Critical care management of systemic mastocytosis: when every wasp is a killer bee.

Since the critical care physician will most likely be involved in a life-threatening expression of systemic mastocytosis, recognition of this disease is of utmost importance in the critical care management of these patients. Mastocytosis is a severely under-recognized disease because it typically occurs secondary to another condition and thus may occur more frequently than assumed. In this article, we will review the current knowledge on the treatment of mastocytosis crises with an emphasis on critical care management. Mastocytosis is characterized by the clonal proliferation and accumulation of mast cells in different tissues. Mast cell mediators contain a wide range of biologically active substances that may lead to itching and hives but may ultimately lead to anaphylactic shock caused by the release of histamine and other mediators from mast cells. The mainstay of therapy is the avoidance of potential triggers of mast cell degranulation and, if unsuccessful, blocking the cascade of mast cell mediators. The critical care physician should be well aware of the special precautions which should be kept in mind throughout the management of a mastocytosis crisis to avoid massive mast cell degranulation. Histamine-releasing drugs and certain physical triggers like temperature change should be avoided.

Chronic hepatitis E infection in lung transplant recipients.

BACKGROUND: Hepatitis E virus (HEV) genotype 3 has been identified in patients with autochthonous HEV infections in developed countries and is currently being recognized as an emerging zoonotic pathogen. HEV infection may lead to a chronic hepatitis in immune-compromised patients. METHODS: We studied the incidence of HEV in adult lung transplant recipients at the Medical University Vienna and the University Medical Center Groningen. These recipients presented with elevated liver test results during the post-transplant follow-up period. The time of infection was investigated using stored specimens, and the HEV genotype was determined by sequence analysis of the open reading frame (ORF)1 and ORF2 region. RESULTS: The study included 468 adult lung transplant recipients. Ten patients (2.1%) tested positive for HEV RNA. At the time of HEV detection, all patients had elevated liver test results, with median alanine aminotransferase levels of 77 U/liter and showed a mild hepatitis. A chronic HEV infection was diagnosed in the 8 lung transplant recipients who survived longer than 6 months after transplantation. Viral genotyping revealed only genotype 3 strains. In 2 of the lung transplant recipients treated with oral ribavirin monotherapy, HEV RNA was cleared from the plasma within 2 months with simultaneous normalization of alanine aminotransferase levels. CONCLUSIONS: Chronic HEV is an important cause of liver test abnormalities after lung transplantation; therefore, routine screening for HEV RNA is strongly recommended in lung transplant recipients. Oral ribavirin appears to be a safe and effective treatment for chronic HEV infection in lung transplant recipients.