The demographics of autoimmune hepatitis in human immunodeficiency virus-infected patients: a United States cross-sectional study.

Introduction: Autoimmune hepatitis (AIH) is a chronic inflammatory condition of the liver with increasing global prevalence. However, no epidemiological data exist for AIH in human immunodeficiency virus (HIV)-infected patients. Aim: To determine the demographics and comorbid conditions associated with AIH among HIV-infected individuals in the United States. Material and methods: The United States National Inpatient Sample database was used to identify HIV hospital encounters in 2012-2014. The encounters were then classified into 2 groups based on a concomitant primary diagnosis of AIH. Primary outcomes included the demographics and comorbid conditions of AIH among HIV-infected patients. Secondary outcomes assessed the independent predictors of AIH. Results: A total of 48,3310 patients with an HIV diagnosis were included. The estimated AIH prevalence was 52.8/100,000 HIV hospital encounters. The female gender was more likely to have AIH with an odds ratio (OR) of 1.82; 95% confidence interval (CI) 1.42-2.32, p < 0.0001. The age intervals of 35-50 and 51-65 years had higher odds of AIH 110 (43.1%) and 115 (45.1%) with OR = 1.30; 95% CI: 1.02-1.67, p = 0.03 and OR = 1.34; 95% CI: 1.05-1.71, p = 0.02, respectively. African American and Hispanic races were more commonly affected. Moreover, HIV-infected patients with AIH had a higher risk of having elevated transaminases, long-term steroid use, rheumatoid arthritis, and ulcerative colitis. Conclusions: This study illustrates that the estimated prevalence of AIH in HIV-infected patients in the United States is 52.8/100,000. AIH in HIV-positive individuals has a predilection for the female gender and African American and Hispanic races, and shows a higher correlation with rheumatoid arthritis and ulcerative colitis.

Gastrointestinal and Liver Manifestations in COVID-19 Population.

The coronavirus was first identified as the cause of pneumonia in Wuhan, a town in the Hubei Province of China, in December 2019. It usually has respiratory symptoms such as myalgia, headache, cough, and dyspnea. In the medical literature, digestive symptoms and liver disease have been reported in Coronavirus disease in 2019 (COVID-19) patients. In this review article, we summarized the recent studies of gastrointestinal and hepatic manifestations and management of COVID-19. The most common gastrointestinal symptoms were poor appetite/anorexia, nausea/vomiting, diarrhea, and abdominal pain. Elevated aminotransferase has been reported in patients with COVID-19. COVID-19 gastrointestinal and hepatic management is usually symptomatic except for high-risk populations such as patients with inflammatory bowel disease or autoimmune hepatitis, which require special attention.

Morbidity and mortality of infections in the cirrhotic patients: a US population-based study.

AIM: This study aims to investigate the morbidity, mortality, and health care utilization of infection in patients with cirrhosis, with the hope of making clinical recommendations. BACKGROUND: The pathophysiology of liver cirrhosis makes patients susceptible to a variety of complications including infection. It contributes to a staggering rate of death and places a tremendous financial burden on the health care system. METHODS: The pathophysiology of liver cirrhosis makes patients susceptible to a variety of complications including infection. It contributes to a staggering rate of death and places a tremendous financial burden on the health care system. RESULTS: In this cross-sectional study, we queried the National Inpatient Sample (NIS) database for patients discharged from United States (US) hospitals with International classification of diseases (ICD) diagnostic codes consistent with liver cirrhosis, between January 2011 and December 2014. The patients were classified based upon the presence or absence of an infection, as well as their demographics and comorbidities. The data was then analyzed using the IBM SPSS version 25 statistical software. CONCLUSION: From 2011 to 2014, 660,727 cirrhotic patients were identified. Of these, 20.6% were found to have an infection. The mortality rate during hospitalization was 4.7% of all cirrhotic patients. The hospital length of stay was significantly longer for the study group than the control group (8.22 days versus 5.11 days) (P <0.0001). Similarly, the mean hospital cost was higher in the study group compared to the control group ($74,729.53 ± $125,963.75 vs. $46,413.32 ± $71,936.50 P< 0.0001).

Stomach Ulcer as a Rare Cause of Pancreatitis: An Unusual Complication of a Displaced Percutaneous Endoscopic Gastrostomy Tube.

A 33-year-old man was admitted to the hospital with upper abdominal pain and melena. Laboratory tests were suggestive of pancreatitis. Computed tomography (CT) of the abdomen showed peripancreatic fat stranding but showed no free air in the peritoneal cavity. Esophagogastroduodenoscopy (EGD) was performed, which revealed an ulcer on the posterior wall of the stomach, caused by the inner tip of the gastrostomy tube, and which had penetrated the pancreas. He had no signs of peritonitis. The gastrostomy tube was exchanged. The patient recovered well with conservative therapy within days.

Betel Chewing and Nonalcoholic Steatohepatitis.

Betel chewing is a common social practice in many regions of the world particularly in Southeast Asia and among the Asian immigrant populations in the West. Several studies have shown betel chewing to be associated with increased risk for various health complications including liver cirrhosis and hepatocellular carcinoma. The exact mechanism by which betel causes liver damage has not been elucidated. We present a 31-year-old Asian immigrant in the United States of America (USA) with no family history of the liver disease and non-smoker who was found to have an unexplained persistent mild elevation of liver transaminases. She reported more than 16 kilograms of weight gain over an eight-year period in association with heavy betel chewing. Despite diet and exercise, she was not able to lose weight. Besides, she developed dyslipidemia and gradual worsening of glucose tolerance. Liver biopsy showed severe steatosis with features of nonalcoholic steatohepatitis (NASH). The gradual development and worsening of metabolic syndrome and NASH paralleling betel use are very indicative of the hepatic steatosis being caused by betel.

Gastric intestinal metaplasia is associated with gastric dysplasia but is inversely correlated with esophageal dysplasia.

AIM: To determine which clinical factors might be associated with gastric intestinal metaplasia (IM) in a North American population. METHODS: Pathology and endoscopy databases at an academic medical center were reviewed to identify patients with and without gastric IM on biopsies for a retrospective cohort study. Patient demographics, insurance status, and other clinical factors were reviewed. RESULTS: Four hundred and sixty-eight patients with gastric IM (mean age: 61.0 years ± 14.4 years, 55.5% female) and 171 without gastric IM (mean age: 48.8 years ± 20.8 years, 55.0% female) were compared. The endoscopic appearance of atrophic gastritis correlated with finding gastric IM on histopathology (OR = 2.05, P = 0.051). Gastric IM was associated with histologic findings of chronic gastritis (OR = 2.56, P < 0.001), gastric ulcer (OR = 6.97, P = 0.015), gastric dysplasia (OR = 6.11, P = 0.038), and gastric cancer (OR = 6.53, P = 0.027). Histologic findings of Barrett's esophagus (OR = 0.28, P = 0.003) and esophageal dysplasia (OR = 0.11, P = 0.014) were inversely associated with gastric IM. Tobacco use (OR = 1.73, P = 0.005) was associated with gastric IM. CONCLUSION: Patients who smoke or have the endoscopic finding of atrophic gastritis are more likely to have gastric IM and should have screening gastric biopsies during esophagogastroduodenoscopy (EGD). Patients with gastric IM are at increased risk for having gastric dysplasia and cancer, and surveillance EGD with gastric biopsies in these patients might be reasonable.

Underwater endoscopic mucosal resection of colorectal neoplasia is easily learned, efficacious, and safe.

BACKGROUND: Underwater endoscopic mucosal resection (UEMR) without submucosal injection is a novel endoscopic procedure. It is not known if UEMR can be easily taught and learned, and the efficacy and safety of UEMR has not been demonstrated at multiple medical centers. Our aims were to demonstrate that (1) UEMR is a technique that can be easily learned by an endoscopist trained in traditional EMR, (2) endoscopic ultrasound (EUS) may not be required before UEMR, and (3) UEMR is an efficacious and safe method for resection of large or flat neoplastic colorectal lesions. METHODS: An experienced interventional endoscopist began performing UEMR after observing UEMR procedures. Colorectal UEMR was performed using a pediatric colonoscope with a cap, a waterjet, and a 'duck-bill' snare using blended current. Submucosal injection was not used. Patient data were collected prospectively. RESULTS: A total of 21 patients (17 men, mean age 64.9 years, range 51-83) referred for polypectomy of large colorectal lesions underwent UEMR. A total of 43 colorectal lesions with a mean size of 20 mm (range 8-50) were resected by UEMR. Lesions were found in the right colon (N = 16), transverse colon (N = 5), left colon (N = 19), and rectum (N = 3). Pathology demonstrated tubular adenoma (N = 29), tubulovillous adenoma (N = 5), high-grade dysplasia (N = 3), serrated sessile adenoma without dysplasia (N = 3), and non-neoplastic tissue (N = 3). EUS was used in only two cases of rectal neoplasia (4.7 %). Of the UEMRs, 97.7 % were successful with complete resection of colorectal polyps. The only adverse event was one case (2.3 %) of delayed post-UEMR bleeding. CONCLUSIONS: UEMR was easily learned by an endoscopist already skilled in conventional EMR. EUS may not be required prior to most UEMR procedures. UEMR appears to be an efficacious and safe alternative to traditional EMR or ESD for large or flat colorectal neoplasms.

Peripheral platelet count correlates with liver atrophy and predicts long-term mortality on the liver transplant waiting list.

Several studies have shown a direct role of liver atrophy in the pathogenesis of thrombocytopenia of cirrhosis via reduced production of thrombopoeitin. About 181 patients listed for liver transplantation at a single transplant center were evaluated at the time of listing with laboratory tests and volumetric liver measurements using computed tomography. Expected normal liver volume was calculated using the Heinemann formula. Liver volume ratio (LVR) was calculated as actual liver volume over expected liver volume. Patients were predominantly male (70.7%), with viral hepatitis (60.2%), had a mean age of 51.8 years (SD 8.7), model for end stage liver disease (MELD) of 14 (SD 6.4), LVR of 0.95 (SD 0.3), and platelet count of 105,000/mcL (SD 66,000). Platelet count (P < 0.0001) correlated more strongly with LVR than MELD, MELD components (P = 0.27) or serum albumin (P = 0.003). Platelet count (HR 0.987, 95% CI 0.979-0.994, P = 0.001) was a strong independent predictor of mortality. Patients with platelet count < 100,000/mcL had a shorter survival (935 vs. 1396 days, P = 0.002) and higher death rate (42.2% vs. 23.6%, P = 0.01), but no different transplantation rate (36.7% vs. 33.3%, P = 0.64) compared to those with platelet count ≥ 100,000/mcL. Low platelet count corresponds to higher waiting list mortality and is a sign of advanced liver atrophy.

Hepatic encephalopathy.

Chronic liver disease and cirrhosis affect hundreds of millions of patients all over the world. The majority of patients with cirrhosis will eventually develop complications related to portal hypertension. One of these recurrent and difficult to treat complications is hepatic encephalopathy. Studies have indicated that overt hepatic encephalopathy affects 30 to 45% of patients with cirrhosis and a higher percentage may be affected by minimal degree of encephalopathy. All of these factors add to the impact of hepatic encephalopathy on the healthcare system and presents a major challenge to the gastroenterologist, hospitalist and primary care physician.

Heightened NTPDase-1/CD39 expression and angiogenesis in radiation proctitis.

Radiation proctitis is an inflammatory process associated with persistent and refractory lower gastrointestinal bleeding. Purinergic signaling regulates hemostasis, inflammation, and angiogenesis. For example, CD39, the vascular ectonucleotidase, blocks platelet activation and is required for angiogenesis. Whether CD39 expression is affected by radiation injury is unknown. The aim of this work was to study CD39 expression patterns after clinical radiation injury to the rectum. We prospectively enrolled eight patients with radiation proctitis and five gender-matched controls. Biopsies were taken from normal-appearing rectal mucosa of controls and from the normal sigmoid and abnormal rectum of patients. Expression patterns of CD39, P2Y2 receptor, CD31, CD61 integrin, and vascular endothelial growth factor receptor 2 were examined by immunostaining; levels of CD39 were further evaluated by Western blots. Chronic inflammatory lesions of radiation proctitis were associated with heightened levels of angiogenesis. Immunohistochemical stains showed increased vascular expression of CD39, as confirmed by Western blots. CD39 was co-localized with vascular endothelial markers CD31 and CD61 integrin, as well as expressed by stromal tissues. Development of neovasculature and associated CD39 expression in radiation proctitis may be associated with the chronic, refractory bleeding observed in this condition.

Deletion of cd39/entpd1 results in hepatic insulin resistance.

OBJECTIVE: Extracellular nucleotides are important mediators of inflammatory responses and could also impact metabolic homeostasis. Type 2 purinergic (P2) receptors bind extracellular nucleotides and are expressed by major peripheral tissues responsible for glucose homeostasis. CD39/ENTPD1 is the dominant vascular and immune cell ectoenzyme that hydrolyzes extracellular nucleotides to regulate purinergic signaling. RESEARCH DESIGN AND METHODS: We have studied Cd39/Entpd1-null mice to determine whether any associated changes in extracellular nucleotide concentrations influence glucose homeostasis. RESULTS: Cd39/Entpd1-null mice have impaired glucose tolerance and decreased insulin sensitivity with significantly higher plasma insulin levels. Hyperinsulinemic-euglycemic clamp studies indicate altered hepatic glucose metabolism. These effects are mimicked in vivo by injection into wild-type mice of either exogenous ATP or an ecto-ATPase inhibitor, ARL-67156, and by exposure of hepatocytes to extracellular nucleotides in vitro. Increased serum interleukin-1beta, interleukin-6, interferon-gamma, and tumor necrosis factor-alpha levels are observed in Cd39/Entpd1-null mice in keeping with a proinflammatory phenotype. Impaired insulin sensitivity is accompanied by increased activation of hepatic c-Jun NH(2)-terminal kinase/stress-activated protein kinase in Cd39/Entpd1 mice after injection of ATP in vivo. This results in decreased tyrosine phosphorylation of insulin receptor substrate-2 with impeded insulin signaling. CONCLUSIONS: CD39/Entpd1 is a modulator of extracellular nucleotide signaling and also influences metabolism. Deletion of Cd39/Entpd1 both directly and indirectly impacts insulin regulation and hepatic glucose metabolism. Extracellular nucleotides serve as "metabolokines," indicating further links between inflammation and associated metabolic derangements.

Current status of antiviral therapy for hepatitis B.

Chronic hepatitis B (CHB) is a major public health problem affecting up to 400 million people globally. Complications of CHB including liver failure and hepatocellular carcinoma result in 1.2 million deaths per year, making CHB the 10th leading cause of mortality worldwide. The natural history of CHB is variable and complex. The past decade witnessed important developments for the therapy of hepatitis B and marked the new era of oral therapy. The ultimate goal of CHB therapy is to arrest the progression of liver injury and to prevent the development of liver failure and hepatocellular carcinoma. Currently, six agents are approved for the treatment of CHB. Each of these agents, given as monotherapy, has been shown to produce virological, biochemical, and histological benefits for both HBeAg positive and negative CHB. There are, however, limitations in spite of their efficacy. The significant side-effect profile of interferon, for example, limits its long-term use. The approved oral agents are tolerable with prolonged use but drug resistance could limit long-term monotherapy. To date, combination therapy with nucleoside analogue and pegylated interferon or two nucleos(t)ide analogues given for one year does not show superiority in durability of response compared to monotherapy. Ongoing research effort is critical to identify the ideal hepatitis B therapy that is safe, effective, and produces durable response with a finite course of therapy. It is equally important to conduct a well designed, prospective natural history study to identify predictors of disease progression. This will accurately guide treatment strategy for this important disease.

The clinical significance of incidental computer tomography finding of gastrointestinal luminal wall thickening as evaluated by endoscopy.

The widespread use of computerized tomography in evaluating patients with various abdominal complaints gave rise to reports of incidental gastrointestinal luminal wall thickening (GILWT), the clinical significance of which remains uncertain. In order to determine the endoscopic significance of GILWT we reviewed 1609 abdominal and/or pelvic CT scans. Ninety-two patients with GILWT were identified. Patients with obvious clinical cause of this abnormality were excluded from the study. The median age of the patients was 58 years, with no significant difference in gender distribution. The GILWTs were distributed along the GI tract as follows: 24 upper (esophageal, gastric, and duodenum), 13 small intestine (jejunum and ileum), 3 combined small and large intestine, and 52 colon. Fifty of these patients underwent endoscopic evaluation. Six patients (12%) had cancer, all of which involved the colon. The endoscopy was unremarkable in 19 (38%) and revealed a nonmalignant finding in the remaining 25 patients (50%). None of the upper GI or small bowel GILWTs were malignant, while 6 of the 34 colonic GILWTs (18%) were malignant. The mean age of the colonic GILWT group was 59. None of the patients younger than 50 had cancer, while 6 of the 24 older patients (25%) had colon cancer. We conclude that as GILWT is not a common finding and could be the initial presentation of malignancy, particularly when involving the colon in patients older than 50, endoscopic evaluation should be strongly recommended in patients who do not have an alternative diagnosis that can satisfactorily explain GILWT.

Concurrent immune thrombocytopenic purpura and Guillain-Barre syndrome in a patient with Hashimoto's thyroiditis.

Immune thrombocytopenic purpura (ITP), Guillain-Barre syndrome (GBS), and Hashimoto's thyroiditis (HT) are autoimmune disorders caused by impaired self-tolerance mechanisms triggered by interaction between genetic and environmental factors. ITP is an immune-mediated destruction of platelets resulting in mucocutaneous bleeding, GBS is an ascending motor paralysis caused by an inflammatory demyelination of peripheral nerves, and HT is characterized by autoimmune-mediated destruction of the thyroid gland. The concurrent development of ITP and GBS has only rarely been reported in the literature, and GBS itself rarely occurs with other autoimmune disorders. We present a 21 year-old patient with known Hashimoto's hypothyroidism that simultaneously developed GBS and ITP after an upper respiratory tract infection. To the best of our knowledge, this is the first reported case of these three autoimmune disorders in the same patient. This points to a possible common genetic predisposition to these disorders.

A case report comparing various radiological tests in the diagnosis of calcific uremic arteriolopathy.

BACKGROUND: Calcific uremic arteriolopathy (CUA) is a rare necrotizing skin condition characterized by calcification in arterioles, leading to ischemia and skin ulcerations. This disease affects 1% to 4% of patients with chronic kidney disease and has a reported mortality rate up to 80%. The diagnosis of CUA is based on clinical judgment suggested by the characteristic skin lesions. Although skin biopsy is the gold standard for establishing the diagnosis, it is performed infrequently because of poor healing and risk for secondary infections. METHODS: In this case report, we compare the ability of various radiological tests to show arteriolar calcifications of patients with CUA. Our patient had biopsy-proven CUA manifesting as chronic nonhealing ulcers of the calves. She underwent soft-tissue x-ray of the affected extremities and high-resolution (0.5-mm slice) computed tomographic (CT) scanning with 3-dimensional image reconstruction. We also used a dedicated mammography machine to obtain images of the patient's calves. Images were compared based on the ability to show small-vessel calcification. RESULTS: Plain soft-tissue x-ray showed mildly increased soft-tissue density and very few calcified vessels, whereas CT showed few calcified small- and medium-sized arterioles. Diffuse calcification of small arterioles in a mesh-like pattern was shown by means of the mammography technique. CONCLUSION: Simple, safe, and inexpensive x-ray imaging using the mammography technique was superior to plain soft-tissue x-ray and 3-dimensional CT in showing the hallmark arteriolar calcifications of patients with CUA. Thus, we propose a possible role for this technique in diagnosing CUA.