, we confirmed the flow-restricted arterial duct, with the minimal duct diameter of ϕ3.3 mm, decreased pulmonary blood flow, and mPAP . Subsequently, we initiated macitentan and tadalafil. Cardiac catheterization 6 months after initiating the pulmonary vasodilators revealed a decrease in Rp and Rp/Rs in response to the acute vasodilator testing, which was low enough for the transcatheter occlusion. 1 , 2 , 6 Such banding converted the shape of the duct to a ‘conical’ duct form, called type A (the smallest diameter ϕ2.8 mm, the aortic side ϕ17.4 mm) . The transcatheter occlusion of the residual PDA was easily performed using the Amplatzer™ Duct Occluder I (ADOI) (Abbott Laboratories, Abbott Park, IL, USA) with a size of 8/6 mm . The macitentan and tadalafil were continued. No apparent device-related adverse events were observed. Cardiac catheterization 8 months after PDA occlusion revealed a favourable haemodynamics ( Table 1 ). Exercise tolerance improved after the duct occlusion.
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https://doi.org/10.1093/ehjcr/ytae354
|
Without proper management, large PDA with increased pulmonary flow leads to advanced pulmonary vasculopathy with high pulmonary artery resistance, in which the extreme form of the disease is Eisenmenger syndrome. 2 Although the treat-and-repair strategy has been applied to atrial septal defect with increased Rp, 1 , 2 it was unclear whether this strategy can be applied to large arterial duct with PAH. Since the administration of pulmonary vasodilators to patients with unrestrictive PDA may carry the risk of acute heart failure due to the excessive pulmonary blood flow, we overcame this issue by performing palliative duct banding in the present case. Furthermore, the palliative surgical duct banding gave us the opportunity to easily and safely occlude the remaining duct by percutaneous catheter occlusion using ADOI for the surgically created type A arterial duct. To the best of our knowledge, this is the first case report to show the successful treat and repair for large arterial duct after palliative duct banding, which was followed by transcatheter occlusion of the duct. The present ‘proof-of-concept’ case warrants further studies to establish a treat-and-repair approach for large PDA with the high pulmonary vascular resistance.
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https://doi.org/10.1093/ehjcr/ytae354
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Post-transplant lymphoproliferative disorders (PTLD) are lymphomas arising in immunosuppressed transplant patients, in both solid transplant and haematopoietic stem cell recipients, and can be a serious and sometimes fatal complication. They can be considered a spectrum of disorders involving lymphoproliferative processes of B- and T-cells. The majority of cases are associated with Epstein-Barr virus (EBV) infection and involve B-cell proliferation. As T-cell activity is suppressed in the immunosuppressed state, this is thought to alter immune surveillance, resulting in the proliferation of latently infected B-cells. Proliferation of a malignant B-cell clone results in a lymphoma . However, the role of EBV is not fully understood, as EBV-negative cases have been reported . PTLD can be heterogeneous in presentation where cutaneous manifestations are relatively rare. We present the case of a patient with PTLD with cutaneous involvement, which highlights the need for dermatologists to maintain a high index of suspicion of this entity in the context of an immunosuppressed transplant recipient.
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39104985
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https://doi.org/10.7759/cureus.63951
|
A 36-year-old man presented with a three-month history of a painless ulcer on the right lower leg. He had a complex medical background; he had received a cardiac transplant four years ago secondary to congenital heart disease and had since been on long-term immunosuppression (ciclosporin, azathioprine and prednisolone). He was receiving haemodialysis for end-stage renal failure.
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https://doi.org/10.7759/cureus.63951
|
The differential diagnoses included pyoderma gangrenosum or an atypical infection. An X-ray did not identify any evidence of osteomyelitis. A skin biopsy showed an atypical lymphoid infiltrate in the dermis, extending to the subcutaneous fat, composed of medium to large-sized lymphoid cells with hyperchromatic nuclei and small amounts of cytoplasm, associated with karyorrhectic necrosis. Some of the small vessels in the dermis showed fibrinoid necrosis of the wall. Immunohistochemistry staining was performed . Atypical lymphoid cells were positive for PAX5 (expressed in B-cell neoplasms), B-cell marker CD20 and MUM1 (expressed in B-cells and activated T-lymphoid cells), but negative for CD3, BCL6, CD10, cyclin D1, C-MYC, CD4 and CD8. In-situ hybridisation for EBV was positive . The Ki-67 cell proliferation index was high at 70% . Tissue cultures for fungi and mycobacteria were negative. Serum EBV viral load was undetectable at < 500 copies per ml.
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39104985
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https://doi.org/10.7759/cureus.63951
|
Based on the history, skin biopsy and immunohistochemistry findings, our patient was diagnosed with monomorphic B-cell post-transplant lymphoproliferative disorder (PTLD) consistent with diffuse large B-cell lymphoma, non-germinal centre subtype. A whole-body fluorodeoxyglucose (FDG) positron emission tomography (PET) scan showed increased tracer uptake corresponding to the site of the cutaneous ulcer . In addition, three other sites showed increased tracer uptake (anterior cortex of the right lower tibia, an area adjacent to the right superficial femoral artery and the right inguinal node) and this was of uncertain significance, although the presence of PTLD remained a possibility.
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https://doi.org/10.7759/cureus.63951
|
Initially, azathioprine was stopped. The patient was commenced on intravenous anti-CD20 antibody, rituximab, which was administered weekly for eight weeks and was tolerated well. Clinical resolution of the ulcer was subsequently observed. A post-treatment FDG-PET scan demonstrated a negative signal in all the areas enhanced in the baseline scan, demonstrating a complete response to treatment . To our knowledge, there has been no disease reoccurrence to date.
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39104985
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https://doi.org/10.7759/cureus.63951
|
After squamous cell carcinoma, PTLD is the main cause of cancer-related death among solid organ transplant recipients . According to the World Health Organisation classification , PTLD is divided into several categories: early lesions, monomorphic PTLD (B-cell, T-cell or NK cell), polymorphic PTLD and classic Hodgkin’s lymphoma type. Our patient had monomorphic PTLD, which is a more aggressive subtype and typically responds poorly to a reduction in immunosuppression. Our case is unusual because although PTLD is heterogeneous in presentation and extra-nodal sites are commonly affected, cutaneous involvement tends to be much rarer with only 5% of cases of PTLD reported to affect the skin , and only a handful of such cases reported to date. Cutaneous manifestations of PTLD are highly variable, ranging from papules to nodules with ulceration, as well as maculopapular eruptions . Affected sites can include the face, trunk and lower limbs. Our patient initially presented with a painless ulcer on the leg, which appeared relatively innocuous, thus highlighting the need to maintain a low threshold to investigate any new cutaneous lesion in a transplant recipient.
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39104985
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https://doi.org/10.7759/cureus.63951
|
In summary, we report a rare case of an aggressive form of PTLD in a patient with a cardiac transplant, presenting with a painless leg ulcer. PTLD seldom affects the skin and is highly variable in presentation, yet can be aggressive and potentially fatal. It can also present many years post-transplant. Treatment with rituximab resulted in disease resolution. Therefore, it is important for dermatologists to consider PTLD in their differential diagnoses so that prompt diagnosis and treatment can ensue.
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39104985
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https://doi.org/10.7759/cureus.63951
|
LEOPARD syndrome (LS) is a rare genetic disorder in which left ventricular hypertrophy (LVH) is the most common cardiac manifestation, although it may rarely manifest as apical cardiac hypertrophy ( 1 , 2 ). The apical left ventricular (LV) region may be difficult to evaluate by a transthoracic echocardiogram (TTE) ( 3 ). Cardiac magnetic resonance (CMR) provides high spatial and temporal resolution in any plane, making it a more accurate tool to assess apical hypertrophy ( 4 ). Coronary computer tomography angiography (CCTA) may be helpful in assessing coronary atherosclerosis and anomalies. In this case report, the unusual presentation of apical hypertrophy and coronary artery dilatation was comprehensively diagnosed by TTE, CMR, and CCTA and supported by clinical manifestations and further genetic testing.
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39105075
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https://doi.org/10.3389/fcvm.2024.1378078
|
A 41-year-old woman, with a body height of 150 cm and weight of 51 kg, presented with a LV apical hypoechogenic tissue detected by TTE, initially suspected as an LV myocardial tumor . Subsequent CMR examination identified it as focal left ventricular hypertrophy with a mass-like protrusion of the apical myocardium measuring 17 mm in diameter, as shown in four-chamber views at the end diastole . Cine CMR showed that the lesion was contracting with systole and relaxing with diastole coincident with the normal myocardium, with no reverse motion observed ( Supplementary Video ). The valves demonstrated normal function and flow. The resting LV systolic function was normal, with an LV ejection fraction of 65%. The T1-weighted, T2-weighted, and T1/T2-mapping CMR images demonstrated myocardial characteristics similar to surrounding normal tissue . A linear area of hyperintensity at T1-weighted and T2-weighted CMR was seen within the lesion, becoming hypointense in fat-suppressed T2 images, suggesting myocardial fat deposition. The first-pass perfusion did not show filling defects, and late gadolinium enhancement (LGE) was unremarkable .
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39105075
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https://doi.org/10.3389/fcvm.2024.1378078
|
From the previous history of the patient, it became evident that she presented with abnormal electrocardiographic findings at the age of 2 years. A recent electrocardiogram (ECG) revealed a left-sided electrical axis deviation with inverted T waves . Since the age of 4, she has been presenting with multiple lentigines (brown macules) dispersed mainly on the face, neck, and limbs, mostly flat within the skin, which gradually increase over time and reach a peak in terms of both number and extent in adolescence . The cutaneous manifestation intensified and deepened during the summer months because of sunlight exposure, which led to the finding of intradermal nevus by the pathological examination. In recent years, she has been experiencing exertional dyspnea. The physical examination was unremarkable, as borne out by normal eye spacing (3.0 cm), cognitive and auditory functions, and no malformations of the skeletal and reproductive systems. An ultrasonographic evaluation of the genitourinary system indicated hydronephrosis in the left kidney and a Nabothian cyst in the cervix, with no additional abnormalities observed. A chest computed tomography showed no thoracic skeletal deformities or hydrothorax. The patient has no children. A screening showed no multiple lentigines or related symptoms in the immediate family, which excluded the clinical possibility of LS according to the study of Voron et al ( 5 ). Complete blood cell count, urine analysis, and serum carcinoembryonic antigen showed no abnormalities. Serum biochemical indices showed a slightly higher level of low-density lipoprotein cholesterol with a value of 3.71 mmol/L (0–3.64 mmol/L). The HCM-AF score was 14 (less than 17), meaning that the risk of the patient developing new-onset atrial fibrillation was low ( 6 ).
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39105075
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https://doi.org/10.3389/fcvm.2024.1378078
|
Given the patient’s clinical features and history, ECG, TTE, and CMR, a diagnosis of Leopard syndrome was highly likely ( 5 ). A supplemental genetic testing revealed a heterozygous missense mutation in the PTPN11 gene (c.836A>G, p.Tyr279Cys), confirming its suspicion. Medical therapy (metoprolol or verapamil) was recommended to minimize cardiac burden and alleviate exertional dyspnea. For the multiple lentigines, intense pulsed light therapy was advised ( 7 ). However, the patient insisted that her current clinical presentation was not severe enough to affect her daily life and therefore refused further treatment with full awareness of the adverse cardiovascular events that may occur. We followed up the patient closely, and after 3 months, she developed transient chest pain that resolved spontaneously. Cardiac biomarkers such as troponin T (0.047 ng/ml), troponin I (0.051 g/L), creatine kinase isoenzyme (12 U/L), and natriuretic peptide (12 pg/ml) did not show any significant abnormality in the first 24 h after admission. A supplemental CCTA revealed minor non-calcified plaques in the left anterior descending artery and right coronary artery with mild luminal stenosis, which was unlikely to cause episodes of chest pain. In addition, a mild diffuse dilatation of the left anterior descending and right coronary arteries was noted . However, apical hypertrophy was unchanged from the CMR imaging study performed three months earlier . Unfortunately, the patient again refused further treatment ( Table 1 ).
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39105075
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https://doi.org/10.3389/fcvm.2024.1378078
|
The patient's clinical symptoms were atypical, presenting only as shortness of breath after activity, leading to her undiagnosed condition. During the follow-up period, she experienced transient apical pain that relieved spontaneously, and CTA did not show severe coronary artery stenosis. Despite no progression in the lesion observed in a 3-month follow-up CMR, early intervention to prevent irreversible cardiac damage remains paramount. Rapamycin has shown promise in reversing PTPN11 mutant hypertrophic cardiomyopathy in mouse models by inhibiting the mTOR pathway; however, its application in human subjects requires further clinical validation ( 31 , 32 ). Symptomatic treatment continues to be the most common treatment modality in clinical practice, with beta-blockers or non-dihydropyridine calcium channel blockers recommended for managing symptomatic non-obstructive myocardial hypertrophy to reduce chest pain and enhance exercise capacity. In the absence of any improvement with medication, surgical removal of the left ventricular outflow obstruction is indicated for obstructive myocardial hypertrophy ( 15 , 16 , 33 , 34 ). Although the patient declined further treatment, we will maintain rigorous monitoring and strive to secure her consent for prompt intervention.
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39105075
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https://doi.org/10.3389/fcvm.2024.1378078
|
This case report shows the value of multimodality imaging by echocardiography, cardiac magnetic resonance imaging, and coronary computed tomography to unravel the diagnostic challenges posed by unusual cardiac manifestations (apical hypertrophy, coronary dilatation) in complex disorders such as Leopard syndrome.
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39105075
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https://doi.org/10.3389/fcvm.2024.1378078
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In March 2024, a 29-year-old female patient presented to our emergency department with bilateral hip pain and fever for 3 days. One day prior to the onset of symptoms, the patient had cosmetic filler injections in the trochanteric areas bilaterally. She received 30 mL of HA filler injections on each side under sterile conditions and local anesthesia. There were no immediate adverse events except for the expected mild redness and swelling at the injection sites postprocedure. The patient was reassured and discharged on prophylactic amoxicillin–clavulanic acid 1 g twice daily along with symptomatic relief medications. On the next day, the patient started experiencing fever at night, documented at 38°C with some night sweats. There was no increase in redness or swelling. The fever continued to occur, and on the third day, the patient developed sudden-onset severe hip pain bilaterally with increasing redness and local warmth at the site of injections. Pain was characterized as sharp and shooting, aggravated by movement, with no relief with simple analgesics.
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39105124
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https://doi.org/10.1093/asjof/ojae052
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Upon examination, vitals were within normal limits except for mild tachycardia that settled after adequate pain control with a morphine injection. Local skin examination revealed bilateral swelling and redness ∼9 × 11 cm in size, with increased warmth, tenderness, and multiple indurations on palpation. Initial laboratory tests revealed mild neutrophilic leukocytosis with an elevated c-reactive protein of 150. The patient underwent ultrasound imaging of bilateral hips, which showed superficial, ill-defined hypo-hyperechoic areas with subcutaneous edema, the largest being 1.87 cc (1.5 × 1.8 × 1.2 cm) in the right hip and 15 cc (2.2 × 1.3 × 2.5 cm) in the left hip.
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39105124
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https://doi.org/10.1093/asjof/ojae052
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The patient was admitted under the plastic surgery team. She was started on IV clindamycin along with adequate pain medications, requiring multiple doses of morphine injections without significant pain relief. After serial examinations, bedside incision and drainage were performed for pain relief, which yielded frank pus. Swabs were taken for culture and sensitivity testing. The patient was scheduled for theater incision and drainage under spinal anesthesia the next day . Intraoperative findings revealed multiple superficial abscesses at the sites of filler injections. Approximately 60 mL of pus was drained from each side, and washout of filler injections was performed. A drain was inserted along with ribbon gauze packs.
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39105124
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https://doi.org/10.1093/asjof/ojae052
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The patient had no immediate complications. She reported improving pain postoperatively. The cultures of the tested swab grew profuse Extended Spectrum Beta-Lactamase (ESBL)-producing S. marcescens , resistant to ampicillin and amoxicillin–clavulanate, but sensitive to ertapenem and trimethoprim-sulfamethoxazole (TMP–SMX). The antibiotics were then changed to daily IV ertapenem with daily dressing of the wounds. A follow-up soft-tissue ultrasound showed resolution of the previous collections with only mild soft-tissue edema. Subsequently, the patient continued to show clinical improvement with inflammatory markers trending down. The patient was then discharged after confirming resolution of the wound infection and proper healing, with future follow-up scheduled in the plastic surgery outpatient department.
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| 0.999996 |
39105124
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https://doi.org/10.1093/asjof/ojae052
|
Our report presents a case of an immediate S. marcescens infection in an immunocompetent female following trochanteric HA filler injection. The product used in our case was a cross-linked HA, each 1 mL of the product contains 6.9 mg of sodium chloride, 2 mg of HA, and 20 mg of cross-linked HA. Two similar cases were reported in the literature. The first case involved a 62-year-old immunocompetent female who developed cutaneous S. marcescens infection of the glabella following glabella and forehead HA filler injections. However, this patient also received a glabellar area permanent filler injection containing polymethylmethacrylate 2 years prior to her presentation, and the HA injection took place 3 months prior to her presentation. Therefore, this could have served as a niche for the entry of S. marcescens microorganisms. Initially, topical and systemic antibiotics were tried along with multiple incisional drainages, yet the condition persisted, fluctuating in severity over time. However, after tissue and pus cultures confirmed the pathogen and sensitivity results, the patient was treated with 2 incision and drainage procedures along with oral TMP–SMX and ciprofloxacin, resulting in full resolution of the infection without recurrence after 1 year of follow-up. The other case involved a 70-year-old immunocompetent male patient with no comorbid disorders who presented with painful nodules in the nasolabial fold around 28 days after cosmetic eyelid surgery and filler injection. No information was provided regarding the type of filler injected in the area. A total of 13 cases were reported in the same paper, and 17 strains were isolated from the wounds. All of them were resistant to cefazolin, and 16 out of 17 were resistant to amoxicillin–clavulanic acid and ampicillin. Additionally, all remained susceptible to third- and fourth-generation cephalosporins, gentamicin, levofloxacin, and meropenem.
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39105124
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https://doi.org/10.1093/asjof/ojae052
|
In comparison with other cases, we find our case unique, because, to our knowledge, it is the first case to report S. marcescens infection posttrochanteric HA filler injection. Moreover, our patient is younger (29 years) compared with the other 2 patients (62 and 70 years), highlighting that it can present in a wide age range. Furthermore, our susceptibility results showed resistance to amoxicillin–clavulanic acid and ampicillin, similar to the majority of cutaneous S. marcescens cases mentioned in the aforementioned study. 10 , 11 Additionally, the early presentation of the case (a few days after the procedure) was a critical factor in early intervention and control of the infection. Source control was achieved by incision and drainage, and the placement of a drain after the surgery helped reduce the risk of re-collection in the cavity and expedited the healing process. 12 This case report describes a single patient, which limits the ability to draw a broader conclusion regarding post-HA filler infections. In addition, it lacks comprehensive information about the setting of which the procedure was performed in. Therefore, it is difficult to establish at which stage the pathogen was introduced. Moreover, there is no control group to help differentiate if the postdermal filler infection was due to the technique used or the patient's health status. Although these types of infections are rare, thorough explanation and discussion with the patients, along with informed consent signing, should take place before any procedure. 13 This will allow patients to make an informed decision before undergoing any procedure. Also, it is essential to preserve complete documentation of the consent in the patient's notes.
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https://doi.org/10.1093/asjof/ojae052
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On October 19, 2021, a 14-year-old boy presented to a local hospital in India with complaints of intermittent fever and abdominal distension with left upper quadrant dragging sensation in the last month. The complete blood count was hemoglobin (Hb) 10.0 g/dL, white blood cell (WBC) count 430,000/ μ L, and platelet (Plt) count 120,000/ μ L. The peripheral blood (PB) smear differential cell count exhibited neutrophils and band cells at 38%, lymphocytes at 8%, monocytes at 2%, eosinophils at 4%, basophils at 2%, myelocytes at 20%, metamyelocytes at 20%, promyelocytes at 2%, and blasts at 4%.
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39104564
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https://doi.org/10.1155/2024/5534445
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A bone marrow (BM) aspiration showed a hypercellular marrow with a heavily increased myeloid-to-erythroid ratio, an impressive myeloid shift to the left, with slightly increased basophils of 3% and blasts of 7%. This prompted a diagnosis of CML which was confirmed by cytogenetics applying the fluorescence in situ hybridization (FISH) technique demonstrating translocation t(9;22)(q34;q11.2)—the Philadelphia chromosome—in 98% of the interphase cells. The child was started on hydroxyurea (50 mg/kg), allopurinol (300 mg/sqm), and imatinib (300 mg/sqm) and was referred to Tata Memorial Hospital in Mumbai.
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39104564
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https://doi.org/10.1155/2024/5534445
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The family took about a week to reach the referral hospital, and 4 days prior to presentation in the referral hospital, the boy developed a continuous, painful penile erection, and in addition, he complained of decreased vision on his left eye for the last 2–3 days. A full blood count at the referral hospital showed Hb 9.0 g/dL, WBC 180,000/ μ L, and Plts 810,000/ μ L. The PB smear differential count showed neutrophils at 62%, lymphocytes at 4%, monocytes at 7%, eosinophils at 8%, basophils at 8%, myelocytes at 4%, metamyelocytes at 6%, and blasts at 1%. Karyotyping (FISH techniques) of interphase cells from PB confirmed the BCR::ABL1 gene fusion in 98% of cells, and a molecular analysis by reverse transcription-polymerase chain reaction (RT-PCR) detected the BCR::ABL1 (p210) transcript. The BM analysis confirmed the morphological findings from the referring hospital with the exception that only 1% of blasts were detected. In an immunophenotypic (FACS) analysis, no abnormal blasts were identified. A molecular analysis on tyrosine kinase domain mutations detected no variant BCR::ABL1.
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https://doi.org/10.1155/2024/5534445
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Treatment was initiated with hydration paralleled with cytarabine (100 mg/m 2 ) × 4 days, and hydroxyurea and imatinib were continued. This prompted a reduction of the WBC to 57,000/ μ L by Day 5, and therefore, the leukostasis syndrome measures were stopped while hydroxyurea and imatinib were continued. By Day 10, the WBC had dropped to 12,000/ μ L and hydroxyurea was tapered while imatinib was continued.
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39104564
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https://doi.org/10.1155/2024/5534445
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Approaches to treat the priapism comprised wide bore needle aspiration which did not result in penile detumescence. Therefore, on Day 2 of admission to the referral hospital (7 days from the onset of priapism), a distal shunt surgery was performed with a Bennett shunt. Ophthalmologic inspection confirmed left eye painless loss of vision. Findings concluded a vitreous hemorrhage. During the course of treatment, the boy developed secondary glaucoma which was controlled on topical antiglaucoma measures.
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39104564
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https://doi.org/10.1155/2024/5534445
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Results of the follow-up examinations at defined time points as indicated are listed in Table 1 . Cytogenetic remission was confirmed in the PB at Month 8 and major molecular response (MMR) (MR3 = <0.1% BCR::ABL1 transcript ratio) at Month 11. With a good adherence to imatinib treatment, the child is doing well. However, the left eye has no vision and there is a total loss of penile erectile function.
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https://doi.org/10.1155/2024/5534445
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(a) Visual impairment at diagnosis of pCML is described in the form of pediatric case reports, but no systematic analysis has been performed. The boy discussed here experienced loss of left eye vision 2–3 days prior to first admission. While retinal infiltration usually resolves when CML is treated appropriately, vitreous hemorrhage and/or retinal vein occlusion, exudative retinal detachment, and/or choroidal infiltration and hemorrhage may have caused the permanent loss of vision in this boy [ 21 – 23 ]. Once TKI treatment has been started and normal white cell counts are achieved, surgical intervention can be planned if conservative measures do not resolve the ophthalmological complications .
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39104564
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https://doi.org/10.1155/2024/5534445
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The reasons behind the delayed presentation of childhood cancers in LMICs can be multiple, including delayed care-seeking by the family, lack of awareness in the primary physician/pediatrician, unavailability of the needed expertise at the primary/secondary healthcare set-ups, and delayed referral to a tertiary care facility . As outlined in the case history, the diagnosis of CML was made before the boy developed organ damage. However, lack of adequate warning regarding the consequences of uncontrolled/unmonitored hyperleukocytosis by the referring physician, leading to the unduly long gap (1 week in this case), from referral to presentation to our centre, contributed to the dismal outcome. Transport infrastructure is unlikely to be the predominant cause for such delays, as currently, barring a few remote areas, most of the places in India are well connected to bigger cities, with centres having requisite expertise for managing children with cancer.
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39104564
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https://doi.org/10.1155/2024/5534445
|
Sarcoidosis is a systemic condition characterized by non-caseating epithelioid granulomas . First described by Norwegian dermatologist Caesar Boeck in 1899, the disease presents a wide array of clinical symptoms involving multiple medical specialties . It is thought to arise from immune reactions triggered by various environmental factors . In the United States, the annual incidence is about 10 cases per 100,000 individuals . The condition most commonly affects individuals aged 20 to 39 years and occurs across all races and ethnicities . In over 90% of cases, sarcoidosis affects the lungs . Although extrapulmonary manifestations can be subtle, they contribute significantly to morbidity . Bone marrow sarcoidosis is rarely documented among these manifestations. We present a case of sarcoidosis confirmed by lung and bone marrow biopsy.
| 3.970703 | 0.908691 |
sec[0]/p[0]
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en
| 0.999997 |
39109141
|
https://doi.org/10.7759/cureus.63991
|
A 50-year-old female presented with chronic lower back pain to her primary care physician. Routine blood work showed significant hypercalcemia (15.1 mg/dL), prompting a visit to the emergency room. She had no other complaints. Her medical history included hypertension, hyperlipidemia, diabetes mellitus, chronic kidney disease secondary to glomerulosclerosis and hypertensive nephrosclerosis (baseline creatinine 1.6 mg/dL), major depressive disorder, and generalized anxiety disorder. Her medications were tirzepatide 15 mg/0.5 mL weekly, allopurinol 100 mg daily, atorvastatin 10 mg daily, buspirone 5 mg daily, and escitalopram 20 mg daily, and vitamin D3 50,000 IU weekly. A CT scan of the abdomen and pelvis without contrast showed bilateral non-obstructive renal stones, mild liver surface nodularity, and mild splenomegaly .
| 3.642578 | 0.987305 |
sec[1]/p[0]
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en
| 0.999996 |
39109141
|
https://doi.org/10.7759/cureus.63991
|
Bronchoalveolar lavage was negative for malignant cells, showing respiratory epithelial cells and mixed inflammation. Pneumocystis pneumonia stain and acid-fast bacilli were negative. Angiotensin-converting enzyme was normal at 10 U/L. Mycology/Fungal panel was negative for beta-D-glucan, Coccidioides IgG and IgM, Histoplasma , and TB QuantiFERON. Malignancy markers were unremarkable with carcinoembryonic antigen of 1.46 ng/dL, cancer antigen 125 of 20.6 U/L, cancer antigen 19-9 of 21.7 U/L, and alpha-fetoprotein of <1.82 ng/mL. A nuclear medicine liver scan indicated decreased uptake of sulfur colloid by the liver’s Kupffer cells and increased uptake by the spleen, suggesting possible functional damage to the liver’s reticuloendothelial system. A liver biopsy showed benign hepatic parenchyma with bridging fibrosis, focal regenerative nodule formation, and no granulomas. There was mild portal chronic inflammation and minimal (less than 5%) macrovesicular steatosis. Bone marrow biopsy revealed significant replacement of marrow space by multifocal single and clustered epithelioid non-caseating granulomas with numerous multinucleated giant cells, suggestive of bone marrow sarcoidosis. Extrapulmonary manifestations of sarcoidosis are uncommon.
| 4.230469 | 0.702148 |
sec[1]/p[2]
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en
| 0.999998 |
39109141
|
https://doi.org/10.7759/cureus.63991
|
POEMS syndrome, also known as Crow Fukase syndrome, was proposed by Bardwick in 1980 ( 1 ). It is a rare multisystem disease caused by plasma cell proliferation. The clinical manifestations of POEMS mainly include peripheral neuropathy, organomegaly, endocrinopathy, M protein elevation, and skin changes ( 2 , 3 ). Patients rarely present with hydrothorax and ascites as the main clinical manifestations. Therefore, these patients may be misdiagnosed or their diagnosis may be missed. We reported a case of a POEMS patient with portal hypertension as the main clinical manifestation.
| 3.761719 | 0.919922 |
sec[0]/p[0]
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en
| 0.999995 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
The patient, a 70-year-old male, was diagnosed with liver cirrhosis 11 months prior, and he had been experiencing abdominal distension and shortness of breath for more than 1 month. He visited our hospital in June 2023. The patient developed abdominal distension without an obvious cause 11 months prior and was diagnosed with liver cirrhosis at a local hospital. Albumin supplementation and diuretic treatment alleviated symptoms to some extent. One-month prior, the patient experienced abdominal distension accompanied by shortness of breath. After admission to the local hospital for albumin supplementation, diuresis, and paracentesis, his condition improved. However, the discomfort described above persisted. To further clarify the diagnosis and treatment, the patient sought medical attention at our hospital. During the disease course, the patient experienced a poor appetite, poor sleep, normal defecation, and decreased urination.
| 3.175781 | 0.989746 |
sec[1]/p[0]
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en
| 0.999997 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
He had been taking oral tablets to control hypertension. Renal dysfunction was discovered 3 months prior. He denied a history of alcohol use. Physical examination revealed the following: a height of 176 cm, a weight of 64 kg, a body temperature of 36.3°C, a pulse of 62 beats/min, an exhalation of 19 beaths/min, and a blood pressure of 147/84 mmHg. The typical signs of liver cirrhosis, including spider haemangioma, engorged paraumbilical veins, or palm erythema, were all negative. Cognitive function appeared normal, and cyanosis of the lips, jaundice of the skin or sclera, and palpable swelling of superficial lymph nodes were all absent. He presented with coarse breathing sounds in both lungs and weak vocal resonance in the right lung. His heart rhythm was consistent, with no additional heartbeats, murmurs, or pericardial friction sounds. The abdomen was full, without tenderness, rebound pain, or muscle tension. The liver and spleen were not palpable, but shifting dullness was detected. Both lower limbs were free of oedema. The diagnostic examination results are shown in Table 1 .
| 3.664063 | 0.986328 |
sec[1]/p[1]
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en
| 0.999998 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
The final diagnoses were noncirrhotic portal hypertension, splenic hyperfunction, hypoalbuminaemia, ascites, right hydrothorax, chronic renal insufficiency (chronic kidney disease, stage 3), and grade 3 hypertension (extremely high-risk group). The patient received symptomatic treatment including albumin supplementation, diuresis, improvement of renal perfusion, and thoracic and abdominal paracentesis. Given the refractory hydrothorax and ascites and the patient’s advanced age, a transjugular intrahepatic portosystemic shunt (TIPS) was applied, and a transjugular liver biopsy was performed to determine the cause of the condition. After TIPS placement, the patient was discharged without any discomfort.
| 3.685547 | 0.982422 |
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en
| 0.999997 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
Two weeks after TIPS placement, the patient was admitted to the local hospital for symptomatic treatment due to pleural effusion and ascites. One and a half months after TIPS surgery, the patient was referred to our hospital again due to nausea, fatigue, abdominal distension, and shortness of breath. Re-examination via computed tomography showed no thrombosis or stenosis in the TIPS stent. After symptomatic treatment involving liver protection, diuresis, albumin supplementation, and fluid drainage, the patient’s condition improved slightly. Considering the persistent recurrent pleural and abdominal fluid accumulation after TIPS placement and concomitant, lower limb weakness but lack of hepatic encephalopathy, the patient’s medical history was traced again. One-year prior, the patient had developed weakness in both lower limbs, and in May of this year, melanin deposition appeared on the skin of both feet. One and a half months after TIPS placement, the weakness in both lower limbs gradually worsened, and hydrothorax and ascites recurred. However, the patient did not experience significant relief after reducing portal pressure. Based on the above symptoms, relevant examinations of the blood system improved, and the diagnosis of POEMS syndrome with portal hypertension was ultimately confirmed. Subsequently, bortezomib combined with glucocorticoids was administered for treatment. After two courses of treatment, the patient died due to pneumonia and infection. The diagnostic process is shown in Figure 1 .
| 3.810547 | 0.984375 |
sec[1]/p[3]
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en
| 0.999996 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
The patient in this case was an elderly male with refractory hydrothorax and ascites. Combined with routine laboratory and imaging examinations, the initial diagnosis was consistent with the clinical characteristics of liver cirrhosis ( 4 ). Ascites is a common complication of liver cirrhosis, with an annual incidence rate of 5–10%. The 1-year and 5-year mortality rates for patients with cirrhosis and ascites are 30% and 70%, respectively, and the median survival time for patients with refractory ascites is only 6 months ( 5 , 6 ). TIPS placement is one of the main methods used to reduce portal vein pressure by establishing a new channel between the portal vein and hepatic vein, which can quickly reduce portal vein pressure in patients with cirrhosis and without cirrhosis, achieve hemostasis, and relieve ascites ( 7–10 ). In addition, compared with the treatment of complications of portal hypertension in cirrhosis, TIPS placement is advantageous for treating complications of noncirrhotic portal hypertension as the latter has relatively good liver function with low incidences of liver failure, and hepatic encephalopathy ( 11 ). Compared to abdominal paracentesis, TIPS placement significantly improves the transplant-free survival rate of patients with refractory ascites and cirrhosis and reduces the risk of recurrent ascites and hepatorenal syndrome, but increases the risk of HE ( 12 ).
| 4.265625 | 0.679688 |
sec[2]/p[0]
|
en
| 0.999998 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
Viral infection and autoimmune liver disease were ruled out for this patient. To further clarify the cause of liver disease, the patient underwent liver biopsy. Due to the presence of ascites in the patient, a transjugular liver biopsy was performed ( 13 ). Transjugular liver biopsy has expanded the indications for liver biopsy, and research has shown that its effectiveness is comparable to that of percutaneous liver biopsy ( 14 , 15 ). Finally, the patient was diagnosed with noncirrhotic portal hypertension. However, the patient’s symptoms of hydrothorax and ascites did not improve after TIPS. The common cause of persistent ascites after TIPS surgery is obstruction or stenosis of the TIPS. However subsequent CT scans showed no abnormalities, and lower limb symptoms worsened after surgery without significant abnormalities in blood ammonia levels or direction or computational ability.
| 4.035156 | 0.934082 |
sec[2]/p[1]
|
en
| 0.999997 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
To clarify the etiology of portal hypertension, a combination of patient history and further relevant examinations were needed ( 16 ). The patient had peripheral nerve damage, abnormal monoclonal plasma cell proliferation (IgA-λ), clerosing bone lesions, elevated VEGF, and abnormal thyroid function. Ultimately, POEMS syndrome diagnosed. Portal hypertension may be associated with POEMS.
| 3.027344 | 0.859375 |
sec[2]/p[2]
|
en
| 0.999997 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
The diagnostic process of this case was somewhat convoluted. The patient did not have typical clinical signs of liver disease except for ascites. Routine blood routine, liver function tests, coagulation tests, abdominal CT, and liver stiffness tests all supported the initial diagnosis of liver cirrhosis. However, the cause was unknown and common liver diseases related to viral infection, fatty liver, and autoimmune diseases were ruled out. TIPS reduced portal hypertension. Transjugular liver biopsy confirmed the diagnosis as noncirrhotic portal hypertension. However, the symptoms did not improve significantly after the decrease in portal vein pressure. Moreover, the patient’s lower limb weakness gradually increased after TIPS placement, which was not related to postoperative hepatic encephalopathy. After tracing the medical history and performing relevant examinations, the diagnosis of POEMS with portal hypertension was confirmed. The time from onset to diagnosis was 13 months. Because the patient had atypical symptoms, diagnosis was more difficult. Furthermore, the patient was elderly, the condition was severe, and suffered from a concurrent infection after chemotherapy.
| 4.003906 | 0.971191 |
sec[2]/p[10]
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en
| 0.999997 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
This patient had relatively complete diagnosis, treatment, and follow-up data. In the future cardiogenic, nephrogenic, hepatogenic, endocrine, tumor, hematological, and rheumatic immune system diseases should be differentiated in patient presenting with concurrent abdominal fluid, pleural fluid, and a small amount of pericardial fluid. Moreover, some symptoms were overlooked in the patient’s diagnosis and treatment process, including the fact that the patient had symptoms of lower limb weakness 1 year prior and did not undergo thyroid function testing at the first visit. The IgA level was slightly elevated but the globulin level was within the normal range. Further immune electrophoresis and other tests were not performed. The patient’s abdominal CT showed lesions in the lumbar vertebrae, which were not further clarified. Additionally, the serum-pleural effusion albumin gap before and after TIPS was differed (13.1 g/L vs. 6.4 g/L). A decrease in the serum-pleural effusion albumin gap of less than 11 g/L after TIPS was another indication of an etiology other than portal hypertension. Therefore, for noncirrhotic patients with portal hypertension, additional causes, such as rheumatism and blood tumors, should be explored.
| 4.082031 | 0.90625 |
sec[2]/p[11]
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en
| 0.999998 |
39109224
|
https://doi.org/10.3389/fmed.2024.1373397
|
In this context, we report the steroid-modified autopsy case with a pathologically-diagnosed MS with initial axonal loss, despite the clinically and radiologically lymphoma-like manifestations. This discrepancy cautioned the high probability of misinvolvement of other diseases even at autopsy in the Marburg variant.
| 3.314453 | 0.956055 |
sec[0]/p[2]
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en
| 0.999997 |
39108350
|
https://doi.org/10.1016/j.ensci.2024.100515
|
A 74-year-old female with a history of diabetes mellitus (DM) experienced two weeks of headache, appetite loss, and fatigue with unknown etiology. Then, the neurological onset was monoplegia of the right upper limb without ipsilateral lower limb involvement. About a week later, the patient developed tetraplegia, leading to hospitalization. Vital signs, including body temperature, were within the normal range. Magnetic resonance imaging (MRI) with contrast-enhanced fluid-attenuated inversion recovery (CE-FLAIR) showed several extending fused lesions appearing to arise from choroid plexus to the white matter of lateral ventricles with lymphoma-suggesting “C opening sign” . The surface lesions showed mass effects protruding to the lateral ventricle . Notably, there was a lesion growing from the skull dura mater, which was even the outside the brain parenchyma . All lesions exhibited high intensity on diffusion-weighted imaging (DWI), and low intensity on apparent diffusion coefficient (ADC) with mass effect . Laboratory testing showed a mild elevation of soluble interleukin 2 receptor (sIL2R) (515 U/mL), along with elevated transaminase, and hyperglycemia due to DM. Other tests to explain brain lesions were all within normal range, including the anti-myelin oligodendrocyte glycoprotein antibody, anti-aquaporin 4 antibody, anti-neutrophil cytoplasmic antibody, anti-nuclear antibody, angiotensin-converting enzyme, or tumor markers. Paraneoplastic syndrome and related antibodies were not evaluated due to the tumor-like mass effects on MRI. Cerebrospinal fluid (CSF) showed lymphocytic pleocytosis with elevated protein and a relatively decreased glucose (initial/final pressure 11/9.5 cm H 2 O, all mononuclear 54 cells/μL, protein 59 mg/dL, glucose 81 mg/dL, serum glucose for reference 194 mg/dL), and cytology showed class 3 without mitosis, suggestive of reactive lymphocyte . CSF also showed an oligoclonal band consisting of a single strong band with an extremely weak band (which appeared as if “mono”clonal band) . Whole-body computed tomography identified a small right thyroid papillary carcinoma (< 1.0 cm diameter), but it was considered an unlikely cause of central nervous system (CNS) lesions due to its static nature and absence of lymph node metastasis. In a few days after admission, lymphoma emerged as a most likely differential diagnosis, but CSF flow cytometry (requiring additional lumber puncture), brain biopsy, or empiric chemotherapy were not available, because of the worsening severe dysphagia, a drowsy state, and the patient's refusal of additional invasive procedures. Given these manifestations suggesting some malignancy like lymphoma and the patient's will, palliative radiation including whole brain and upper spinal cord (30 Gray/ 10 Fractions), steroids (dexamethasone 3.3 mg/day for 15 days), and intravenous morphine was administered. Following treatment, the patient's condition initially stabilized, but she eventually succumbed to severe aspiration pneumonia with worsening dysphagia and consciousness. In contrast to clinical diagnosis, histopathological observations at autopsy could not detect extending fused lesions with mass effect on MRI, such as malignancy (including lymphoma and thyroid carcinoma), infection like tuberculosis, or any granuloma. Instead, all brain and spinal cord lesions were pathologically diagnosed as Marburg variant of MS, with sharply margined myelin loss , myelin phagocyting , intact astrocytes with minor enlargement , and initial axonal damage despite demyelinating disease . In the lesion of myelin loss, no inflammatory cells were detected. All lesions of myelin loss were completely matched with DWI-high (and ADC-low) intensity lesions . In addition, most of the lesions appeared to grow from the brain surface, lateral and fourth ventricles, or spinal central canal , appearing as if via-CSF dissemination of the lesion. Fig. 1 CE-FLAIR MRI of the coronal section shows fused, clustered lesion with the C opening sign arising from choroid plexus (A), and several lesions protrude to the lateral ventricle (A, B, C, D). A lesion growing from the dura mater on the skull, which is not even the brain parenchyma, at the coronal and axial view (E, F). All lesions are high in DWI and low in ADC map (G, H). CSF shows class 3 in cytology, unlike MS (I), and oligoclonal band with strong single band (J). Fig. 1 Fig. 2 In pathology, there is no mass effect protruding to the lateral ventricle, or mass growing from the dura mater on the skull observed on MRI (K). KB and GFAP staining shows selective myelin damage without astrocytic involvement. Some astrocytes show enlargement (L, M, Q). The KB-unstained lesion is completely matched to the DWI-high lesion (with low ADC map lesion) on MRI (N, O). Myelin was phagocyted (P). The lesion is sharply marginated (R, yellow arrows). Initial axonal damages with swelling are shown in neurofilament staining (S). Most of the lesions of KB-unstained lesions appear to arise from the brain surface, fourth ventricle, or central canal (L, N, T). Fig. 2
| 4.152344 | 0.97168 |
sec[1]/p[0]
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en
| 0.999998 |
39108350
|
https://doi.org/10.1016/j.ensci.2024.100515
|
The major issue in the present case is the “negative” result in pathology. Although histopathological evaluations are the most reliable for diagnoses, brain biopsy is more invasive, and it might be avoided especially in patients with deteriorating general status like the Marburg variant. In addition, cases with assumed treatable demyelinating diseases like MS, or terminal stage requiring palliative care might be treated by steroids antecedently, which increases the probability of “vanishing tumor” (mainly lymphoma) . On the other hand, an autopsy is regarded as the gold standard/final diagnosis and determines the “negative” case (as if diagnostic testing with 100% sensitivity). Furthermore, “negative” studies are usually unpublished . Therefore, it is an inevitable pitfall for pathology to recognize vanishing tumors with sentinel demyelinating lesions after steroid use as demyelinating disease or malignancy-negative cases, even if clinical and radiological manifestations are significantly inconsistent with MS. The allowance of initial axonal loss in Marburg's variant despite demyelinating disease is exacerbating this pitfall. In addition, unlike the Marburg variant, diagnosable cases of vanishing tumors were confined to slow-progressing or surviving cases because it requires a time course to confirm recurrence .
| 4.238281 | 0.469482 |
sec[2]/p[3]
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| 0.999996 |
39108350
|
https://doi.org/10.1016/j.ensci.2024.100515
|
Multiple sclerosis (MS) is a chronic autoimmune disease that primarily affects women and young adults and characterized by demyelination of the central nervous system. 1 Current management approaches are concentrated on symptom relief, acute attack treatment, and lowering biological activity through disease‐modifying therapies (DMT). 2 The first oral DMT licensed for the treatment of MS is fingolimod. 3 Atypical demyelinating disorders exhibiting tumor‐like features present significant diagnostic and therapeutic challenges for neurologists. Tumefactive demyelinating lesions (TDLs) are rare tumor‐like lesions in the central nervous system presenting diverse symptoms that predominantly affect motor, cognitive, sensory, cerebellar, and brainstem functions. 4 Balo's concentric sclerosis (BCS) emerges as an uncommon variant of TDLs, distinguished radiologically by a “tree trunk” or “onion bulb” appearance on magnetic resonance imaging (MRI), characterized by alternating bands of myelin preservation and loss around them. 5 , 6 Despite TDLs being observed in MS patients on fingolimod, 7 documentation on Balo‐like lesions remains limited. Herein, we present a young female MS patient treated with fingolimod who was admitted to our clinic with hemiparesis and a Balo‐like lesion in her MRI.
| 4.296875 | 0.846191 |
sec[0]/p[0]
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en
| 0.999997 |
39109309
|
https://doi.org/10.1002/ccr3.9266
|
A 37‐year‐old female with a 9‐year history of relapsing–remitting MS (RRMS) and 3‐year fingolimod treatment presented to Sina Hospital's emergency department in Tehran, Iran, exhibiting acute right‐sided hemiparesis persisting for 5 days. The patient had no complaints of fever, headache, diplopia, imbalance, or aphasia. She was alert and oriented at admission, and her vital signs were stable. Her pupils were normal in size and had a normal reaction to light. Eye movements were normal in all directions, with no observed ptosis, lid lag, or nystagmus. A physical examination of muscles revealed normal tone in upper and lower limbs on both sides and a medical research council score of 3/5 for proximal and distal muscles of the right upper and lower limbs and 4/5 for proximal and distal muscles of the left upper limb and 5/5 for proximal and distal muscles of the left lower limb. Deep tendon reflexes were assessed using a reflex hammer on the biceps, triceps, brachioradialis, patellar, and Achilles tendon. The reflex responses were normal on the left side and increased on the right side.
| 3.998047 | 0.980469 |
sec[1]/p[0]
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en
| 0.999998 |
39109309
|
https://doi.org/10.1002/ccr3.9266
|
A brain MRI was requested, revealing closed ring and target lesions in the left parietal lobe, prompting consideration of infectious etiologies . Subsequent lumbar puncture yielded normal cerebrospinal fluid (CSF) biochemistry results (WBC: 0, RBC: 2, glucose: 69 mg/dL, and protein: 16 mg/dL). Additional studies on CSF, including tuberculosis, brucella, cryptococcus, wright, coombs wright, venereal disease research laboratory, and angiotensin‐converting enzyme, were negative. Moreover, CSF cytologic assessments did not reveal any signs of malignant cells. Patient had anemia and lymphopnia on complete blood count assessment (Hb: 9.2 gr/dL, WBC: 4.4 × 10 3 /μL, lymphocyte: 12.7%, and neutrophil: 84.3%). Further laboratory examinations, including renal and liver function tests, erythrocyte sedimentation rate, C‐reactive protein, blood sugar, arterial blood gas, toxoplasmosis, JC virus, urine analysis, urine culture, stool exam, stool culture, and serum electrolytes, did not yield any pathologic findings. Viral markers, including hepatitis B core antibody, hepatitis B surface antigen, hepatitis C virus antibody, and human immunodeficiency virus antibody, were nonreactive. Additional abdominopelvic CT scan was performed to assess any signs of malignancy or metastases, which did not reveal any pathologic findings.
| 3.994141 | 0.961914 |
sec[2]/p[0]
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en
| 0.999995 |
39109309
|
https://doi.org/10.1002/ccr3.9266
|
With infectious causes ruled out, fingolimod‐induced BCS emerged as the leading diagnosis. As the BCS could be caused by fingolimod, the drug was discontinued, and 1 g/day of IV methylprednisolone was administered for 5 days, resulting in improved limb strength by the fifth day of corticosteroid therapy. Subsequently, rituximab was initiated 15 days after fingolimod cessation. We followed the patient monthly and she exhibited improvement in symptoms, with the absence of any new focal neurological deficits noted during 8‐month follow‐up assessments.
| 3.792969 | 0.971191 |
sec[3]/p[0]
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en
| 0.999998 |
39109309
|
https://doi.org/10.1002/ccr3.9266
|
In this case report, we describe a young patient diagnosed with MS who had been under treatment with fingolimod for 3 years. The patient presented to our clinic exhibiting symptoms of hemiparesis, and upon examination, we detected a Balo‐like lesion in her MRI scan without any symptomatic indications of infection.
| 3.15625 | 0.989258 |
sec[4]/p[0]
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en
| 0.999998 |
39109309
|
https://doi.org/10.1002/ccr3.9266
|
The case described herein involves a known MS patient who had been undergoing fingolimod therapy for 3 years preceding the identification of a Balo‐like lesion on MRI. A comprehensive diagnostic evaluation excluded alternative diagnoses mimicking Balo‐like lesions, including intracranial neoplasms and infectious etiologies. There is a growing body of literature suggesting a possible association between fingolimod therapy and the development of new TDLs in MS patients, 7 , 13 , 25 In a study by Baghbanian et al., a 32‐year‐old MS patient receiving fingolimod treatment who acquired Balo‐like lesions was described. She had symptoms such as fatigue, uncontrolled crying, and paralysis of the left side, but testing revealed no indication of cancer or metastases. The patient responded dramatically to corticosteroid pulse therapy. 7 Nevertheless, reports of Balo‐like lesion development in MS patients receiving fingolimod remain largely anecdotal. Furthermore, while BCS is usually considered to be a precursor to MS, the occurrence of new BCS lesions in MS patients undergoing fingolimod therapy is unusual. 26 It is unclear whether the development of a Balo‐like lesion in this case is associated with a new MS attack or the use of fingolimod. However, the possibility of an association between new BCS and fingolimod use needs further investigation.
| 4.199219 | 0.888184 |
sec[4]/p[5]
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en
| 0.999996 |
39109309
|
https://doi.org/10.1002/ccr3.9266
|
The patient was a male infant aged six months and 10 days, delivered via the high route on a scarred uterus, with a normal birth weight of 3700 g, no neonatal distress, no known maternal-fetal infections during pregnancy, and exclusive breastfeeding. At the age of five months, he presented with feeding difficulties and vomiting, indicating an inability to achieve diversification. He also had chronic constipation. The infant had shown psychomotor regression since the age of four months, which worsened over time with a deterioration in general condition.
| 3.066406 | 0.990234 |
sec[1]/p[0]
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en
| 0.999998 |
39109106
|
https://doi.org/10.7759/cureus.64000
|
Clinical examination revealed a pale, hypotonic, hyporeactive infant with delayed stature-weight development. The weight and height were below the second percentile, with a normal voiding. On neurological examination, he showed generalized hypotonia with symmetrical osteotendinous reflexes. Contact was poor, with no smile-response or eye pursuit. He could not hold his head, and the sitting position had not yet been acquired.
| 3.322266 | 0.986816 |
sec[1]/p[1]
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en
| 0.999997 |
39109106
|
https://doi.org/10.7759/cureus.64000
|
The patient underwent an initial biological assessment revealing bicytopenia: macrocytic hypochromic anemia at 7.1, along with neutropenia at 460/uL; white blood cells and platelets were within normal range. As for the biological signs of malnutrition, albumin level was normal at 47 g/l with a correct protein level at 70 g/l. He also had a low prothrombin time (PT) of 57% (exclusively breast-fed infant, not supplemented with vitamin K), and the rest of his liver work-up was normal. A thyroid workup was performed, with no particular findings, and IgA anti-transglutaminase antibodies were normal. A vitamin assay confirmed severe vitamin B12 deficiency at 69 pg/ml, associated with elevated homocysteinemia at 53 umol/l. A maternal workup showed vitamin B12 deficiency at 149 pg/ml (Table 1 ). In the context of investigating Biermer's disease, the measurement of anti-intrinsic factor antibodies was performed and returned normal.
| 4.023438 | 0.966797 |
sec[1]/p[2]
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en
| 0.999997 |
39109106
|
https://doi.org/10.7759/cureus.64000
|
A bone marrow aspiration was performed to rule out a neoplastic origin . It revealed numerous megakaryocytes, sometimes dysplastic, with cellular gigantism: megaloblasts and giant metamyelocytes, a cytological appearance pointing to an anti-megaloblastic vitamin deficiency (vitamins B12 and B9). A cerebral MRI revealed bilateral frontoparietal cortical atrophy, with enlargement of the lateral ventricles and cortical sulci . Substitutive treatment with vitamin B12 supplementation was initiated with intramuscular injections of 1 mg/day for eight days, then 1 mg/week for one month, then 1 mg/month. Only one presentation of hydroxycobalamin is available on the Moroccan market, in the form of ampoules containing 5000 ug.
| 3.927734 | 0.912109 |
sec[1]/p[3]
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en
| 0.999996 |
39109106
|
https://doi.org/10.7759/cureus.64000
|
Vitamin B12 deficiency should be suspected in infants showing psychomotor regression, associated with anemia and stagnation of weight and height. Our patient presented with an identical clinically evident presentation and showed significant improvement in clinical, hematological, and neurological aspects from the start of the treatment. Follow-up was conducted regularly and consistently maintained for several months to ensure normal neurological development and growth of the child.
| 3.337891 | 0.956055 |
sec[3]/p[0]
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en
| 0.999998 |
39109106
|
https://doi.org/10.7759/cureus.64000
|
In light of these suspected neurocardiogenic links with vaccination, we present a unique case, a 40-year-old South Asian woman who developed symptoms suggestive of POTS one week post-dTdap booster vaccination.
| 3.058594 | 0.975586 |
sec[0]/p[2]
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en
| 0.999997 |
39109119
|
https://doi.org/10.7759/cureus.64008
|
A 40-year-old South Asian woman with an unremarkable medical history presented to the emergency department with a one-week history of recurrent presyncope and syncope. The presyncope episodes manifested as prodromal faintness, lightheadedness, and dizziness. Syncopal events were fleeting and devoid of any ictal features. The patient reported experiencing in excess of 10 episodes of both presyncope and syncope daily. She did not report any antecedent infection or recent ill contacts upon evaluation. The patient denied head trauma, current prescription, complementary and alternative medication use, having pets, or pertinent travel history. She maintained her usual dietary intake and physical activity levels, with no lifestyle modifications preceding the onset of symptoms. She also reported being physically active before the development of symptoms and exercising regularly. Notably, the patient received a dTdap booster vaccination one week prior to the emergence of the symptom complex. Historically, she also completed a two-dose series, including a subsequent booster of the COVID-19 vaccine, approximately 15 months earlier. COVID-19 polymerase chain reaction testing performed upon presentation returned a negative result.
| 3.916016 | 0.982422 |
sec[1]/p[0]
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en
| 0.999997 |
39109119
|
https://doi.org/10.7759/cureus.64008
|
The initial evaluation revealed the following vital signs: a blood pressure of 112/57 mmHg, a heart rate of 110 beats per minute (bpm), and oxygen saturation of 99% on room air. The patient was afebrile and had a body mass index of 26.5 kg/m². Neurological examination demonstrated an alert and oriented patient with no focal deficits. Cardiopulmonary auscultation revealed normal heart sounds and vesicular breath sounds bilaterally. Peripheral edema was absent. An extensive workup, including a two-dimensional transthoracic echocardiogram, brain computed tomography, magnetic resonance imaging with angiography, and 24-hour ambulatory electroencephalogram, were all unremarkable and did not reveal any significant abnormalities. The 72-hour Holter did demonstrate persistent sinus tachycardia and head-up tilt-table testing confirmed POTS . Following a passive head-up tilt-table testing, the patient’s heart rate increased by >30 bpm to a maximum of 144 bpm, clinching the diagnostic criteria for POTS. The patient’s heart rate returned to baseline upon returning to a prone position. The patient did not experience significant blood pressure changes or symptoms during the tilt-table testing despite the administration of isosorbide dinitrate at a 70-degree tilt angle.
| 3.908203 | 0.977051 |
sec[1]/p[1]
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en
| 0.999994 |
39109119
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https://doi.org/10.7759/cureus.64008
|
The patient’s three-day hospitalization course included the initiation of a pharmacotherapeutic regimen for POTS. She received fludrocortisone 0.1 mg orally every eight hours and ivabradine 2.5 mg every 12 hours. In addition, she was counseled on lifestyle modifications to optimize her circulatory status and mitigate symptoms. These recommendations included increased dietary sodium and fluid intake, sun exposure minimization to prevent dehydration, and participation in a graded moderate-intensity exercise program. The patient demonstrated a progressive clinical response, and her constellation of symptoms, including exercise intolerance and fatigue, gradually improved. The frequency of syncopal episodes subsequently decreased on consecutive days, ultimately resolving by discharge. At a one-month follow-up appointment, the patient’s cardiovascular medications were successfully de-escalated to low-dose fludrocortisone and ivabradine once daily. She reported no interval serious adverse events (SAEs).
| 3.746094 | 0.972656 |
sec[1]/p[2]
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en
| 0.999994 |
39109119
|
https://doi.org/10.7759/cureus.64008
|
Tetanus toxoid is a vaccine approved by the Food and Drug Administration (FDA) to prevent tetanus, which can be combined with other vaccines. It targets the neurotoxin tetanospasmin, which inhibits the release of a key inhibitory neurotransmitter, leading to uncontrolled muscle contractions and spasms . Adverse events following immunization (AEFI) include any untoward medical occurrences post-vaccination that do not necessarily imply causation. Tetanus toxoid vaccination demonstrates a favorable safety profile, with most symptoms categorized as mild and localized and include pain, erythema, and induration at the injection site, typically resolving within 48 hours. Although less frequent, systemic reactions may encompass low-grade fever, headache, fatigue, and nausea, which are also transient . Some life-threatening AEFIs include anaphylaxis, Guillain-Barré syndrome (GBS), and thrombosis with thrombocytopenia syndrome (TTS), which can result in protracted morbidity and be fatal . A case report previously documented extreme cachexia (wasting syndrome) associated with severe dysautonomia, potentially stemming from autoimmune/inflammatory syndrome induced by adjuvants (ASIA) syndrome triggered by the Tdap vaccine . However, this current discussion focuses on a case of suspected POTS following dTdap booster vaccination.
| 4.402344 | 0.432617 |
sec[2]/p[0]
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en
| 0.999996 |
39109119
|
https://doi.org/10.7759/cureus.64008
|
This case presentation highlights a possible association between dTdap booster vaccination and the subsequent development of POTS in a 40-year-old female patient. The temporal relationship between vaccination and symptom onset, confirmed diagnosis via tilt table testing, absence of alternative etiologies, and concordance with typical POTS demographics strengthen the argument for a vaccine-adverse event (VAE). Reporting this case to the Vaccine Adverse Event Reporting System (VAERS) contributes to ongoing vaccine safety surveillance.
| 3.964844 | 0.955078 |
sec[2]/p[4]
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| 0.999997 |
39109119
|
https://doi.org/10.7759/cureus.64008
|
In this report, we presented a case of a 40-year-old South Asian woman who developed symptoms consistent with POTS one week following a dTdap booster vaccination. The patient’s clinical presentation and diagnostic workup confirmed POTS, which responded favorably to a treatment regimen of fludrocortisone and ivabradine. This case presentation contributes to the emerging literature exploring AEFI and VAEs associated with dTdap vaccination.
| 3.947266 | 0.973633 |
sec[3]/p[0]
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en
| 0.999996 |
39109119
|
https://doi.org/10.7759/cureus.64008
|
A 4-year-old boy (patient 1) presented with CMC-associated recurring oral candidiasis and candida-associated paronychia since infancy, body-wide scaly seborrheic eczemas that extended to the eyelids, and a dystrophic growth of both thumbnails due to a chronic inflammation of the nail folds . His 14-month-old brother (patient 2) developed a severe oral thrush 3 months later . In 1991, 28 years earlier, their father (patient 3) developed a SAA when he was 4 years old. At that time, his white blood cell count was 3.6 × 10 9 /L (age-adjusted normal range, 4.1 to 14.6 × 10 9 /L) with an absolute neutrophil count of 324 × 10 6 /L (normal, 200 × 10 6 /L) and a red blood cell count of 1.08 × 10 12 /L (normal, 3.98 to 5.33 × 10 9 /L). His hemoglobin was 3.6 g/dL (normal, 10.7 g/dL to 14.2 g/dL) and his platelets were 10 × 10 9 /L (normal, 168 to 453 × 10 9 /L) ( 32 ). Eleven months earlier, he had a hepatitis A infection; 6 months earlier, a bronchitis; and 2 months, earlier a whooping cough. When he was 3 years old, he had developed a mild psoriasis-like seborrheic eczema but none of the more specific CMC signs. The patient became transfusion-dependent 2 months after first presentation and was, therefore, treated unsuccessfully with high-dose corticosteroids and anti-lymphocyte globulin. Six months later, he was transplanted with cord blood cells from his newly born brother. The conditioning consisted of cyclophosphamide at 200 mg/kg and 5 Gy of total nodal irradiation and the graft-versus-host prophylaxis of ciclosporin A and methotrexate. Stem cell engraftment was delayed, but, following G-CSF treatment, his white blood cell count rose over 1.0 × 10 3 /µL on day +39. He received his last platelet transfusion on day +40 and the last unit of packed red blood cells on day +47. Since then, the now 37-year-old father has normal blood cell counts, had never experienced any CMC symptoms, and remained healthy. Also, the clinical course of the two affected boys is so far benign. They require only occasionally symptomatic antifungal treatment. Fluorescence activated cell sorting (FACS) analyses of peripheral blood mononuclear cells of the two brothers and their transplanted father revealed a normal distribution of lymphocyte subpopulations. Their levels of immunoglobulins and immunoglobulin G (IgG) subclasses were normal and none of them had developed autoantibodies or endocrine deficiencies.
| 4.152344 | 0.959473 |
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en
| 0.999999 |
39114664
|
https://doi.org/10.3389/fimmu.2024.1430938
|
In addition to these two cases and the one presented herein, only three other STAT1 -associated CMC cases with SAA and one with a PRCA were reported ( Table 1 ) ( 13 – 16 ). The first of these concerns a 10-year-old girl who originally suffered from a life-threatening Evans syndrome with episodes of AIHA and ITP (case 3, Table 1 ) ( 16 ). Later on, she developed a SAA together with a suspected macrophage activation syndrome. She was treated with steroids, intravenous immunoglobulins, the anti-CD20 antibody rituximab, the anti-complement C5 antibody eculizumab, and, thereafter, with anti-thymocyte globulin and ciclosporin A. Only the latter restored her bone marrow function to some extent but did not produce a complete remission. Following the detection of a STAT1 GOF pathogenic variant and the subsequent meticulous in vitro assessment of its functional consequences, she received the JAK1/2 inhibitor ruxolitinib. Continuous treatment with this inhibitor alone resolved all her autoimmune-mediated problems, and she was reported to be still in complete remission 18 months later.
| 4.085938 | 0.556641 |
sec[3]/p[2]
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| 0.999998 |
39114664
|
https://doi.org/10.3389/fimmu.2024.1430938
|
The second case concerns an 18-year-old man with oral ulcers and CMC who developed SAA with an only moderately decreased number of platelets, but weekly transfusion-dependent anemia and several episodes of febrile neutropenia (case 4, Table 1 ) ( 15 ). He was treated with the JAK1 inhibitor itacitinib for 20 months without any adverse effects that resulted in a rapid and remarkable recovery of hematopoiesis, before he self-discontinued this treatment. Three years after initial presentation and approximately 12 months off itacitinib therapy, he was still in continuous hematologic remission. Based on the discovery and insight that a significant proportion of other patients with “idiopathic” forms of SAA share similar STAT1-mediated pathophysiologic changes, the authors were the first to suggest that such “idiopathic” cases might also benefit from treatment with JAK inhibitors in a similar manner.
| 4.128906 | 0.896973 |
sec[3]/p[3]
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en
| 0.999996 |
39114664
|
https://doi.org/10.3389/fimmu.2024.1430938
|
Because PRCA and SAA are BMF syndromes with a closely related etiology, we also include the girl with CMC and a PRCA (case 6, Table 1 ) ( 14 ). With 1 year, she already suffered from a systemic lupus erythematosus before she developed CMC-typical infections and eventually PRCA with 8 years. Because conventional immunosuppressive therapies were not effective, she received the JAK inhibitor ruxolitinib and was transplanted after she had transiently improved but succumbed to transplant-related complications.
| 3.591797 | 0.876953 |
sec[3]/p[5]
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en
| 0.999997 |
39114664
|
https://doi.org/10.3389/fimmu.2024.1430938
|
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