Modified citrus pectin stops progression of liver fibrosis by inhibiting galectin-3 and inducing apoptosis of stellate cells.

Modified citrus pectin (MCP) is a pH modified form of the dietary soluble citrus peel fiber known as pectin. The current study aims at testing its effect on liver fibrosis progression. Rats were injected with CCl4 (1 mL/kg, 40% v/v, i.p., twice a week for 8 weeks). Concurrently, MCP (400 or 1200 mg/kg) was administered daily in drinking water from the first week in groups I and II (prophylactic model) and in the beginning of week 5 in groups III and IV (therapeutic model). Liver function biomarkers (ATL, AST, and ALP), fibrosis markers (laminin and hyaluronic acid), and antioxidant biomarkers (reduced glutathione (GSH) and superoxide dismutase (SOD)) were measured. Stained liver sections were scored for fibrosis and necroinflammation. Additionally, expression of galectin-3 (Gal-3), α-smooth muscle actin (SMA), tissue inhibitor metalloproteinase (TIMP)-1, collagen (Col)1A1, caspase (Cas)-3, and apoptosis related factor (FAS) were assigned. Modified pectin late administration significantly (p < 0.05) decreased malondialdehyde (MDA), TIMP-1, Col1A1, α-SMA, and Gal-3 levels and increased levels of FAS, Cas-3, GSH, and SOD. It also decreased percentage of fibrosis and necroinflammation significantly (p < 0.05). It can be concluded that MCP can attenuate liver fibrosis through an antioxidant effect, inhibition of Gal-3 mediated hepatic stellate cells activation, and induction of apoptosis.

Endoscopic ultrasound of isolated gastric corrosive stricture mimicking linitis plastica.

Isolated gastric outlet obstruction after 1 month of asymptomatic ingestion of corrosive is a rare phenomenon and rarely reported. In this type of cases, diagnosis is very difficult due to no symptoms at the time of poisoning, and biased history. We report a case of a young male presented with isolated gastric outlet obstruction after 1 month of asymptomatic ingestion of toilet cleaner, which was known to us later, mimicking linitis plastica. On upper endoscopy, the stomach was grossly edematous, antrum edematous and inflamed with reduced distensibility and narrow pyloric canal. Endoscopic ultrasound of the stomach revealed diffuse thickening of the gastric wall, mainly the antrum, involving submucosa and muscularis propria. We propose corrosive injury to be in the differential diagnosis of gastric linitis plastica.

Post-splenectomy splenosis presenting as hepatocellular carcinoma in the left lateral section of the liver: A case report.

INTRODUCTION: Defined as heterotrophic autotransplantation of splenic tissue after splenic trauma or surgery. PRESENTATION OF CASE: We present a case of 45 years old female patient with past history of splenectomy for haemolyticanaemia. Complaining of abdominal pain the patient was investigated by abdominal CT scan which revealed a focal lesion in the left lateral section of the liver suspicious to be hepatocellular carcinoma and gall bladder stones. Serum α-fetoprotein was within normal range. Exploration revealed a well encapsulated lesion completely separable from the liver and the diaphragm. Histopathological examination confirmed the diagnosis of splenosis. Although it is a rare condition, we recommend that the diagnosis of splenosis should be put in consideration in every patient with past history of splenectomy for proper management. DISCUSSION: Although several cases of hepatic splenosis have been reported in the literature, supra-hepatic splenosis as our case has been rarely described. CONCLUSION: Considering patients past history of splenectomy or splenic trauma should add splenosis to the list of possible differential diagnosis to avoid unnecessary surgical intervention.