Hyponatremia in Empty Sella Syndrome: Is it a Covid Sequelae?

The symptoms associated with empty sella syndrome (ESS) include headache, giddiness, vomiting, visual field deficits, and endocrine problems, as well as the radiological appearance of an enlarged sella turcica. This case report highlights a 45-year-old female who had a COVID-19 infection 2 months back and presented with chronic headache, giddiness, and lethargy having persistent hyponatremia later diagnosed as empty sella syndrome on brain magnetic resonance imaging. In this case, we tried to correlate all of these clinical and radiological features as COVID-19 sequelae due to post-Covid hypothalamic-pituitary axis dysfunction.Copyright © 2023 Authors. All rights reserved.

A Case of Membranous Nephropathy Post SARS-CoV-2 Vaccination

Introduction: Emergency use authorization and mass vaccination programs worldwide have lowered the burden of the COVID-19 pandemic. Vaccine complications not previously seen in clinical studies continue to manifest. We present a case of membranous nephropathy (MN) following the SARS-CoV-2 vaccination with successful treatment. Case Description: Our patient is a 58-year-old woman with past medical history of hypothyroidism seen at a nephrology clinic for evaluation of new onset symptoms of dyspnea, severe bilateral pedal edema, and proximal muscle weakness for 4 months. The patient had 3+ proteinuria and microscopic hematuria on urinalysis obtained by primary care provider. She also had a rapid decline in serum albumin to 2.2 g/dL and new onset hypercholesteremia at 415 mg/dL. Before initial presentation, she had normal labs and no symptoms. Upon presentation to our nephrology clinic, the patient had proteinuria of 2,360 mg/day on a 24-hour urine collection, random urine protein-to-creatinine ratio (UPCR) of 5,459 mg/g and random urine albumin-to-creatinine ratio (UACR) of 3,539 mg/g. She had no risk factors for chronic kidney disease. The only recent change in the health management of the patient was the administration of two doses of the SARS-CoV-2 vaccine several weeks prior to presenting with her initial symptoms 4 months ago. The phospholipase A2 receptor (PLA2R) antibody was elevated at 287 IU/mL. Serological tests for other sources of proteinuria were negative. Renal biopsy performed was consistent with primary MN. The patient was started on rituximab infusion given 2 weeks apart based on Mentor Trial. Additional treatment included apixaban, sulfamethoxazole/ trimethoprim DS, losartan, and L-carnitine. After two doses of rituximab, she had resolution of dyspnea, pedal edema and muscle weakness. Repeat labs revealed UPCR to 1000 mg/g, UACR to 629 mg/g, improvement of PLA2R to 8 IU/mL. Our patient achieved immunological remission and partial clinical remission. Discussion(s): This case illustrates a potential association of the SARS-CoV-2 vaccination and autoimmune mimicry leading to MN. We hope that this will help clinicians become aware of a potential complication not widely recognized and an effective management strategy. We hope further investigations of this possible association are performed as more cases are discovered.

Can COVID-19 Vaccination Be the Culprit for New-Onset Crescentic Glomerulonephritis? The Correlation vs. Causation Conundrum

Introduction: While the development, delivery, and implementation of the mRNA vaccines have been spectacular, consideration for potential rare side effects on organ systems was not clear. Although emergency use authorization trials of these vaccines in the USA did not demonstrate major safety concerns, unique side effects after massscale vaccination are now being reported more frequently. Here, we describe a case of new-onset crescentic & sclerosing GN with linear basement membrane staining for IgG, kappa, and lambda by Immunofluorescence in a 30-yo healthy female three days after receiving her Tozinameran (Pfizer-BioNTech) booster vaccine. Case Description: 30 y/o Caucasian female with no PMH presented with a CC of gross hematuria 3 days after receiving her booster of Tozinameran. Retrospectively reported symptoms of pedal edema, generalized athralgia, tinnitus, and paresthesia of lower limbs. UA revealed dysmorphic RBCs and proteinuria. CT urethrogram, & cystoscopy revealed left hydronephrosis, no nephrolithiasis or urothelial lesions. Kidney biopsy revealed crescentic & sclerosis GN, with linear GBM staining for IgG, Kappa, & Lambda on IF. Several glomeruli showed segmental scars & fibrous crescents in addition to focal cellular crescents of varying ages raising the possibility of concurrent ANCA vasculitis. Her GBM antibody was 25. Additional workup of ANCA, PLA2R, PR3, ana, c3/c4 levels, dsDNA, and hepatitis studies returned negative. On admission, BP was 175/103, and HR 104. Labs were notable for hemoglobin 13.3, WBC 16.6k, & BUN/creatinine 16/1.5. The PE was unremarkable. She received pulse IV steroid therapy, cyclophosphamide, Lupron, and daily plasma exchange (PLEX) for 5 days until her GBM antibody cleared. She responded well to treatment. Her renal function improved, and she was discharged without requiring dialysis. Discussion(s): Our case demonstrates a possible correlation & causation scenario after receiving a Tozinameran booster shot activating anti-GBM disease with concurrent ANCA-negative vasculitis demonstrated by kidney biopsy. Although the mechanism of de novo anti-GBM disease & ANCA-negative vasculitis post-SARS-CoV-2 vaccine remains to be explained, pharmacovigilance is vital in our efforts to ascertain answers.

Severe progression of autoimmune hepatitis in a young COVID-19 adult patient: A case report

Rationale: The impact of COVID-19 in patients with autoimmune liver disease treated with immunosuppressive therapy has not been described so far. This case report describes the clinical course of a patient with autoimmune hepatitis (AIH) who developed COVID-19 and the features of cytokine syndrome leading to its deterioration in our intensive care unit. Patient's Concern: A 28-year-old male presented with generalized anasarca for two weeks and chronic liver disease for 8 months. Diagnosis: AIH and Covid-19 with features of cytokine storm syndrome. Interventions: Intravenous furosemide, mannitol, syrup lactulose, steroids (prednisolone 40 mg), azathioprine 1 mg/kg body weight, rifaximin, vitamin K, and blood products. Outcomes: The patient had hepatic encephalopathy and AIH and died on the 10th day after admission despite ventilatory support, sustained low-efficiency hemodialysis, and resuscition. Lessons: The dramatic release of cytokines and the inflammatory-immune responses not only alter the pathophysiology but also affects the onset and severity of disease progression in patients with AIH.

CLINICAL, LABORATORY PROFILE, TREATMENT AND OUTCOME OF PRIMARY AMYLOIDOSIS IN THE ERA OF NOVEL AGENTS: AN EXPERIENCE FROM A TERTIARY CARE HOSPITAL IN INDIA

Background: Diagnosis of AL amyloidosis requires demonstration of amyloid in affected tissues along with clonal plasma cells in bone marrow or presence of monoclonal light chains in blood. With increasing awareness among physicians and availability of proper diagnostics, more cases of AL amyloidosis are being diagnosed. Here we present our experience of AL amyloidosis diagnosis and treatment in the era of modern diagnostics and therapy with novel agents. Aims: We aimed to describe the clinical presentations, laboratory features and outcomes of patients with AL amyloidosis in a single center using standard diagnostic tests and treatment with novel agents. Methods: A retrospective analysis of AL amyloidosis patients, diagnosed in our hospital, a tertiary care center in India from January 2016 to December 2021. The data was collected from departmental database. All statistical analyses were done by SPSS version 17. Results: Diagnosis of AL amyloidosis was done in 27 patients. Median age of presentation was 59 years. 22 (81.5%) were males. Major symptoms were pedal edema (37%), shortness of breath (22.2%), frothy urine (11.1%) and fatigue (11.1%). Twenty two (81.5%) presented with ECOG PS ≥ 2. Most common system involved was renal in 16 (59.2%), followed by cardiac in 13 (48.1%) and gastro-intestinal in 9 (33.3%). Fifteen (55.6%) had two or more system involvement while 12 (44.4%) had single system involvement. Lambda monoclonal light chain was present in 22/27 (81.5%) and kappa monoclonal light chain was present in 5/27 (18.5%). Median Hb was 11.6 g/dl (range 6.7- 14.8 g/dl), median M-protein was 0.69 g/dL (range 0-2 g/dL) and median bone marrow plasma cells were 7% (range- 1-18%). Fourteen patients were treated;cyclophosphamide, bortezomib and dexamethasone (CyBORD) in 10/14 (71.4%) and bortezomib + dexamethasone in 4/14 (28.6%). Among 14 patients followed up with median follow up of 13 months (range 6-60 months), 5 expired;3 due to COVID, one due to cardiac arrhythmia (during first cycle) and one due to relapse and rest 9 were alive. Among the 9 patients who were alive 6 were in complete hematological response and 3 were in partial response after 6 cycles of therapy. Summary/Conclusion: Our study presents the spectrum of clinical manifestations, management and outcomes of primary amyloidosis in Indian context. There is a need to increase the awareness among the physicians about amyloidosis so that early diagnosis can be made and timely treatment can be done with novel agents to improve the dismal historical results.

SLE ONSET POST COVID-19 VACCINATION: COINCIDENTAL or ASSOCIATION?

Background: Numerous immune-mediated diseases fare or new disease onset after SARS-CoV2-vaccination have been reported. There were case reports showed the immune-mediated disease fare post vaccination but study on new disease occurs post Covid-19 vaccination is still lacking. Objectives: To describe two SLE cases that diagnosed post Covid-19 vaccination. Methods: Case report Results: 14 years old girl, post Covid-19 vaccination 1st dose 3 weeks ago presented with 2 day history of giddiness, breathlessness, vomiting and diarrhea prior to admission. She also complained of frothy urine for the past 1 week associated with lower limbs swelling and facial puffiness. Clinical examination noted she had sparse hair, oral ulcers and discoid lupus at the ear concha. She also noted to have periorbital puffiness with pedal edema. Lung auscultation noted bi-basal crepitations. Blood investigation noted ANA positive (1:640, speckled) with low complement 3 (0.1g/L). Her full blood count showed leucopenia (3100 UL) with low lymphocyte count of 810UL. UFEME noted protein of 3 + and red blood cell of 2+ with normal renal profile. Her serum albumin was 22g/L. Chest x ray showed clear lung field with no cardiomegaly. Her 24-hour urine protein showed proteinuria of 2.345g/dl and her renal biopsy showed mesangial proliferative lupus nephritis class iI. She was given intravenous methyl-prednisolone 500mg OD for 3 days and discharged with tapering dose of prednisolone, hydroxychloroquine, calcium supplements, perindopril and frusemide. Another case was a 17 year-old female, post covid-19 vaccination 10 weeks, presented with 3 weeks history of bilateral lower limbs weakness with difficulty in getting up from chair. She also had fever on and off with cough for 1 week. There was no alopecia, oral ulcer, facial rash or photosensitivity. No joints pain. Clinical examination noted presence of proximal myopathy with stable vital signs. Other systemic examinations were unremarkable. Blood investigation noted ANA positive (1: 640, homogenous and speckled) with low complements level (C3 0.19g/L and C4 0.049 g/L).Her creatine kinase was 2367U/L and EMG showed evidence of irritable myopathic process which is consistent with inflammatory myositis. Her TFT was normal. Myositis panel showed anti-Ku and anti-Ro 52 were positive. She was treated as SLE with myositis and intravenous methylprednisolone was given. She discharge well with tapering dose of prednisolone and azathioprine. Her creatine kinase showed improvement with immunosuppression therapy and she was advised on intensive physiotherapy. Conclusion: The onset of these two SLE cases were occurred within the 2 month of post covid-19 vaccination. Whether Covid-19 vaccination direct contribute to the occurrence of SLE remained inconclusive. More studies are required to show its correlation between onset of SLE and Covid-19 vaccination.

Coronavirus-2019 Disease with Pancytopenia with Leptospirosis and Herpes Simplex Virus Co-infection

Aim and background: COVID-19 pandemic has affected the whole world. Besides COVID, many infections may emerge during the course of the disease. Lymphopenia, use of immunosuppressants underlying comorbidities, and immune dysregulation secondary to SARS-CoV-2 could be the likely cause of the emergence such infections. We hereby describe a case of COVID-19 disease which presented with pancytopenia and was found to have Leptospirosis and Herpes Simplex Virus co-infection. Case summary: A 23-yearold postpartum female with no comorbidities and uneventful obstetric history was referred to our hospital 2 weeks after a full-term normal vaginal delivery. She developed generalized convulsive status epilepticus on the 10th day of her delivery, which was managed elsewhere with anti-epileptic drugs (AEDs). During her hospital stay, RTPCR for COVID-19 turned out to be positive but she remained asymptomatic throughout the course of her illness and seizures remained well-controlled on AEDs. On admission to our hospital, she was fully conscious, alert with no focal neurological deficits. Notable findings on evaluation were pancytopenia with megaloblastic features, bilateral pedal edema, and hepatosplenomegaly. NCCT brain was done which was suggestive of subarachnoid hemorrhage (SAH) along bilateral parietooccipital region for which conservative management was planned. 2D echocardiography was normal. Ultrasonography of abdomen revealed gross splenomegaly and mild hepatomegaly with mesenteric lymphadenopathy. NCCT thorax and abdomen were unremarkable apart from hepatosplenomegaly. In the panel sent for pancytopenia workup, IgM anti-HSV 1 antibodies turned out to be positive in blood. In addition, tropical workup was suggestive of Leptospirosis (IgM antibodies were positive). Workup for tuberculosis was negative. Bone marrow workup revealed features of trilineage hematopoiesis with micronormoblastic maturation consistent with iron deficiency anemia with no evidence of hemophagocytosis. Subsequently, IV acyclovir, IV doxycycline, and iron replacement were added. She improved clinically after these therapies and was subsequently discharged in a stable condition. MRI brain with MR angiography and venography done before discharge showed T1 sulcal hyperintensities along bilateral parietooccipital regions suggestive of SAH which was not progressing (as compared to NCCT brain scan done at admission). On day 60 of telephonic follow-up, patient was doing well and leading normal life without any persistence or emergence of symptoms.

A Case Report of Coronavirus (COVID-19) Disease and Herpesviridae Viral Co-Infections: A Lethal Combination? ABS0138)

Introduction: COVID-19 pandemic has affected the whole world. Besides COVID, other viral infections may emerge during the course of the disease owing to lymphopenia, use of immunosuppressants, underlying comorbidities, and immune dysregulation, which may pose additional threats.1 We hereby describe two cases of COVID- 19 with viral co-infections belonging to the Herpesviridae family with undulating clinical course. Case 1: Cytomegalovirus (CMV) Co-infection: A 55-year-old male, COVID unvaccinated, chronic smoker, overweight and hypertensive was admitted to our ICU with a 1-week history of fever, cough, and breathlessness. SARSCoV- 2 reverse transcriptase-polymerase chain reaction (RT-PCR) test was positive. At admission, he had hypoxaemia (SpO2 86%on room air), respiratory rate 35-40/minute, and ground-glass opacities in chest X-ray involving 50% of bilateral lung parenchyma suggestive of severe COVID-19 pneumonia. He was managed with lung-protective invasive mechanical ventilation, restrictive fluid strategy, 16-18 hour/day proning sessions (4-5), intravenous (IV) remdesivir, IV dexamethasone 6 mg 12 hourly, and enoxaparin thromboprophylaxis. After 2 weeks of ICU stay, weaning was attempted but the weaning attempts failed due to underlying neuromuscular weakness. On examination, bilateral (B/L) cranial nerve palsies, areflexia, and motor power 0/5 in bilateral upper and lower limbs were noticed. possibility of Guillain-Barre syndrome (GBS) was kept and IV immunoglobulin therapy was empirically administered for 5 days with some improvement in power up to 1/5 in upper limbs. On day 35 of hospitalization, he developed pancytopenia along with features of deranged liver function and gut dysfunction. In evaluation, PCR for CMV turned out to be positive in blood. Bone marrow aspiration and biopsy showed hemopoiesis with viral inclusion bodies and hemophagocytosis (HLH) [Figs 1 and 2]. A diagnosis of secondary HLH related to CMV was contemplated and IV ganciclovir was initiated along with steroids. Histological evidence of CMV co-infection was present and moreover, the quantitative viral load of CMV showed a decreasing trend after initiating IV gancyclovir. However, the patient continued to deteriorate and succumbed to his illness in the 8th week of the ICU stay. Case 2: Herpes Simplex Virus (HSV) Co-infection: Twenty-three years postpartum female with no comorbidities and uneventful obstetric history was referred to our hospital two weeks after a full-term normal vaginal delivery. She developed generalized status epilepticus on the 10th day of delivery, which was managed with anti-epileptic drugs (AEDs). During the hospital stay, RTPCR for COVID-19 turned out to be positive but she remained asymptomatic and seizures were well-controlled on AEDs. On admission to our hospital, she was fully conscious and alert with no neurological deficits. Notable findings were pancytopenia with megaloblastic features, B/L pedal edema, and hepatosplenomegaly. NCCT brain revealed mild subarachnoid hemorrhage (SAH) along the bilateral parietooccipital region for which conservative management was planned. 2D echocardiography was normal. Ultrasonography of the abdomen showed gross splenomegaly and mild hepatomegaly with mesenteric lymphadenopathy. NCCT thorax and abdomen were unremarkable apart from hepatosplenomegaly. In pancytopenia workup, IgM anti-HSV-1 antibodies turned out to be positive in blood. In addition, tropical workup was suggestive of Leptospirosis (IgM antibodies positive). Serological evidence was suggestive of acute HSV-1 infection (based on antibody titers). Bone marrow workup had features of trilineage hematopoiesis with micronormoblastic maturation consistent with iron deficiency anemia without any evidence of hemophagocytosis. IV acyclovir, IV doxycycline, and iron replacement were added, after which she improved clinically and was discharged in stable condition. Tables 1 and 2 show a detailed description of these cases. Discussion: Herpesviridae family is the most important group of viruses responsible for persistent vi al infections in humans, of which CMV contributes to 60-90% of infections in adults, especially in developing countries.2 In healthy individuals, these viruses are kept dormant by the body's immune mechanisms but in an immunocompromised population, reactivation from the latent state can occur. SARS-CoV-2 infection predisposes patients to concomitant viral co-infections, owing to T-cell lymphopenia, decreased NK cell number, and use of immunosuppressive medications.3,4 The first case of CMV co-infection was first reported by D'Ardes and co-workers in 2020.5 Since then, many studies have been emerging in this area. In an observational study from France, 38 COVID-19 patients on >7 days of MV were studied for HSV and CMV pulmonary co-infections (by quantitative real-time PCR in tracheal samples) out of which 47% of patients had one of these infections (24% HSV, 5% CMV, 18% both).6 Another study looking for HSV-1 in patients on invasive MV found HSV-1 reactivation between days 11 and 40, which correlated with immunological markers of decreased innate immunity.7 A case series looking for CMV infection (by PCR in plasma or BAL) in COVID-19, also found CMV reactivation between day 7 and 45 of illness. Most of these patients were above 60 years of age and immunosuppressed (HIV, diabetes mellitus, medications).8 Although immunocompromised individuals are more vulnerable, healthy immunocompetent adults who are critically ill or on prolonged MV may also be susceptible to these infections.9-12 This may be explained by a state of immunoparalysis inherent to prolonged critical illness. In case 1, an ICU stay of around 9 weeks complicated with recurrent nosocomial infections, multiple blood product transfusions, and steroid usage could have the likely triggers. Whether viral co-infections are merely bystanders or truly pathogenic is difficult to comment but timely management is essential to avoid end-organ damage (EOD) which may occur directly (by enhanced viral load secondary to compromised host immunity) or indirectly (by inflammatory changes consequent to prolonged cell-mediated immunity required to maintain viral dormancy).2-4,13 It also seems imperative to study if a viral co-infection has a proclivity to develop more severe hematological anomalies (besides the inherent risk of HLH with COVID) as was seen in case 1, in which the patient had a downward spiral of illness with multiorgan dysfunction.14-15 Limitations: Dynamics of PCR trends and virology studies of samples from trachea, gut, and urine could not be analysed in our patients. Conclusion: Viral co-infections can occur in COVID-19 disease as these patients are often immunocompromised and critically ill. A high index of suspicion and prompt management is needed to improve the outcome of patients. Patients with organ dysfunctions especially hematologic abnormalities with bone marrow involvement should be worked up in detail to look for concomitant viral co-infections. In the future, large-scale research is needed to better elucidate the relationship between SARS-CoV-2 and other viral co-infections.

Proteinuria in Thin Basement Membrane Nephropathy: A Rare Finding

Hydrothorax occurs in approximately 2% of patients on peritoneal dialysis caused by migration of fluid from the peritoneal cavity into the pleural space via pleuroperitoneal fistulas. These diaphragmatic defects are usually congenital and right-sided, explaining the predominance of right-sided effusion.. Thoracocentesis with biochemical analysis of pleural fluid reveals a transudate with a very high glucose concentration. In uncertain cases, or when there is a clinical need to demonstrate the anatomy of the communication, an imaging approach such as peritoneal scintigraphy is required. 66-year-old Hispanic female with past medical history significant for end stage kidney disease on peritoneal dialysis for past 5 months, hypertension ,cerebrovascular accident with no residual deficit, and recent exposure to COVID19 presented with fever, shortness of breath, left eye gaze abnormality and + COVID PCR. She had been having issues with meeting ultrafiltration goals outpatient. On examination she has decreased breath sounds at right lung base, Abdomen non-tender with PD catheter in place with clean dressing, no pedal edema. Laboratory findings were consistent with a transudative effusion;no organisms were cultured and no malignant cells were visualized. CT failed to identify dispersal of contrast material into the right hemithorax. A nuclear isotope scan was subsequently done. Following administration of technetium 99m via the PD catheter, a high volume of radioactive dialysate was detected entering the right hemithorax. No tracer activity was seen in the left hemithorax. PD was stopped and switched to intermittent hemodialysis.Unfortunately she succumbed to covid 19 pneumonia and died few days later. 50% of the cases, a conservative approach allows reinstitution of CAPD Conservative approach with temporary cessation of peritoneal dialysis remains the first-line treatment. 1-4 months has been shown to be adequate cessation time and restarting with low volume PD. If conservative approach fails, Invasive approach with video-assisted thoracoscopic pleurodesis or diaphragmatic repair or both allows most of them to continue with CAPD

A Case of Hydrothorax Complicating Peritoneal Dialysis

Hydrothorax occurs in approximately 2% of patients on peritoneal dialysis caused by migration of fluid from the peritoneal cavity into the pleural space via pleuroperitoneal fistulas. These diaphragmatic defects are usually congenital and right-sided, explaining the predominance of right-sided effusion.. Thoracocentesis with biochemical analysis of pleural fluid reveals a transudate with a very high glucose concentration. In uncertain cases, or when there is a clinical need to demonstrate the anatomy of the communication, an imaging approach such as peritoneal scintigraphy is required. 66-year-old Hispanic female with past medical history significant for end stage kidney disease on peritoneal dialysis for past 5 months, hypertension ,cerebrovascular accident with no residual deficit, and recent exposure to COVID19 presented with fever, shortness of breath, left eye gaze abnormality and + COVID PCR. She had been having issues with meeting ultrafiltration goals outpatient. On examination she has decreased breath sounds at right lung base, Abdomen non-tender with PD catheter in place with clean dressing, no pedal edema. Laboratory findings were consistent with a transudative effusion;no organisms were cultured and no malignant cells were visualized. CT failed to identify dispersal of contrast material into the right hemithorax. A nuclear isotope scan was subsequently done. Following administration of technetium 99m via the PD catheter, a high volume of radioactive dialysate was detected entering the right hemithorax. No tracer activity was seen in the left hemithorax. PD was stopped and switched to intermittent hemodialysis.Unfortunately she succumbed to covid 19 pneumonia and died few days later. 50% of the cases, a conservative approach allows reinstitution of CAPD Conservative approach with temporary cessation of peritoneal dialysis remains the first-line treatment. 1-4 months has been shown to be adequate cessation time and restarting with low volume PD. If conservative approach fails, Invasive approach with video-assisted thoracoscopic pleurodesis or diaphragmatic repair or both allows most of them to continue with CAPD

Chronic Eosinophilic Pneumonia - A Challenging Case with Multiple Triggers

Introduction Eosinophilic pneumonia is a class of lung diseases characterized by accumulation of eosinophils in the lung. Chronic eosinophilic pneumonia (CEP) is diagnosed through radiographic imaging and bronchoalveolar lavage (BAL) with elevated eosinophil count (>25%) in the setting of pulmonary symptoms for more than 2 weeks. While CEP is often an idiopathic disease, it may also be caused by medications, illicit substances, or infections. Identifying the trigger is imperative for successful treatment. A 71-year-old man presented with fever and chronic shortness of breath that started after COVID-19 infection (6 months prior to presentation). Medical history was also significant for multiple myeloma, asthma, hypertension, type 2 diabetes, coronary artery disease, chronic kidney disease, and Alzheimer's dementia. Current medications included bortezomib, pomalidomide, aspirin, clopidogrel , donepezil, tramadol and insulin. Lenalidomide was discontinued 3 months prior due to generalized skin rash and high peripheral eosinophilia (19%). On presentation, physical exam revealed mild respiratory distress, bibasilar crackles, and bilateral pedal edema. Long COVID Syndrome was suspected. He was started on antibiotics and diuretics with no improvement. Labs revealed mild peripheral eosinophilia. Chest X-ray showed diffuse bilateral reticular nodular opacities predominantly on the right. CT chest revealed reticulonodular infiltrates in both lungs predominantly in the right upper lobe with small pleural effusion. Bronchoscopy with BAL was negative for infection but revealed 28% eosinophils. Pomalidomide was discontinued and oral prednisone started. Discussion: CEP is part of a group of eosinophilic lung diseases characterized by abnormal accumulation of eosinophils in the lung tissue. Symptoms include dyspnea and cough in the majority of cases, but may also include fever, sinusitis, rhinitis, fatigue and weight loss. The radiographic hallmarks are bilateral alveolar infiltrates peripherally predominantly in the upper lobes and may be ground glass or consolidation. The presence of an elevated eosinophil count (>25%) in a BAL confirms the diagnosis. Though often idiopathic, identification of possible causes is important for proper management. In our case, the patient has multiple risk factors including possible Long COVID Syndrome and malignancy. Medications such as bortezomib, lenalinomide and pomalidomide have been known to cause diffuse lung injury. To the best of our knowledge there is one case report illustrating Lenalinomide related CEP. History of asthma is present in most cases of idiopathic CEP. Our patient had multiple potential triggers for CEP. We suspect that CEP was medication-related in this case. (Figure Presented).

MISDIAGNOSIS OF KIKUCHI-FUJIMOTO DISEASE: THE IMPORTANCE OF TIMELY HISTOPATHOLOGY IN LYMPHADENITIS

Background: Febrile lymphadenopathy not responding to first line antibiotics in a patient hailing from or with a history of travel to tuberculosis endemic countries is often primarily diagnosed as extra-pulmonary tuberculosis. However, histiocytic necrotizing lymphadenitis or Kikuchi-Fujimoto Disease(KFD) presents with similar clinical features. Etiological theories of KFD include viral agents, autoimmunity, and physicochemical factors such as leaking implants. Although KFD has classically been described in young Asian females, recent studies show men and women can be equally affected, with cases increasingly being reported from the USA and Europe as well. Availability bias amongst physicians can lead to misdiagnoses, especially in patients from tuberculosis endemic countries. Objectives: To describe a case of misdiagnosis of KFD in an adolescent. Design/Method: Case report. Results: A 16-year-old male from a tuberculosis endemic country, with a history of asthma, eczema and excision of omental infarct, presented with sub-occipital lymphadenopathy which resolved with antibiotics. Six months later, he complained of tender left cervical lymphadenopathy, associated with fever and fatigue, which lasted for a month. Two courses of antibiotics failed to decrease symptoms. Based on his clinical history, he was started on empirical anti-tubercular medications despite negative tests for tuberculosis. However, his symptoms began to worsen after three weeks of this treatment, and he developed high evening rise of temperature associated with chills, night sweats, frontal headache, pedal edema and generalized pruritic maculopapular rash. Laboratory workups revealed leukopenia (WBC:3830/μL);elevated Erythrocyte sedimentation rate (29 mm/h), C-reactive protein (68.6 mg/dL), Aspartate Aminotransferase(95 U/L) and Alanine Aminotransferase(61 U/L). Rapid antigen test for SARS-CoV2 was negative, and no appreciable levels of SARS-CoV-2 IgG antibodies were detected. Investigations for Tuberculosis, EBV, CMV, Dengue, Malaria, Typhoid, Leptospirosis and Scrub typhus were all negative. Chest X-ray and abdomen ultrasound scan were normal. Histopathological analysis of the excised cervical lymph nodes demonstrated crescentic histiocytes and karyorrhexis in a background of coagulative necrosis. Neutrophils, granulomas and acid-fast bacilli were absent. Immunohistochemistry was positive for CD3, CD20, CD68;and negative for CD15, CD30 and PAX-5. A diagnosis of KFD was made, and patient was given supportive treatment only. His symptoms rapidly resolved within 48 hours, with complete resolution by three months. Conclusion: It is important to raise awareness of KFD, a benign and self-limiting condition with good prognosis, which has many clinical symptoms mimicking grave conditions like extra-pulmonary tuberculosis, SLE and lymphomas. Timely histopathological analysis can help avoid anxiety surrounding a misdiagnosis and adverse reactions due to unnecessary toxic treatments.

A case report of granulomatosis with polyangiitis in a middle aged women

Background: Wegener's granulomatosis (Granulomatosis with polyangiitis) is a rare systemic autoimmune disease of unknown etiology characterised by triad of necrotising granulomatous inflammation of upper and lower respiratory tract, glomerulonephritis, and disseminated vasculitis. Case Study: A 50 year old female presented with complaints of running nose since last 8 months. Patient also had low grade fever, generalised body pain, productive cough, shortness of breath on exertion, pedal oedema for last 2 months. She had an 2-3 episodes of blood in sputum 15 days back. On examination saddle nose found. HRCT chest shows multiple cavitating nodules with consolidation. Lab findings shows raised ESR, CRP, COVID RT PCR negative and positive C-ANCA (Anti neutrophilic cytoplasmic antibody), red blood cell casts, and albumin present in urine. Sputum for AFB negative. Patient discharged on corticosteroids and cyclophosphamide and advised for regular follow up. Discussion: Wegener's granulomatosis is an antineutrophilic cytoplasmic antibody associated small vessel vasculitis. Prevalence of this disease varies from 3/1,00,000 to 16/1,00,000. Typically this involve the lungs and kidneys. It can be of generalised severe form or localised limited form. Our patient clinical course, CT findings and his strongly positive C-ANCA were considered diagnostic of wegener's granulomatosis. Treatment include corticosteroids and immunosuppressants. Conclusion: The early diagnosis and prompt treatment of multisystem disorder is necessary to prevent complication such as diffuse alveolar haemorrhage CT is the imaging modality of choice for diagnosis, surveillance and follow up in patients with wegener's granulomatosis.

POS-162 'COLA COLOURED URINE' : NOT ALWAYS GLOMERULAR HEMATURIA

Introduction: Hematuria is a common condition for which a patient seeks nephrology consultation. The presence of gross hematuria is a frightening experience for patient. The reasons for this gross hematuria can be various like nephrolithiasis, malignancies, glomerular diseases, trauma, urinary tract infections, drugs, hemoglobinuria, etc. To differentiate between the various causes of gross hematuria one must begin by taking good history and clinical examination, followed by urine examination and then other tests. Glomerular hematuria is smoky or cola coloured and is usually accompanied by signs and symptoms of fluid overload, high blood pressure, and proteinuria. However cola coloured urine should not be considered synonymous with glomerular hematuria Methods: We report a case of 22 year old pregnant female who was Gravida-3 (22 weeks gestation) but no live issues. Her previous 2 pregnancies ended up in Intra Uterine Death (IUD) of foetus at 6 months gestation. She was referred to us in view of history of cola coloured urine. History of similar episodes of hematuria in previous 2 pregnancies were also present.The history taking was limited because of the prevailing 2ndpeak of COVID-19 pandemic in India and hence most history taking was done indirectly via phone. Clinically she had mild pedal edema and her BP was 110/70 mm of Hg. Her workup showed that she had severe anaemia. Her Complete Blood Count showed Hb-5.8 gm/dL,TLC-3600/mm3,Plt-1.64lakh/mm3,PBS-Microcytic hypochromic with target cells. Renal function was normal. Liver function showed mild indirect hyperbilirubinemia. Urinalysis showed 3+ protein, 50-60 RBCs, 5-10 Pus cell, No casts. Urine culture was sterile. 24 hour urine protein was 1.29 grams. Ultrasonography-bilateral normal sized kidneys. Her COVID-19 RTPCR was negative Results: Differentials we considered were : Primary Glomerulonephritis;Pregnancy Induced Hypertension (PIH);Anti-Phospholipid Antibody Syndrome (APLA) & Atypical Hemolytic Uremic Syndrome (a-HUS). These were ruled out based on further relevant tests.Kidney biopsy was not offered as there was no nephrotic syndrome. Anti-Nuclear Antigen was negative. Complements were normal. APLA antibodies were negative.BP was always normal making PIH less likely. However LDH was raised (2700 U/L) & serum haptoglobulin was low. So a clear cut evidence of hemolytic anaemia but normal renal function, compelled us to revisit the history by calling the patient in-person despite the pandemic. She admitted that anaemia was present since her childhood days and she had suppressed this history due to social issues. Also the hematuria was episodic with clear urine in between. Hence Flowcytometry for Paroxysmal Nocturnal Hemoglobinuria was done which confirmed the diagnosis as PNH. Conclusions: Our case report highlights the fact that while evaluating cases of hematuria one must keep all possibilities open. Especially when dealing with cola coloured urine it should not be assumed to be glomerular hematuria It also stresses the well established fact that history taking is the key to making any diagnosis. In situations where social factors may lead to suppression of facts,efforts must be made to gain the confidence of patient and provide a conducive environment for complete history. Finally, even after diagnosis of PNH, the definitive treatment is still out of reach for many patients in this part of world. No conflict of interest

Not your typical presentation: A case of pediatric systemic lupus erythematous

Case Report Pediatric Systemic Lupus Erythematous (pSLE) is a multi-system autoimmune disease with varied clinical presentations. Although rare, it can be associated with significant morbidity and mortality. We report a case of a newly diagnosed pSLE patient who's presenting symptoms were concerning for viral pericarditis. Our 17-year-old African American female presented with non-radiating substernal chest pain and shortness of breath for three days. Pain was described as a constant pressure, exacerbated by lying down, and improved with leaning forward. Shortness of breath was most notable with ambulation. Other associated symptoms included subjective fever, chills, fatigue, two-week history of mild cough, intermittent headaches, nausea, emesis, pedal edema, myalgias, arthralgias, and a 10-pound weight loss. Detailed enquiry revealed a long-standing history of lymphadenopathy, neutropenia, microcytic anemia, and migraine headaches. Previous evaluation included normal thyroid studies, Hemoglobin A1c, complete metabolic panel, HIV testing, monospot, and a reassuring peripheral blood smear. Initial evaluation for her chest pain revealed normal EKG and chest x-ray. On physical exam at our facility, she was afebrile with normal vital signs. Soft, mobile, non-tender, <2 cm posterior cervical lymph nodes were palpated. Cardiac exam was unrevealing and no arthritis or rashes were noted. Her lungs were clear, but she had conversational dyspnea. Initial differential diagnoses included systemic processes such as rheumatologic, oncologic, and infectious. Testing revealed elevated troponin, proteinuria, pancytopenia, and elevated inflammatory markers. Coombs test and ACE were negative. D-dimer and creatinine kinase to evaluate for deep vein thrombosis and myositis were normal. EKG was concerning for ST elevation in anterolateral leads, and an echocardiogram revealed a small, globally distributed pericardial effusion. COVID PCR was positive concerning for pericarditis secondary to multisystem inflammatory syndrome in children (MIS-C). Though she met diagnostic criteria for MIS-C with her history of fever, elevated inflammatory markers, and multisystem involvement (cardiac and abdominal), the presence of her symptoms over several months was more concerning for a chronic process. Further evaluation into an underlying etiology revealed low C3/C4, positive ANA, positive ds-DNA, and positive SS-A, SS-B, chromatin, Anti-Smith, and RNP antibodies. The immunologic profile along with her clinical presentation was consistent with pSLE. Treatment with high-dose intravenous steroids resulted in complete resolution of her chest pain and she was discharged on oral hydroxychloroquine. pSLE is a multi-faceted and diagnostically challenging disease. Our case highlights the importance of obtaining a thorough history and a low threshold of suspicion for this complex autoimmune condition.

Clinical features and laboratory findings of multisystem inflammatory syndrome in children (MIS-C)

Introduction: Children mostly have mild or asymptomatic forms of SARS-CoV-2 infection, but during pandemic a higher incidence of Kawasaki disease, Kawasaki-like syndrome and the emergence of a new clinical entity, multisystem inflammatory post-covid syndrome (MIS-C) has also been observed. Objectives: The aim of this study is to determine clinical features and laboratory findings in patients with MIS-C. Methods: Retrospective analysis of clinical features and laboratory findings of MIS-C patients treated at our tertiary referal center (Clinic of Pediatric, University Clinical Centre Nis, Serbia). Results: From 18th of March 2020 till 30st of April 2021 there were 10 patients diagnosed as MIS-C according to CDC criteria. Eight patients were male and two were female. Patients age was 2 to 13 years (average 7.9 years, median 7 years). All patients had SARS -CoV-2 N-protein IgG antibodies but without history of disease symptoms and had positive contact four weeks prior to the onset of MIS-C symptoms. First symptom of MIS-C was fever (over 38C) which lasted in average for 4.4 days (3-7 days). Muco-cutaneous and gastrointestinal manifestations were most common. All patients had bulbar conjuctivitis, rash was present in 8 patients (80%), hand/foot oedema in 6 cases (60%), anterior cervical lymphadenopathy and cheliitis in 4 cases (40%) and periobital oedema in one case (details presented in Table 1. Clinical features of MIS-C patients). Nine patients (90%) presented with gastrointestinal symptoms while nervous system was affected in 5 patients. Three patients developed heart insuffitiency and one patient developed early signs of right coronary arthery aneurism. All patients had elevated inflammatory markers. Complete blood count showed elevated levels of white blood cells in 9 patients. Hypoalbuminemia and hypoproteinemia, low levels of serum potassium and sodium were present during ten days after the onset of symptoms. Troponines were elevated in 4 cases, proBNP in 5 cases. Abdominal ultrasound was performed and 6 patients presented with hepatoplenomegaly, 3 with enlarged spleen, one with enlagred liver and 4 had ascites. All patients were treated with combination of two antibiotics till cultures were proven negative, corticosteroid therapy and antiaggregation therapy. Three patients received a IVIG in a single dose (2gr/kg). All patients had good response to corticosteroid therapy (2mg/kg). Corticosteroid therapy was continued for four weeks (tapering). Conclusion: MIS-C can be a life-threatening condition in children. Early diagnosis and timely adequate treatment are of paramount importance. In children less than 5 years of age, the distinction between Kawasaki (Kawasaki shock) syndrome and MIS-C might be difficult, influencing the decision to use IVIG or steroids alone.

A case of recurrent pulmonary embolism

Background: Nephrotic syndrome is known to be associated with hypercoagulable status. Pulmonary artery thromboembolism is one of the life- threatening complications in patients with nephrotic syndrome but rarely occurs before the diagnosis of nephrotic syndrome. Methods and Results: A 33-year-old man without any co-morbidities presented to a primary care clinic with sudden onset shortness of breath. An electrocardiogram showed sinus tachycardia with S1Q3T3. ECHO and CTPA revealed thrombi of the bilateral pulmonary arteries and he was COVID-19 negative by PCR analysis. Anticoagulant therapy was initiated immediately. Hypercoagulability workup showed normal levels of protein C, protein S, and AT III. He was ANA- and APLA negative and his homocysteine levels were normal. Lower limb Doppler showed multiple deep venous system thrombi. Three months following this episode, he presented with recurrence of acute worsening of breathlessness with pedal edema and abdominal distention. He was referred to our Cardiology emergency care. 2D Echocardiography showed classic Mc Connells sign with akinesia of RV free wall and RV systolic pressure of 60 mm Hg. CT pulmonary angiography definitively proved fresh (recurrence of) pulmonary embolism with large clots in both LPA and RPA and CXR showed classical signs of pulmonary embolism (Fig. 1). USG abdomen showed ascites, normal kidneys and no renal vein thrombosis. Laboratory examination showed he was COVID-19 negative again by PCR analysis. They also revealed low serum albumin (2.2g/dl) and nephrotic-range proteinuria (>10 gm in 24 hours) with transudative ascitic fluid. Since patient was on anticoagulation renal biopsy was deferred by the consultant nephrologist in view of possible bleeding complications. In view of possible primary membranous nephropathy, Serum Anti-Pla2r antibody was done which was strongly positive. The constellation of nephrotic-range proteinuria, pulmonary thromboembolic complications and associated serum anti-Pla2R antibody suggested primary membranous nephropathy. Immunosuppression was started as per modified Ponticelli regimen. Proteinuria resolved after three weeks and patient continues to be doing well on anticoagulation on oral VKA [Formula presented] Conclusion: Previous case reports of pulmonary artery thromboembolism associated with nephrotic syndrome are very few, particularly in adults. In the rare cases where they do occur, the patients initially present with the symptoms derived from nephrotic syndrome, unlike in our patient where the presentation was extremely rare and the investigation of the thromboembolic event led us “backwards” to the diagnosis of nephrotic syndrome. Awareness regarding the potential complications of hypercoagulable in nephrotic syndrome is thus essential.