Gastrointestinal Manifestations of IgA Vasculitis-Henoch-Schönlein Purpura

Immunoglobulin A vasculitis, formerly called Henoch-Schönlein purpura (HSP), is the most common systemic vasculitis in childhood. It is a small-vessel vasculitis mediated by type III hypersensitivity, manifested as rash accompanied by gastrointestinal (GI) symptoms, arthritis, and nephritis. The etiology of this disease (a leukocytoclastic vasculitis) is still uncertain, but immune complexes of IgA and unidentified antigens seem to have a central pathogenic role. Most often the diagnosis is established after the clinical examination; it is easy at first glance when the clinical presentation includes the classic tetrad of rash (nonthrombocytopenic palpable purpura), arthralgia/arthritis, abdominal pain, and renal manifestations but may be difficult when the gastrointestinal manifestations precede the skin purpuric rash. Gastrointestinal involvement is frequently seen and varies from mild symptoms to severe complications; sometimes the gastrointestinal symptoms (colicky abdominal pain, nausea, vomiting, diarrhea, gastrointestinal bleeding) are the first manifestations of the disease. Immunoglobulin A vasculitis is usually a self-limited disease with a benign course, and the treatment is often symptomatic; in severe cases corticosteroids are necessary

Clinical Impact of Small Bowel Capsule Endoscopy in Obscure Gastrointestinal Bleeding

Background and objectives: The most frequent indications for small bowel capsule endoscopy (SBCE) are obscure gastrointestinal bleeding (OGIB) and iron deficiency anemia (IDA). The aim of this study was to evaluate the diagnostic yield (DY) of SBCE in overt and occult OGIB, as well as its impact on the clinical outcome. Materials and Methods: This study retrospectively included all cases of OGIB investigated by SBCE in a tertiary care referral center, between 1st January 2016 and 31st December 2018. OGIB was defined by overt or occult gastrointestinal bleeding, with negative upper and lower endoscopy. Occult gastrointestinal bleeding was either proved by a fecal test or presumptively incriminated as a cause for IDA. DY was defined as the detection rate for what were thought to be clinically significant findings. DYs for overt and occult bleeding were assessed and compared. Gender, age, hemoglobin levels, NSAID consumption and the use of anticoagulants were recorded. Following SBCE results, individual therapeutic decisions were made, and follow-up data were recorded. Results: 224 SBCE examinations were performed for OGIB, of which 148 were for overt OGIB, and 76 for unexplained IDA. Positive findings were found in 139 patients, resulting in an overall DY for OGIB of 62%, higher in overt OGIB (75%) compared to IDA (37%). The most frequent findings were small bowel angioectasias (62.2% in overt OGIB and 78.5% in IDA). On multivariate logistic regression analysis, only hemoglobin level <10 g/dL and anticoagulants were the variables independently associated with positive findings. All patients received medical, endoscopic or surgical treatment and had good clinical outcome during follow-up. Conclusion: SBCE has a high diagnostic yield and a positive impact on management of patients with OGIB

Natural course of nonmalignant partial portal vein thrombosis in cirrhotic patients

Background/Aim: Portal vein thrombosis (PVT) has a high incidence in patients with liver cirrhosis and determines a poor prognosis of hepatic disease. The aim of our study was to define the natural course of partial PVT in cirrhotic patients, including survival and decompensation rates. Patients and Methods: We performed a prospective, cohort study, in a tertiary referral center. There were 22 cirrhotic patients with partial nonmalignant PVT, without anticoagulant treatment, who were followed-up between January 2011 and October 2013. All patients were evaluated by Doppler abdominal ultrasound and computed tomography. Kaplan-Meier method was used to determine the difference in clinical events between the study subgroups. Results: After a mean follow-up period of 20.22 months, partial PVT improved in 5 (22.73%), was stable in 11 (50%), and worsened in 6 (27.27%) patients. Hepatic decompensation rate at 6 and 18 months was higher in patients with worsened PVT than in those with stable/improved PVT (50% vs. 25%, P < 0.0001 and 100% vs. 56.25%, P < 0.0001, respectively). The survival rate at 6 months was 66.66% in worsened PVT group vs. 81.25% (P = 0.005) in stable/improved group, and 16.66% vs. 81.25% (P < 0.0001) at 18 months, respectively. Multivariate analysis showed that Model of End-Life Disease was the independent predictor of hepatic decompensation [hazard ratio (HR) 1.42; 95% confidence interval (CI): 1.08-1.87, P = 0.012] and survival (HR 1.76; 95% CI: 1.06-2.92, P = 0.028). Conclusions: Nonmalignant partial PVT remained stable/improved in over half of cirrhotic patients and aggravated in more than one fourth in whom it negatively influenced the survival and decompensation rates

The Prevalence of Liver Steatosis and Fibrosis Assessed by Vibration-Controlled Transient Elastography and Controlled Attenuation Parameter in Apparently Healthy Romanian Medical Students

Vibration-Controlled Transient Elastography (VCTE) with Controlled Attenuation Parameter (CAP) is used as a non-invasive method for evaluating liver steatosis and fibrosis simultaneously. In this prospective study, we aimed to assess the prevalence of liver steatosis and fibrosis, as well as the associated risk factors in Romanian medical students by VCTE and CAP score. We used a cut-off CAP score of ≥248 dB/m for the diagnosis of mild steatosis (S1), ≥268 dB/m for moderate steatosis (S2), and ≥280 dB/m to identify severe steatosis (S3). For liver fibrosis, the cut-off values were: ≤5.5 kPa, indicating no fibrosis (F0), 5.6 kPa for mild fibrosis (F1), 7.2 kPa for significant fibrosis (F2), 9.5 kPa for advanced fibrosis (F3), and 12.5 kPa for cirrhosis (F4). In total, 426 Romanian medical students (67.8% females, mean age of 22.22 ± 1.7 years) were evaluated. Among them, 352 (82.6%) had no steatosis (S0), 32 (7.5%) had mild steatosis (S1), 13 (3.1%) had a moderate degree of steatosis (S2), and 29 (6.8%) had severe steatosis (S3). Based on liver stiffness measurements (LSM), 277 (65%) medical students did not have any fibrosis (F0), 136 (31.9%) had mild fibrosis (F1), 10 (2.4%) participants were identified with significant fibrosis (F2), 3 (0.7%) with advanced fibrosis (F3), and none with cirrhosis (F4). In conclusion, the prevalence of liver steatosis and fibrosis is low among Romanian medical students

Association between Nonalcoholic Fatty Liver Disease and Endocrinopathies: Clinical Implications

Nonalcoholic fatty liver disease (NAFLD) has a rising prevalence worldwide. Its potential for evolution towards liver cirrhosis and hepatocellular carcinoma, as well as associations with extrahepatic manifestations, represents a double burden for patients and physicians alike. Recently, there has been increasing evidence of the association between NAFLD and a number of endocrinopathies, such as hypothyroidism, polycystic ovarian syndrome (PCOS), hypopituitarism, growth hormone deficiency (GHD), hypogonadism, and hypercortisolism. Definite correlations are supported by clear evidence so far, but further studies are needed in order to completely clarify the pathogenic mechanisms and, especially, to identify therapeutic implications. In this review, we present the main relationships between NAFLD and endocrinopathies, emphasizing the reciprocal causality, evolutive interconnections, and current clinical scenarios of presentations of which the clinicians should be aware

Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases: The Heart of the Matter

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most frequent cause of liver disease worldwide, comprising a plethora of conditions, ranging from steatosis to end-stage liver disease. Cardiovascular disease (CVD) has been associated with NAFLD and CVD-related events represent the main cause of death in patients with NAFLD, surpassing liver-related mortality. This association is not surprising as NAFLD has been considered a part of the metabolic syndrome and has been related to numerous CVD risk factors, namely, insulin resistance, abdominal obesity, dyslipidemia, hyperuricemia, chronic kidney disease, and type 2 diabetes. Moreover, both NAFLD and CVD present similar pathophysiological mechanisms, such as increased visceral adiposity, altered lipid metabolism, increased oxidative stress, and systemic inflammation that could explain their association. Whether NAFLD increases the risk for CVD or these diagnostic entities represent distinct manifestations of the metabolic syndrome has not yet been clarified. This review focuses on the relation between NAFLD and the spectrum of CVD, considering the pathophysiological mechanisms, risk factors, current evidence, and future directions