Expression of gut homing markers on T cells was quantified using flow cytometry. Results Expression of GPR15 was significantly increased on CD4+ effector T cells (CD4+ CD127+ CD45RO+) in NAFLD, ALD and PSC patients compared to healthy controls (9.7 ± 0.4, 12.7 ± 0.9 and 20.1 ± 1.8 vs 4.1 ± 1.8, P<0.05), with a significant increase also observed on CD8+ effector T cells (CD8+ CD45RO+) in PSC patients when compared to healthy controls (16.7 ± 2.6 vs 2.3 ± 0.58, P<0.01). There were also trends towards increased expression of gut homing markers CCR9, a4b7 and aEb7 on effector CD4+ and CD8+ T cells in all chronic liver disease groups compared with healthy control tissue. Conclusions For some time, evidence pointed towards b7 integrins as the drivers of the hepatic inflammation seen in patients with AILD and associated inflammatory bowel disease as a result of aberrant effector T cells homing from the gut to the liver. These data reveal a somewhat redundant role for b7 integrins, which could be regarded as a non-disease specific feature of advanced disease, and highlight GPR15 as the primary mediator of effector gut T cell homing.
Patients with known cirrhosis who present with anemia, thrombocytopenia, acute renal failure, and confusion are usually presenting with decompensated cirrhosis. We present a patient with known alcoholic cirrhosis presenting with the above abnormalities, initially thought to be decompensated cirrhosis but found to have acute myeloid leukemia (AML) with acute blast crisis. This case was presented as a poster at the American College of Gastroenterology Annual Scientific Meeting held on October 22-27, 2021.A 59-year-old male with a history of compensated alcoholic cirrhosis presented with unresponsiveness. On physical exam, vitals were normal, he appeared lethargic with generalized pallor, and rectal exam demonstrated an empty rectal vault with no blood or stool noted. Labs were notable for hemoglobin 3.1 g/dL, platelet count 41,000/µL, creatinine 5.2mg/dL, aspartate aminotransferase (AST) 242 U/L, alanine aminotransferase (ALT) 138 U/L, bilirubin 0.8 mg/dL, lactic acid 8.5 mmol/L, international normalized ratio (INR) 1.8, ammonia 51µmol/L. Imaging with CT head was unremarkable and CT abdomen demonstrated cirrhotic morphology of the liver with a small amount of ascites. Upper endoscopy was performed with no evidence of varices. Paracentesis demonstrated a high serum-ascites albumin gradient with low total protein consistent with portal hypertension. He was intubated for airway protection due to worsening encephalopathy. A peripheral smear was performed which showed myeloblasts with no signs of hemolysis. Bone marrow biopsy was subsequently performed which revealed 38% myeloblasts and features of myelodysplastic syndrome suggestive of secondary AML. Chemotherapy was not initiated as he was acutely critically ill and he expired shortly thereafter.AML can present with symptomatic anemia, bleeding, mental status changes due to central nervous system involvement, organomegaly, and renal insufficiency. Diagnosing AML in the setting of decompensated liver cirrhosis can be difficult as the clinical presentations can be similar at times. Thus, hematological causes should be considered when there is profound anemia with no acute blood loss early in the course.
Scabies infection is a very common skin disease that occurs due to infestation with the Sarcoptes scabei mite. Typically, it results in intensely pruritic papules and excoriations in the webs of the hand, groin, or axilla, and remains limited in its spread. In rare cases, the disease can become diffuse and progress to crusted or nodular subtypes. Here, we report the case of crusted scabies infestation in a 69-year-old male who presented with a diffuse pruritic, erythematous, and petechial rash. His medical history was significant for severe idiopathic urticaria treated with omalizumab. Before starting omalizumab, the patient was selfmedicating for several months with corticosteroids obtained through his veterinary practice to alleviate symptoms. His presentation was complicated by immune thrombocytopenic purpura and muscle weakness, likely secondary to omalizumab and corticosteroid use, respectively. The patient underwent an extensive rheumatologic workup until skin biopsy confirmed the underlying etiology as crusted scabies infestation. He was treated with ivermectin and weekly 5% permethrin skin cream with great improvement of his rash; however, unfortunately, he succumbed to bacterial sepsis. Scabies infestation can masquerade as a manifestation of other systemic diseases and is often misdiagnosed. As this case illustrates, initial misdiagnosis and subsequent treatment with immunosuppressive drug regimens can cause preventable, but potentially fatal, concomitant superinfections.
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