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Gianfranco Ciboddo, MD; Francesca Crosti, MD; Giuseppe Di Lucca, MD; Matteo Bellone, MD
Istituto Scientifico San Raffaele Milan, Italy

JAMA. 1987;258(14):1892.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Recently, Mayer et al¹ suggested that hyper-IgM hypogammaglobulinemia might be due to a defect in control of the isotype switch by a specific T-lymphocyte helper cell subpopulation.

Report of a Case.—

A 33-year-old woman with a clinical history of recurrent respiratory tract infections, cervical suppurative lymphadenitis, and ear drainage came under our observation for hypogammaglobulinemia. On admission she was in good health; results of physical examination and laboratory tests were normal, except for serum immunoglobulin values, which showed the typical pattern of hyper-IgM hypogam maglobulinemia. We found the same immunodeficiency in a living 28-yearold brother; two other brothers had died at the ages of 18 months and 10 years, respectively, from overwhelming infections. The patient's parents, a living 32-year-old brother, and her children (a 5 1/2-year-old girl and a 2 1/2-year-old boy) showed normal immunoglobulin values.

Comment.—

The inheritance in this family resembles that of the . . . [Full Text PDF of this Article]

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