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Lawrence F Naarian, MD, Editor PIR
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sydney_sutherland{at}urmc.rochester.edu Lawrence F Naarian, MD
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A reader pointed out a sentence in the September 2008 Index of Suspicion, Case #4, that needs clarification. In the September 2008 issue (PIR.29;pg 328), in the discussion of Case #4 in "Index of Suspicion," the following statement appears: "Progression to DKA is seen exclusively in type 1 diabetes." Although DKA is associated with type 1 diabetes most commonly, it can be the presenting manifestation in as many as 25% of adolescents afflicted with type 2 diabetes." Note: For a further discussion of type 2 diabetes, including the sometimes challenging task of differentiating between types 1 and 2, the reader is referred to Cowell KM. Focus on Diagnosis. Type 2 Diabetes Mellitus. PIR. 2008; 29: 289-292 (August 2008 issue). Conflict of Interest:None declared |
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Martin R Correa, Allergist and Immunologist Florida Center for Allergy and Asthma Care
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user136986{at}aol.com Martin R Correa
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In June, 2007 a japanese group described, and published in Nature for first time the cause of the classical Hyper IgE syndrome (HIES) "Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome. Yoshiyuki Minegishi et. al.... Then in October, 2007 a group lead by Dr Bodo Grimbacher described again in the New England Journal of Medicine "Stat 3 mutations in the Hyper IgE syndrome" STAT3 mutation is the predominant cause of sporadic and familial hyper-IgE syndrome. Although other genomic loci may also be involved for patients with the syndrome reported as autosomal recessive hyper-IgE syndrome. The extraordinary elevation of the IgE level in persons with the disorder, seen from birth through adulthood and uncorrelated with eosinophilia, may reflect the known role of STAT3 in mediating interleukin-21 receptor signaling, since interleukin-21 receptor –knockout mice have elevated IgE levels. In conclusion, the newly recognized genetic cause of the hyper-IgE syndrome — STAT3 mutation — affects complex, compartmentalized somatic and immune regulation. The discovery of this genetic cause opens new doors to understanding organ-specific infection, inflammation, and therapy. Conflict of Interest:None declared |
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lawrence f nazarian, editor-in-chief pediatrics in review
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sydney_sutherland{at}urmc.rochester.edu lawrence f nazarian
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In the September 2008 issue (Pediatr Rev. 29:328), in the discussion of Case #4 in "Index of Suspicion,the following statement appears: "Progression to DKA (diabetic ketoacidosis) is seen exclusively in type 1 diabetes." Although DKA is associated with type 1 diabetes most commonly, it can be the presenting manifestation in as many as 25% of adolescents afflicted with type 2 diabetes. For an additional discussion of type 2 diabetes, including the sometimes challenging task of differentiating between types 1 & 2, the reader is referred to Cowell KM. Focus on Diagnosis. Type 2 Diabetes Mellitus. Pediatri Rev. 2008;29:289-292 (August 2008 issue). Conflict of Interest:None declared |
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