Hyperammonemic Coma—Barking Up the Wrong Tree

Hepatic encephalopathy and myxedema coma share clinical features: coma, ascites, anemia, impaired liver functions, and a “metabolic” electroencephalogram (EEG). Hyperammonemia, a hallmark of hepatic encephalopathy, has also been described in hypothyroidism. Differentiation between the 2 conditions, recognition of their possible coexistence, and the consequent therapeutic implications are of utmost importance. We describe a case of an 82-year-old woman with a history of mild chronic liver disease who presented with hyperammonemic coma unresponsive to conventional therapy. Further investigation disclosed severe hypothyroidism. Thyroid hormone replacement resulted in gain of consciousness and normalization of hyperammonemia. In patients with an elevated ammonia level, altered mental status, and liver disease, who do not have a clear inciting event for liver disease decompensation, overwhelming evidence of hepatic decompensation, or who do not respond to appropriate therapy for hepatic encephalopathy, hypothyroidism should be considered and evaluated

Endocrine therapy for growth retardation in paediatric inflammatory bowel disease

Inflammatory bowel disease, particularly Crohn’s disease (CD), can potentially cause growth failure during childhood as well as a reduction in final adult height. The underlying mechanism is multifactorial and includes poor nutrition, chronic inflammation, and the prolonged use of steroids. Despite major advances in the treatment of CD, current cohorts of children continue to display a deficit in linear growth and may qualify for growth-promoting hormonal therapy. However, currently there is limited evidence to support the use of endocrine therapy directed primarily at improving growth. This review is aimed at summarising the current evidence for growth impairment in inflammatory bowel disease and discusses the rationale for using growth promoting therapy