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Background: Antimicrobial resistance has decreased eradication rates for Helicobacter pylori infection worldwide. A sequential treatment schedule has been reported to be effective, but studies published to date were performed in Italy. We undertook this study to determine whether these results could be replicated in India. Methods: A randomized, open-labeled, prospective controlled trial comparing sequential vs. standard triple-drug therapy was carried out at Lokmanya Tilak Municipal General Hospital, Mumbai. Two hundred and thirty-one patients with dyspepsia were randomized to a 10-day sequential regimen (40 mg of pantoprazole, 1 g of amoxicillin, each administered twice daily for the first 5 days, followed by 40 mg of pantoprazole, 500 mg of clarithromycin, and 500 mg of tinidazole, each administered twice daily for the remaining 5 days) or to standard 14-day therapy (40 mg of pantoprazole, 500 mg of clarithromycin, and 1 g of amoxicillin, each administered twice daily). Results: The eradication rate achieved with the sequential regimen was significantly greater than that obtained with the triple therapy. Per-protocol eradication rate of sequential therapy was 92.4 % (95 % CI 85.8–96.1 %) vs. 81.8 % (95 % CI 73.9–87.8 %) ( p = 0.027) for standard drug therapy. Intention-to-treat eradication rates were 88.2 % (95 % CI 80.9–93.0 %) vs. 79.1 % (95 % CI 71.1–85.4 %), p = 0.029, respectively. The incidence of major and minor side effects between therapy groups was not significantly different (14.6 % in the triple therapy group vs. 23.5 % in sequential group, p = 0.12). Follow up was incomplete in 3.3 % and 4.7 % patients in standard and sequential therapy groups, respectively. Sequential therapy includes one additional antibiotic (tinidazole) that is not contained in standard therapy. Conclusions: Sequential therapy was significantly better than standard therapy for eradicating H. pylori infection. [ABSTRACT FROM AUTHOR]

Abstract: Sweet syndrome,also known as acute febrile neutrophilic dermatosis , is one of the rare cutaneous association of ulcerative colitis.Only few cases of Sweet syndrome associated with ulcerative colitis have been reported in literature. We herein describe a case of young female with acute exacerbation of ulcerative colitis associated with erythematous , papular skin lesions which on biopsy were consistent with Sweet syndrome. Treatment with intravenous steroids resulted in improvement of ulcerative colitis and disappearance of cutaneous lesions. Cutaneous lesions of Sweet syndrome in ulcerative colitis parallel the bowel disease activity in majority of the cases but sometimes may precede the intestinal symptoms and rarely may appear after procto-colectomy for acute severe ulcerative colitis.Introduction., (© Journal of the Association of Physicians of India 2011.)

Mucormycosis is a rare, opportunistic fungal infection that occurs almost exclusively in immunocompromised hosts such as patients with diabetes mellitus, leukemia, lymphoma, renal disease, septicemia, burns, malnutrition, and following long-term treatment with steroids and antibiotics. Based on the clinical presentation and involvement, mucormycosis is classified as six major forms, namely, rhinocerebral, pulmonary, cutaneous, gastrointestinal (GI), disseminated and miscellaneous, with rhinocerebral and pulmonary being the common forms. GI mucormycosis is rare, accounting for only 7% of all cases; however, the mortality rate is as high as 85%. Here we report a case of a young immunocompetent male who developed gastric invasive mucormycosis during an acute illness and succumbed to it despite all supportive care., (© Journal of the Association of Physicians of India 2011.)

Patterson Brown Kelly or Plummer-Vinson syndrome is characterized by dysphagia, iron deficiency anemia and post-cricoidal esophageal web. Waldenstorm introduced the term 'sideropenic dysphagia' because of absence of stainable iron in the bone marrow. There is increased incidence of upper aero-digestive tract carcinoma in patients with Plummer-Vinson syndrome has been well established. The reported rates range from 4% to 16%, with almost all cases occurring at the postcricoid location.We have reported here a case of a 48-year-old woman with dysphagia , upper esophageal web and iron deficiency anemia . Dilatation of esophageal web with subsequent endoscopy showed mid- esophageal growth which on biopsy showed squamous cell carcinoma., (© Journal of the Association of Physicians of India 2011.)

A middle aged male with no known comorbidities presented with history of colicky abdominal pain, low grade fever and weight loss. Laboratory parameters were normal except low albumin. Imaging showed multiple areas of mural thickening with enhancement in jejunum & ileum. On Colonoscopy there was a thickened and deformed ileum with multiple ulcers. The biopsy showed co-infection of CMV and histoplasma, urine antigen for histoplasma was positive and CMV DNA detected in blood. He was successfully treated with combination of Valgancyclovir and Amphotericin-B followed by itraconazole., (© Journal of the Association of Physicians of India 2011.)

Aim: To estimate the prevalence of inherited prothrombotic risk factors in patients with splanchnic venous thrombosis (SVT) and Budd-Chiari syndrome (BCS) and to compare the risk factor profiles between these two groups., Methods: In this prospective study, patients with abdominal venous thrombosis were studied. The patients were divided into two groups on the basis of the veins involved; splanchnic venous thrombosis group [portal (PVT), splenic, superior mesenteric veins (SMV)] and Budd-Chiari group (hepatic vein, IVC thrombosis). Thrombophilia profile including protein C, protein S, antithrombin III, factor V Leiden mutation, activated protein C, factor VIII level, CD55, CD59, IgM cardiolipin, IgG cardiolipin, anti-β2 glycoprotein, JAK2 mutation, homocysteine levels, MTHFR and lupus anticoagulant was done in all patients., Results: Out of 30 patients, 23 patients had SVT, 7 had BCS, including 2 of the 23 patients with SVT had mixed venous thrombosis, PVT and SMV thrombosis. Risk factors were found in 21/30 (70%) patients [17/23 (73.9%) of PVT. 4/7 (57.1% of BCS] and multiple risk factors were overall present in 8/23(34.7%) patients of SVT., Conclusions: Hereditary risk factors play an important role in the etiopathogenesis of abdominal venous thrombosis and hyperhomocysteinemia and protein S deficiency are the most common risk factors., (© Journal of the Association of Physicians of India 2011.)