Uric acid (UA) is the final end product of purine catabolism and is formed from xanthines and hypoxanthines. Hyperuricemia can be secondary to either an exaggerated production of UA that follows high cellular turnover conditions or, most frequently, to a low renal excretion in patients with impaired renal function. Recent data suggest that serum UA (SUA) at high-normal level is associated with cardiovascular disease risk factors and cardiovascular disease, often being a predictor of incident events. Preliminary data suggest that the reduction of SUA level in subjects with normal-high SUA could prevent at least a part of target-organ damage related to high SUA, especially when xanthine oxidase is selectively inhibited.
A 67-year-old woman presented with a year-long history of general malaise, low-grade fever, diarrhea, and a 20-kg weight loss. She had a history of hypertension and depressive disorder. In the previous 4 years, she had undergone several rheumatologic examinations for polyarthritis and, having been diagnosed with seronegative rheumatoid arthritis, she had been treated with steroids, methotrexate, and etanercept, with little benefit. Recent laboratory tests showed: hemoglobin, 8.3 g/dL; mean corpuscular volume, 70 fL; erythrocyte sedimentation rate, 78; and C-reactive protein, 6.4 mg/dL. To evaluate the microcytic anemia and the diarrhea, endoscopic investigations had been performed a few months earlier. Esophagogastroduodenoscopy showed villous atrophy at the level of DII; histology was compatible with intramucosal xanthoma. There were no pathologic findings at colonoscopy. The situation had not been further investigated. At presentation, the physical examination revealed lower limb edema, skin and mucosal pallor, and a body mass index of 17.4 kg/m 2. Laboratory tests showed microcytic anemia (hemoglobin, 10.0 g/dL; mean corpuscular volume, 74 fL), increased acute phase proteins (erythrocyte sedimentation rate, 59; C-reactive protein, 8.53 mg/dL), and malabsorption (albumin, 2.5 g/dL; multiple electrolytes deficiencies including iron, vitamin A, and vitamin D deficiency). Abdominal ultrasound examination revealed 3 small lymph nodes in the periaortic region (maximum diameter, 10 mm), marked mesenteric and ileal wall thickening, mild jejunal wall thickening, an increased number of connivent valves, and a mild amount of peri-intestinal fluid effusion (Figure A, B). What is the likely diagnosis and the appropriate treatment? Look on page 1254 for the answer and see the Gastroenterology website (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and images in GI.
Background: Combination therapy with an angiotensin-converting enzyme (ACE) inhibitor and a thiazide diuretic has proven to be effective in the treatment of hypertension with or without end-organ damage. Discussion: The mechanism of action of such a combination therapy may involve a opposite effect on the renin-angiotensinaldosterone system (RAAS) with possible "functional" synergistic effects. Indeed, while diuretics can initially reduce intravascular volume leading to an activation of the RAA system with consequent vasoconstriction and salt and water retention, the concomitant presence of an ACE inhibitor may prevent such a counterregulatory response on neurohumoral system. This creates the conditions for the achievement of a maximal antihypertensive effect for both the ACE inhibitor and the diuretic.
Helicobacter pylori plays an important role in the pathogenesis of chronic active gastritis, peptic ulcer and gastric mucosa-associated lymphoid tissue-lymphoma, and is also involved in carcinogenesis of the stomach. Since now no current first-line therapy is able to cure the infection in all treated patients. We evaluated data on the most successful therapy regimens-sequential, concomitant and quadruple therapies-and on the standard therapy available for H. pylori eradication. When therapy fails several factors may be involved: we reviewed both bacterial and host factors that can affect the eradication and that can be involved in therapeutic management of the H. pylori infection.
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