1f:T4c3,The purpose of this study was to assess the findings on chest high resolution computed tomography (HRCT) in patients with primary humoral immunodeficiency. HRCT was prospectively and consecutively performed in 19 patients with primary humoral immunodeficiency, aged 15-64 years (mean 36), and in 15 healthy subjects. HRCT results were correlated with clinical and biological data. Bronchial lesions were observed in 11 patients (58%), consisting either of bronchial wall thickening in eight or bronchiectasis in eight; both were present in five patients. Lobar and/or segmental collapses were found in seven patients (37%), scars in eight patients (42%), interstitial lesions in six patients (32%), and lobular air-trapping in two patients (11%). Parenchymal collapses were correlated with the annual frequency of infections (p = 0.03) and with the IgA level (p = 0.01). Scars were correlated with the annual frequency of infections (p = 0.04). No correlation was found between bronchial wall thickening or bronchiectasis and the data analysed. In conclusion, HRCT is a useful method to demonstrate lung disease in primary humoral immunodeficiencies, with special emphasis on bronchial changes and interstitial lesions.20:T454,UNTIL the acquired immunodeficiency syndrome (AIDS) emerged six years ago,¹defects in immunity were considered rare. It is important to realize, however, that it was from patients with genetic abnormalities of the immune system^2-5that the functions and components of the normal immune system were elucidated, information that was later applied to the delineation of the immunologic abnormalities in AIDS.¹Immunodeficiency diseases may involve any of the components of the immune system, including lymphocytes, phagocytic cells, and complement proteins.^2-4Despite considerable advances in understanding of the cellular and molecular abnormalities present in the various known primary immune defects,⁵it is clear that the fundamental biologic errors for most of them remain unknown.^2-4Exceptions include two accompanied by purine salvage pathway enzyme deficiencies—adenosine deaminase (ADA) in some cases of autosomal recessive severe combined immunodeficiency (SCID) and purine nucleoside phosphorylase (PNP) in some patients with Nezelof's

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