The association between hepatitis C virus (HCV) and sarcoidosis is well-documented, but in this case report, we shall discuss an interesting association between hepatitis B virus (HBV) and sarcoidosis, presenting with non-specific symptoms and confirmed with liver biopsy and immunologic markers. The case was complicated by treatment with immunosuppressive medication that led to colonic histoplasmosis. A 58-year-old woman, from the western part of India, who has a past medical history of HBVrelated cirrhosis of the liver for six months, hypertension, and type 2 diabetes presented to our clinic with bilateral pedal edema, anorexia, and mild epigastric discomfort. She had been on entecavir for the last six months. The patient denied any significant surgical, social, or family history. Abdominal ultrasonography revealed hepatosplenomegaly and mesenteric lymphadenopathy. She had a 21.3kPa liver stiffness on elastography and an HBV deoxyribonucleic acid (DNA) level of 89 copies/ml. Liver biopsy showed multiple noncaseating granulomas consisting of Langerhans cells in the parenchyma and portal tract, associated with moderate inflammation. A chest computed tomography (CT) scan showed upper and middle lobe fibrosis of the lungs; this diagnosis was further confirmed with elevated angiotensinconverting enzymes. She was started on prednisone; within a period of three months, she experienced weight loss, diarrhea, and fever. Colonoscopy was done after an abdomen CT showed mural thickening of the ascending colon and terminal ileum, which on biopsy was confirmed as histoplasmosis. Prednisone was stopped, and the patient was treated with hydroxychloroquine and amphotericin B, followed by itraconazole. The patient improved symptomatically, and repeated colonoscopy findings were normal. Studies are scarce to prove the association between hepatitis B and sarcoidosis; however, we reasonably hypothesized that the alterations in the pool of cytokines and immune cells caused by HBV infection might have had a vicious influence on immune regulation and could be a trigger for granuloma. Further studies can impact the future to provide for a better understanding of the pathophysiology of sarcoidosis, HBV correlation, and treatment options.
INTRODUCTION: There have been many documented cases of cirrhosis and associated Parenchymal renal disease (Ig-A nephropathy, glomerulonephritis). We discuss here rare case of hepatorenal syndrome type 2, in-patient with no clinically and imaging finding indicative of portal hypertension. Also, further interesting finding is to have nephrotic range proteinuria in nephritic syndrome. CASE DESCRIPTION/METHODS: 56-Year-old Indian male with no past medical or surgical history presented with complaints of generalized weakness and occasional abdominal discomfort. He denied significant family history and alcohol, tobacco or illicit drug use. Ultrasonography (USG) abdomen showed cirrhotic changes. All work up including autoimmune panel negative, hence diagnosed with idiopathic liver cirrhosis. Patient managed with conservative approach, as there were no changes indicative of portal hypertension including Esophagogastroduodenoscopy. After about a year, on routine follow up he found to have his serum creatinine (Cr) progressed from 0.8 to 3.8 mg/dl. Repeat USG abdomen showed diffuse liver parenchymal disease with mild ascites and normal size of kidney with cortical thickness. Urine Microscopy revealed proteinuria and hematuria with 24 hour measured urinary protein 5 gm. Renal biopsy was performed and showed diffuse proliferative glomerulonephritis-Ig A Nephropathy (nephritic syndrome with nephrotic range proteinuria). Autoimmune profile was negative. Hospital course was complicated by septic shock and hemorrhagic cystitis. Patient was treated with inotropes, Pulse dose of intravenous methylprednisolone, albumin and other supportive approach. Decision was made not to continue cyclophosphamide due to hemorrhagic cystitis. Patient Cr later stabilized after peak of 4.3 mg/dl. Presently, is on diuretics and prednisone with Cr is stable around 1.3 mg/dl. DISCUSSION: Hepatorenal syndrome is divesting complication of liver cirrhosis, which can occur due to various mechanism one of which is described as in our case. Literature has focused mainly on mechanism of Ig-A nephropathy in portal hypertension. Our aim for this case report is to focus on monitoring renal function in cirrhotic patient even without no evidence of portal hypertension as there is no firm correlation between degree of portal hypertension and severity of IG A nephropathy. Thus, further studies can effect future era of hepatic transplant by more effectively understanding complex mechanism and managing complications.
INTRODUCTION: Necrotizing colitis has historically been primarily a disease of premature infants, affecting about 3/1000 live births. Adult necrotizing enterocolitis (ANEC) has seldom been reported, and to our knowledge, only a few case reports exist. We present an adult with necrotizing colitis and hope to provide some insight about presentation, diagnosis, and management. CASE DESCRIPTION/METHODS: A 54-year-old male with history of gastroesophageal reflux disease and hyperlipidemia presented with abdominal pain associated with vomiting, fever, and bloody diarrhea. He had both an unremarkable upper endoscopy and colonoscopy 3 years ago. His abdomen was soft, but tender on the left, with no rebound or guarding. CT scan revealed infectious and inflammatory colitis. Stool studies for bacteria, parasites and clostridium difficile were negative. Initially, the patient deteriorated despite aggressive hydration and antibiotics. Colonoscopy showed extensive ulcerated friable boggy colon, and severe colitis with pseudomembranes. Pathology confirmed necrotizing inflammation suggestive of necrotizing colitis. Ischemic work up with CT angiography showed patent abdominal arteries. Surgery was premeditated, however the patient gradually improved with medical management alone and was eventually discharged. DISCUSSION: Although the exact mechanism of ANEC is unknown, two possible explanations include infectious agents and bowel perfusion disturbances. Infection is the main cause in neonates due to an underdeveloped immune system. Both gram negative bacteria and viruses are culprits, most commonly, E. Coli and Klebsiella. In ANEC, the primary insult may be hypoxia-reperfusion injury due to vasoconstriction of non occlusive mesenteric vessels and bacterial overgrowth as a secondary insult. Patients present with abdominal pain, vomiting and hematochezia. Xray and CT usually show nonspecific findings. CT angiography rules out mesenteric occlusion. Histological analysis demonstrating necrotizing inflammation finalizes the diagnosis. Our patient's diagnosis was based on histology and the exclusion of mesenteric occlusion. Although, stool studies did not identify a causative pathogen, our patient eventually improved with antibiotics. It is postulated that an initial ischemic damage contributed to the patient's clinical deterioration but the second insult of bacterial translocation was treated with antibiotics. Although rare, ANEC is being reported and clinicians need to keep high index of suspicion for timely management.
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