tetano
Editor, Senior Moderator
Pediatr Nephrol. 2010 Nov 7. [Epub ahead of print]
Pandemic H1N1 influenza A infection and (atypical) HUS-more than just another trigger?
Allen U, Licht C.
Division of Infectious Diseases, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Abstract
Atypical hemolytic uremic syndrome (aHUS) is caused by mutations resulting in an exceedingly active alternative complement pathway. While today more than half a dozen genes are involved in aHUS pathology, only about 50% of carriers precipitate the disease. The reason for this phenomenon remains unclear, and triggering events like intercurrent infections have been postulated. In this context, reports on the development of (a)HUS in patients concomitantly diagnosed with pandemic H1N1 influenza A (pH1N1) infection are of great interest. They establish-for the first time in the literature-the link between aHUS and pH1N1 infection. While illnesses associated with pH1N1 infections during the recent pandemics were generally mild, secondary bacterial infections (e.g. Streptococcus pneumoniae) are known in patients with influenza A infections to not only aggravate the disease course, but also serve as a possible HUS trigger. Assuming pH1N1 was the cause of HUS in the cases reported here, it remains an interesting but unanswered hypothesis whether an underlying complement defect served as a susceptibility factor, at least in a subgroup of patients. In the future, pH1N1, but also pH1N1-associated, bacterial infections will have to be considered in (a)HUS patients, and further studies will be required to examine the role of the complement system in this condition.
PMID: 21057815 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21057815
Pandemic H1N1 influenza A infection and (atypical) HUS-more than just another trigger?
Allen U, Licht C.
Division of Infectious Diseases, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Abstract
Atypical hemolytic uremic syndrome (aHUS) is caused by mutations resulting in an exceedingly active alternative complement pathway. While today more than half a dozen genes are involved in aHUS pathology, only about 50% of carriers precipitate the disease. The reason for this phenomenon remains unclear, and triggering events like intercurrent infections have been postulated. In this context, reports on the development of (a)HUS in patients concomitantly diagnosed with pandemic H1N1 influenza A (pH1N1) infection are of great interest. They establish-for the first time in the literature-the link between aHUS and pH1N1 infection. While illnesses associated with pH1N1 infections during the recent pandemics were generally mild, secondary bacterial infections (e.g. Streptococcus pneumoniae) are known in patients with influenza A infections to not only aggravate the disease course, but also serve as a possible HUS trigger. Assuming pH1N1 was the cause of HUS in the cases reported here, it remains an interesting but unanswered hypothesis whether an underlying complement defect served as a susceptibility factor, at least in a subgroup of patients. In the future, pH1N1, but also pH1N1-associated, bacterial infections will have to be considered in (a)HUS patients, and further studies will be required to examine the role of the complement system in this condition.
PMID: 21057815 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21057815