Zoonotic infections are increasingly becoming public health menaces and are usually transmitted to humans due to unsuitable environmental conditions. One of them is hepatic capillariasis, caused by the parasite Capillaria hepatica, primarily a disease of rodents, with hepatic manifestations in humans. Although its prevalence is very low, it can cause significant morbidity and mortality, with cases reported from all over the world. The main infective form for humans is the embryonated egg of the parasite, which hatches in the intestine and ultimately colonize the liver. The larvae mature and reproduce, and eventually form embryonated eggs, which cause chronic focal inflammation and septal hepatic fibrosis. Clinical presentation mainly consists of fever, abdominal pain, hepatomegaly and eosinophilia. Spurious infection with unembryonated eggs cause gastrointestinal symptoms. Diagnostic modalities include liver biopsy, ultrasonography, CT scan, immunological tests like ELISA and IIFT. The infection can be treated mainly with a combination of benzimidazoles like thiabendazole, mebendazole and albendazole; with corticosteroids. The study emphasizes the need for hepatic capillariasis to be considered as a differential diagnosis in cases of suspected hepatitis, leptospirosis, abdominal lymphadenopathy or other hepatic or parasitic infections prevalent in the region concerned; and meticulously assess the cases to facilitate early diagnosis and prompt treatment, thus reducing the distress faced by patients.

Summary Background Although hepatitis B surface antigen (HBsAg) loss is considered the ideal therapeutic endpoint for the treatment of chronic hepatitis B virus (HBV) infection, its impact on clinical outcomes remains uncertain. Aim To assess the impact of HBsAg loss on clinical outcomes following spontaneous and treatment‐related HBsAg loss. Methods We searched PUBMED, Embase, the Cochrane library, and published abstracts through to May 2021 for studies that reported HBsAg loss, had >1 year of follow‐up and reported at least one clinical outcome in adults with chronic HBV infection. Results We identified 57 studies (258 744 HBsAg‐positive patients, 63 270 with HBsAg loss). Based on 24 studies including 160 598 patients with and without HBsAg loss, HBsAg loss was associated with a non‐significant 23% relative risk reduction of developing hepatocellular carcinoma (HCC) compared to those who remained HBsAg‐positive (RR = 0.77; 95% CI: 0.38‐1.57). In subgroup meta‐analysis of 10 studies, treatment‐related HBsAg loss was associated with a non‐significant higher pooled proportion of HCC (0.94%) compared to spontaneous HBsAg loss (0.45%). HCC development after HBsAg loss was significantly higher in males, those with underlying cirrhosis, and those with a family history of HCC. HBsAg loss was associated with lower pooled proportions of incident cirrhosis, hepatic decompensation, overall and liver‐related mortality compared to no HBsAg loss. Substantial heterogeneity was noted across studies for all outcomes. Conclusion HBsAg loss is associated with a reduced risk of clinical outcomes. However, several shortcomings in the published studies prevent a more definitive conclusion on the potential benefits of HBsAg loss.

Vibration controlled transient elastography (VCTE) is validated for the evaluation of hepatic fibrosis in different liver diseases. Sickle cell liver disease (SCLD) results from a cumulative hepatic injury and its lifelong and progressive nature raises the need for a non-invasive tool for fibrosis evaluation.Fifty patients, aged between 23 and 59 years with sickle cell disease and suspected SCLD underwent a VCTE followed by a liver biopsy. Biopsies were evaluated for various scores of liver disease that were then correlated to VCTE score. 90% of our patients had an Ishak Fibrosis (IF) score between 0-2 (Group A-minimal to no fibrosis) and 10% of the patients had IF score between 3-6 (Group B-advanced fibrosis). The median Transient Elastography (TE) for patients in Groups A and B was 4Á8 kilopascals (kPa) and 17Á6 kPa, respectively. A positive correlation was shown between TE and IF score, R = 0Á0Á68 (P = <0Á0001); a positive correlation was also shown with Histology Activity Index fibrosis score, R = 0Á64 (P = <0Á0001). This study emphasises the need for further studies of noninvasive tools and their utility in liver fibrosis evaluation of patients with SCLD.

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KRAS is detected in 30%–50% of colorectal cancer (CRC) and BRAF mutations are found in 10% of CRC. A 62-year-old man with the long-standing smoking history presented to the emergency department with abdominal pain, weight loss and constipation. CT scan of abdomen/pelvis showed obstructive mass which was found to be colon adenocarcinoma which on further molecular analysis tested positive for KRAS, NRAS and BRAF mutations. His tumour progressed despite chemotherapy and surgery and he died within a year of diagnosis. Concomitant KRAS, NRAS and BRAF mutations are rare enough to be considered mutually exclusive but coexistent mutations appear to be a distinct molecular and clinical subset which needs new and effective treatment strategies in a setting of dismal prognosis.

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Technologic innovations, expensive new therapies, and improved access to treatment have all contributed to the Figure. Abstract Search and Selection 1546 Abstracts with word randomized or randomised assessed for eligibility 422 Abstracts not reporting RCT results excluded 75 Nonhuman studies 140 Background or conclusions 28 Nonrandomized 144 Systematic reviews 13 ≥4 pooled studies 22 Other 1124 Abstracts reporting RCT results included 720 Abstracts reporting RCT primary results 404 Abstracts reporting other RCT resultsA total of 1546 abstracts including the words randomized or randomised were selected for review. Of these, 720 presented primary results of a randomized clinical trial (RCT).

The recently developed lipoprotein insulin resistance index (LP‐IR) incorporates lipoprotein particle numbers and sizes and is considered to reflect both hepatic and peripheral IR. As tissue IR is a strong component of nonalcoholic fatty liver disease (NAFLD) pathogenesis, we aimed to assess the degree by which LP‐IR associates with hepatic fat content. This was a single‐center retrospective analysis of patients with NAFLD. LP‐IR, the homeostasis model assessment of insulin resistance (HOMA‐IR), and adipose tissue IR (Adipo‐IR) were measured simultaneously. Liver fat content was estimated by FibroScan controlled attenuated parameter. Associations were assessed using Spearman’s correlation and multivariate linear regression. The study included 61 patients. LP‐IR was correlated with HOMA‐IR (ρ = 0.30; P = 0.02), typically thought to reflect hepatic IR, but not with Adipo‐IR (ρ = 0.15; P = 0.25). Liver fat content was significantly associated with Adipo‐IR (ρ = 0.48; P < 0.001), LP‐IR (ρ = 0.35; P = 0.005), and to a lesser degree with HOMA‐IR (ρ = 0.25; P = 0.051). The association of liver fat with LP‐IR was limited to patients without diabetes (ρ = 0.60; P < 0.0001), whereas no association was seen in those with diabetes. In a multivariate model, Adipo‐IR, LP‐IR, and diabetes were independently associated with liver fat and together explained 35% of the variability in liver fat. Conclusion: LP‐IR is a reasonable measure of IR in non‐diabetic patients with NAFLD and is associated with hepatic fat content. Although adipose tissue is the major contributor to liver fat, the additional contribution of nonadipose tissues can be easily estimated using LP‐IR.