An Immunocompetent Adult With Adenovirus Hepatitis

Introduction: In the US there has been a recent outbreak of adenovirus hepatitis in the pediatric population. However, to our knowledge, there has been only one reported case of adenovirus hepatitis in an immunocompetent adult. We have identified another such case. Case Description/Methods: A 25 year old female with no medical history presented with abdominal pain, nausea, vomiting, diarrhea, and subjective fevers for two weeks and was found to have transaminitis 25-30x the upper limit of normal, which were: AST 791, ALT 542, ALP 92, and total bilirubin of 2.9. The patient reported no prior history of liver disease. She denied alcohol, tobacco, illicit drugs, or herbal medications, but did report taking acetaminophen 1500 mg daily for two weeks. Serum acetaminophen levels were normal and serum and urine toxicology were negative. US with doppler was unremarkable, CT showed cholelithiasis, MRCP showed a normal common bile duct without obstructive calculus. Autoimmune causes of hepatitis, ceruloplasmin and alpha-1 antitrypsin were all unremarkable. HAV, HBV, HCV, HDV, HEV, CMV, HSV, VZV, EBV, HIV, and COVID19 were all negative. Ultimately, the serology for adenovirus was positive. After a week of supportive treatment, the patient's labs trended down and symptoms resolved. Discussion(s): Adenovirus is confirmed by a rise in antibody titer or by virus detection. Coagulative necrosis in histopathology is a finding in liver biopsies if they are pursued in unexplained cases of liver injury. Ultimately, adenovirus hepatitis can be diagnosed once all common causes of hepatitis have been excluded. In the current outbreak, only children have been getting adenovirus hepatitis. In adults, a high prevalence of neutralizing antibodies contributes to immunity, and therefore only in immunocompromised states, do adults get such an infection. Supportive care with IV fluids, electrolyte correction, and antiemetics usually is enough with eventual symptomatic and laboratory improvement as it was for our patient. Studies have shown that extensive disease can be treated with antiviral drugs, cidofovir, and ribavirin. Our patient's history of acetaminophen use is a confounder, however, her normal serum level and her symptoms suggestive of an infectious cause made acetaminophen less of a culprit. We hypothesize that our patient's use of acetaminophen when she was initially exposed to the virus is what made her susceptible to developing adenovirus hepatitis and we hope this case adds insight for clinicians dealing with future adult cases.

IgM Multiple Myeloma Presenting With Diarrhea

Introduction: IgM Multiple Myeloma (MM) is a rare subtype of MM consisting of <1% cases of MM. It is distinguished from Waldenstrom Macroglobinemia, which also produces IgM, by the absence of somatic mutation MYD88. We present a patient with a chief complaint of diarrhea which unknowingly led to his hematological diagnosis Case Description/Methods: A 64 year old male with RA-SLE overlap syndrome on steroids, and recent COVID19 pneumonia, had presented with 5 episodes of watery diarrhea every day and 40 Ib weight loss within 2 months. CT revealed small bowel enteritis and stool studies, including C. diff, cultures, ova and parasites were negative. Diarrhea persisted despite antibiotics, therefore an EGD and Colonoscopy were performed which showed duodenal lymphangiectasia and a normal colon. Duodenal biopsy revealed eosinophilic deposits in the villous lamina propria which stained for IgM and stained negative under congo red ruling out amyloidosis. SPEP and a bone marrow biopsy revealed monoclonal IgMspikes and plasma cells in the bone marrow suggesting MMalong with a co-existing population of CLL. Next-generation sequencing was negative forMYD88, supporting IgM MM instead of Waldenstrom. He developed a protein-losing enteropathy with dramatic hypoalbuminemia (albumin 0.9) and lower extremity edema and DVTs. He was started on chemotherapy and frequent albumin infusions. His diarrhea completely resolved, however not in time, as his other medical comorbidities lagged behind and he developed anasarca and continued to deteriorate. Discussion(s): Plasma cell dyscrasias such as IgM MM or more commonly Waldenstrom have rarely been reported to cause GI symptoms. GI involvement can include direct GI infiltration of plasma cells, IgM deposition, or the finding of a plasmacytoma. It has been speculated that IgM deposits can lead to interstitial viscosity and obstructive lymphangiectasia leading to diarrhea and a protein-losing enteropathy as in our patient. Protein loss has led him to have hypoalbuminemia and possibly loss of antithrombotic proteins that have caused DVTs. Few case reports have suggested that treating the underlying cause with chemotherapy stops diarrhea entirely. Although our patient's diarrhea ceased, we believe that it was not in time for him to entirely recover from the later complications of the disease. We hope that this case can help clinicians to attempt prompt treatment of patients when they find GI specimens showing IgM deposits and they suspect a plasma cell dyscrasia.

Secondary amyloidosis presenting as a rare complication of IBD

Introduction: 35% of patients with Inflammatory Bowel Disease (IBD) experience extraintestinal manifestations. However, amyloidosis is a rare complication of IBD;the incidence in the US is <1% for both Crohn's disease (CD) and Ulcerative Colitis (UC). We hope to shed some light in this underdiagnosed consequence with a clinical vignette. Case description/methods: A 75 year old man with recently diagnosed UC 6 weeks prior and history of thoracic laminectomy presented with bilateral lower extremity weakness that resulted in a fall in the shower and complaints of bloody diarrhea. Prior to his admission he was ambulating with a walker, he then developed loss of motor function of his lower extremities. He had been having several episodes of bloody diarrhea a day along with tenesmus and fecal incontinence for almost a year. He delayed getting medical aid until recently due to the COVID-19 pandemic. He had a colonoscopy which revealed pancolitis and he was started on aggressive steroids and mesalamine. CT and MRI imaging of the spine were inconclusive, but revealed swelling of the iliopsoas muscle with concern for polymyositis. However EMG, muscle enzymes and Immunological studies were all unremarkable. Muscle biopsy of the gastrocnemius revealed interstitial amyloid deposition. Mass spectrometry was indeterminate and could not isolate the type of amyloid protein. The patient's UC flare slowly improved after several weeks and he was transferred to acute rehab and later to a tertiary care center for further evaluation. Discussion: Primary amyloidosis is AL amyloid deposition associated with plasma cell dyscrasias such as multiple myeloma (MM). AA Amyloid can also build up as an acute phase reactant from chronic inflammatory conditions such as IBD and be deposited in extracellular tissue. Amyloidosis is more associated with CD than UC, more found in men and is often associated with renal involvement. One study found that only 15 out of 1709 (0.9%) patients with CD and 1 in 1341 (0.7%) patients with UC had amyloidosis. Our patient's long standing uncontrolled UC likely resulted in amyloid protein production and deposition. Although it is important to rule out MM in cases of amyloidosis, the timing of our patient's lower extremity weakness and diagnosis of amyloidosis in the setting of uncontrolled UC flare strongly suggests secondary amyloidosis. We hope this diagnostic walk through can guide clinicians to approach similar situations in the future.