Decreased vitamin A levels in common variable immunodeficiency: vitamin A supplementation in vivo enhances immunoglobulin production and downregulates inflammatory responses

• Published in: European journal of clinical investigation Vol. 30; no. 3; pp. 252 - 259
• Main Authors: Aukrust, Müller, Ueland, Svardal, Berge, Frøland
• Format: Journal Article
• Language: English
• Published: Oxford BSL Blackwell Science Ltd 01.03.2000
• Subjects: Adult; Aged; Common variable immunodeficiency; Common Variable Immunodeficiency - blood; Common Variable Immunodeficiency - complications; Common Variable Immunodeficiency - immunology; Cytokines - biosynthesis; Dietary Supplements; Down-Regulation; Female; Humans; Immunoglobulin G - biosynthesis; immunoglobulin production; interleukin-10; Lymphocyte Activation; Male; Middle Aged; Monocytes - immunology; Retinol-Binding Proteins - metabolism; Retinol-Binding Proteins, Plasma; T-Lymphocytes - immunology; vitamin A; Vitamin A - blood; Vitamin A - pharmacology; Vitamin A Deficiency - complications; Vitamin A Deficiency - immunology
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1046/j.1365-2362.2000.00619.x

Background Vitamin A has a broad range of immunological effects, and vitamin A deficiency is associated with recurrent infections. Common variable immunodeficiency (CVI) is a group of B‐cell deficiency syndromes with impaired antibody production and recurrent bacterial infections as the major manifestations, but the immunological dysfunctions may also include T cells and macrophages. In the present study we examined the possible role of vitamin A deficiency in CVI. Patients and methods We analysed plasma vitamin A levels in 20 CVI patients and 16 controls, and examined the relationships between vitamin A and clinical, immunological and metabolic parameters in CVI. In the six CVI patients with the lowest vitamin A levels we also studied the effect of vitamin A supplementation in vivo on several immunological functions in these patients. Results (i) The majority of CVI patients had decreased vitamin A levels compared with healthy controls, as found in both cross‐sectional and longitudinal testing. (ii) Low vitamin A levels were associated with the occurrence of chronic bacterial infections and splenomegaly as well as high neopterin levels. Decreased levels of carrier protein and malabsorption were not observed. (iii) Vitamin A supplementation in patients with low vitamin A levels resulted in increased interleukin‐10 (IL‐10) and decreased tumour necrosis factor‐α (TNFα) levels, as found in both plasma and monocyte supernatants, possibly favouring anti‐inflammatory net effects. (iv) Vitamin A supplementation in vivo also enhanced anti‐CD40‐stimulated IgG production, serum IgA levels and phytohaemagglutinin (PHA)‐stimulated peripheral blood mononuclear cell (PBMC) proliferation. Conclusion A considerable subgroup of CVI patients appears to be characterized by low vitamin A levels. Our findings support a possible role for vitamin A supplementation in CVI, perhaps resulting in enhanced immunoglobulin synthesis and downregulated inflammatory responses.