Treatment-Refractory, Primary Immune Thrombocytopenic Purpura in a Patient with Celiac Disease.

BACKGROUND Immune thrombocytopenic purpura (ITP) is primarily caused by antibody-mediated destruction of platelets. Alterations in immune homeostasis can induce loss of peripheral tolerance and promote the development of self-reactive antibodies. Primary ITP is the diagnosis of exclusion made after the extensive work-up rules out other possible causes of thrombocytopenia.

Prevalence of hepatitis C virus infection in patients with cardiomyopathy.

Chronic hepatitis C can be associated with extrahepatic manifestations; thus, we explored the association of this viral infection with dilated cardiomyopathy in a group of sixty-three patients with a cardiac ejection fraction of less than 40% determined by an echocardiogram in a prospective study. Two of the forty-one patients with non-ischemic cardiomyopathy (4.8%) had serum antibodies to the hepatitis C virus and one of those had hepatitis C virus RNA (2.

A study of the mu opioid receptor gene polymorphism A118G in patients with primary biliary cirrhosis with and without pruritus.

The increase in opioidergic tone by the central administration of morphine, which binds to the mu opioid receptor, is associated with pruritus. Pruritus is a symptom of cholestasis, which appears to result, in part, from increased opioidergic tone; a central mechanism has been proposed. The single nucleotide polymorphism Al18G in exon 1 of the opioid receptor mu 1 (OPRM1) gene, which codes for the mu opioid receptor, has been associated with alterations in functions mediated by the endogenous opioid system.

Healing of leg ulcers associated with transjugular intrahepatic portosystemic shunt in decompensated cirrhosis: case series of a possible hepatodermal syndrome.

The occurrence of leg ulcers in patients with cirrhosis is not well documented in the literature. In this case series, we describe 4 patients with cirrhosis complicated by leg ulceration that failed all conventional therapy, yet healed completely following the placement of transjugular intrahepatic portosystemic shunt. The course of disease and the possibility of a hepatodermal syndrome underlying this observation are discussed.