Thursday, November 30, 2017

Hyperammonemic encephalopathy following bariatric surgery

You can add this one to two growing lists: bariatric surgery complications and non hepatic hyperammonemias. [1] [2]

Mechanisms? From the first reference:

The specific mechanisms driving the hyperammonemic state after RYGB may be multifactorial. As it has been almost exclusively observed in women, X-linked partial ornithine transcarbamylase (OTC) deficiency has been implicated (Figure 2). Previously asymptomatic heterozygous OTC-deficient women can present when faced with catabolic stressors, and biochemical profiling is consistent with impaired urea cycle function. Zinc deficiency has also been proposed to interfere with OTC function (5). Nongenetic mechanisms of increased ammoniagenesis have been considered, including portosystemic shunting, severe hepatic dysfunction, and overgrowth of intestinal flora. A profound catabolic state may also play a role, driving protein breakdown and accumulation of nitrogenous waste products.

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