Journal of clinical gastroenterology
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Gut microorganisms have the potential to influence weight gain and fat deposition through a variety of mechanisms. One factor is the ability of microorganisms in the large intestine to release energy by fermenting otherwise indigestible components of the diet ("energy harvest"). This energy becomes available to the host indirectly through the absorption of microbially produced short-chain fatty acids. ⋯ There is conflicting evidence, however, on the extent to which gut microbiota composition differs between obese and nonobese humans. In contrast, there is increasing evidence to suggest that gut microorganisms and their metabolic products can influence gut hormones, inflammation, and gut motility. Any changes in gut microbiota composition that influence energy expenditure, satiety, and food intake have the potential to alter weight gain and weight loss, but a better understanding of the impact of different members of the gut microbial community upon host physiology is needed to establish these relationships.
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J. Clin. Gastroenterol. · Nov 2011
Case ReportsMethylnaltrexone for treatment of acute colonic pseudo-obstruction.
Acute colonic pseudo-obstruction (ACPO) or Ogilvie syndrome is an idiopathic syndrome of dilation of the colon without mechanical obstruction that develops in hospitalized patients usually in the setting of significant medical and surgical conditions. Standard care therapy includes colonoscopic decompression or neostigmine. The latter is not Food and Drug Administration-approved for this indication but has been the recent intervention of choice. ⋯ There was a brisk response to methylnaltrexone, a μ-opioid-receptor antagonist which does not cross the blood-brain barrier. This is the first case report in the literature and in the pharmaceutical company's data bank that illustrates a potential role for methylnaltrexone in ACPO. Prospective, larger studies to determine the role of methylnaltrexone in ACPO are warranted.
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The development of pulmonary arterial hypertension in the setting of portal hypertension is known as portopulmonary hypertension. Portal hypertension is thought to predispose patients to disturbances in the homeostatic regulation of numerous neurohumoral and vasoactive mediators that induce the development of pulmonary arterial hypertension. Portopulmonary hypertension is pathologically indistinguishable from idiopathic pulmonary arterial hypertension and is characterized by the development of vasoconstriction, vascular remodeling, and thrombosis within the pulmonary vasculature. ⋯ However, the diagnosis of portopulmonary hypertension is based on unique hemodynamic criteria as determined by right heart catheterization. Untreated portopulmonary hypertension portends a poor prognosis, and the efficacy of current treatment modalities is limited. At present, the primary goals of therapy are to provide symptomatic relief, prolong survival, and improve pulmonary hemodynamics to facilitate safe and successful liver transplantation.