Background:Unsafe injection practices are common in developing nations. Such practices, through contaminated needles and syringes, place injection recipient, healthcare workers and the community at large at risk of infection with blood borne viruses.Aim:An attempt was made to briefly describe an acute hepatitis outbreak that occurred in Gujarat, India, due to unsafe injection practices with a brief review of the literature.Subjects and Methods:An outbreak of acute hepatitis occurred in February-March 2009 in the Sabarkantha district of Gujarat in India. Blood samples were collected randomly from 25 cases, admitted in the local hospital during the ongoing outbreak. Screening was done using an immunoassay analyzer (Cobas e411; Roche Diagnostics, Indianapolis, IN, USA) for hepatitis B surface antigen (HBsAg), IgM and total antibodies to hepatitis B core antigen (HBc), hepatitis B e antigen (HBeAg) and antibody to HBe, antibodies to HCV, HIV and IgM antibodies to hepatitis A virus (HAV), as per the manufacturer's protocol.Results:Gross and continuous use of contaminated needle and syringes were responsible for this outbreak as all the patients gave history of receiving injections about 2-3 months prior to the development of clinical signs and symptoms, from one particular doctor. Mean age of the patients was 33.4 years (SD 12.9 years). Seventeen of these patients were males and eight were females. All patients were hepatitis B surface antigen positive, with median levels as 35,450 IU/mL (IQR 450-2,49,750 IU/mL). IgM HBc was positive in 22/25 (88%). HBe Ag was positive in 11 patients (44%). The median HBV DNA level was 2.6 × 104 IU/mL (IQR 1.18 × 102 to 6.7 × 106 IU/mL). No significant co-infection with other hepatitis viruses existed. All isolates were genotype D.Conclusions:The findings emphasize the role of unsafe injection practices in the community outbreak of hepatitis B infection, need to start routine surveillance system and increase awareness in health care workers regarding safe injection practices.
Background: Isolated ectopic gastric varices (IGV2) are present either in the body or antrum of the stomach or upper duodenum. The prevalence, natural history and clinical significance of these varices has not been adequately described. Materials and Methods: Consecutive patients with portal hypertension, prospectively studied and diagnosed to have IGV2, were assessed for their time of appearance – primary (at first presentation) or secondary (after obliteration of oesophageal varices), association with other varices, portal hypertensive gastropathy and any overt bleeding. Results: Fifty-three of the 1,128 (4.7%) patients had IGV2. The IGV2 were commonly seen in the antrum (53%), duodenum (32%), or at both sites (11%) and rarely in body and fundus (4%). IGV2 were predominantly (84.9%) secondary in origin, developing after oesophageal variceal obliteration. The median time for emergence of secondary IGV2 was 8.2 months for patients with cirrhosis, 12.8 months for non-cirrhotic portal fibrosis and 10.8 months for extra-hepatic portal vein obstruction. Eight (15%) patients had primary IGV2, 6 of them had underlying portal vein obstruction. Portal gastropathy (p < 0.05) and UGI bleeding were more common in the secondary than in primary IGV2. Bleeding due to IGV2 was seen only in 3 (5.7%) patients during a mean follow-up of 36.3 ± 12.1 months, and could be successfully managed with endoscopic ligation or obliteration. Conclusions: Isolated ectopic gastric varices are not uncommon and generally develop following obliteration of main variceal columns. They rarely bleed and often can be managed with endoscopic interventions.
Therapeutic ERCP procedures like endoscopic sphincterotomy with stenting or nasobiliary drainage are effective in management of bile leaks following blunt abdominal trauma.
Non‐cirrhotic portal hypertension (NCPH) comprises of diseases having an increase in portal pressure (PP) due to intraheptic or prehepatic lesions, in the absence of cirrhosis. The lesions are generally vascular, either in the portal vein, its branches or in the perisinusoidal area. Because the wedged hepatic venous pressure (WHVP) is near normal, measurement of intravariceal or intrasplenic pressure is needed to assess portal pressure. The majority of the diseases included in the category of NCPH are well characterized disease entities where portal hypertension (PHT) is a late manifestation and hence, these are not discussed. Two diseases which present only with features of PHT and are common in developing countries are NCPF and extra‐hepatic portal vein obstruction (EHPVO). Non‐cirrhotic portal fibrosis is a syndrome of obscure etiology, characterized by ‘Obliterative portovenopathy’ leading to PHT, massive splenomegaly, repeated well tolerated episodes of variceal bleeding and anemia in young adults from low socio‐economic strata of life. The hepatic parenchymal functions are nearly normal. Jaundice, ascites and hepatic encephalopathy are rare. Management of variceal bleeding remains the main concern as nearly 85% of patients with NCPF present with variceal bleeding. Endoscopic variceal ligation or sclerotherapy are equally effective in about 90–95% of the patients. Gastric varices are seen in about 25% patients and a bleed from them can be managed with cyanoacrylate glue injection or surgery. Other indications for surgery include failure of endoscopic therapy to control acute bleed and symptomatic hypersplenism. The prognosis of patients with NCPF is good and 5‐years survival rates in patients in whom variceal bleeding can be controlled is about > 95%. © 2002 Blackwell Publishing Asia Pty Ltd
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