High dose intravenous immunoglobulin in atopic dermatitis and hyper-IgE syndrome.
BACKGROUND
High dose intravenous immunoglobulin (IVIG) has immunoregulatory and anti-inflammatory properties that might benefit illnesses with exaggerated IgE responses including atopic dermatitis and hyper-IgE immunodeficiency syndrome.


OBJECTIVE
To determine if high-dose IVIG would be of benefit to patients with severe atopic dermatitis and/or hyper-IgE syndrome using serial clinical, pulmonary, and laboratory studies for evaluation.


METHODS
This was an open label study in which we gave patients with hyper-IgE syndrome (n = 1) or severe atopic dermatitis (n = 9) IVIG as a 10% solution (Venoglobulin I-Alpha Therapeutic Corporation, Los Angeles, CA) at a dose of 2 g/kg every 30 days for seven infusions.


RESULTS
Therapy was completed in nine of the ten patients. Skin disease improved slightly in six patients, remained unchanged in two patients, and worsened slightly in one patient. The average daily prednisone dosage was 6.8 mg/day prior to treatment and 5.1 mg/day during IVIG therapy (P = .1250). The three patients with abnormal pulmonary function showed very mild improvement of pulmonary function during treatment, but returned to baseline during follow-up. Flow cytometric studies showed no consistent pattern of change. IgA and IgM levels were unchanged. The mean serum IgE levels went from 3221+/-2454 IU/mL (SD) before IVIG to 2944+/-2491 IU/mL (P = .4609) during IVIG and then to 2321+/-2229 IU/mL (P = .1484) during the 6-month follow-up period. In vitro IgE production of peripheral blood mononuclear cells (PBMC) following IL-4 and anti-CD40 stimulation before IVIG was 6.6+/-3.1 ng/mL (SD) and 4.3+/-3.1 ng/mL (P = .1641) after six IVIG treatments. There were no significant trends in lymphocyte proliferative responses to PHA (phytohemaglutinin), Candida, tetanus, and anti-CD3 monoclonal antibody. Radioallergosorbent (RAST) testing showed no clear changes from positivity to negativity.


CONCLUSIONS
We conclude that IVIG was of no clear clinical benefit in these nine patients and did not significantly decrease IgE levels, IgE synthesis, or other measures of immunologic function.
Department of Pediatrics, UCLA School of Medicine, Los Angeles, California 90095-1752, USA.
M
M
Wakim
M
M
Alazard
A
A
Yajima
D
D
Speights
A
A
Saxon
E R
ER
Stiehm
D000293:Adolescent; D000328:Adult; D000906:Antibodies / Q000494:pharmacology; D015703:Antigens, CD / Q000032:analysis; D001402:B-Lymphocytes / Q000276:immunology; D019013:CD40 Antigens / Q000276:immunology; D002478:Cells, Cultured; D002648:Child; D003876:Dermatitis, Atopic / Q000628:therapy*; D004305:Dose-Response Relationship, Drug; D004485:Eczema / Q000473:pathology; D005434:Flow Cytometry; D005541:Forced Expiratory Volume; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis / Q000096:biosynthesis / Q000187:drug effects; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage* / Q000009:adverse effects / Q000627:therapeutic use*; D015847:Interleukin-4 / Q000494:pharmacology; D007589:Job Syndrome / Q000628:therapy*; D007694:Killer Cells, Natural / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects; D008213:Lymphocyte Activation; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D011241:Prednisone / Q000008:administration & dosage; D011852:Radioallergosorbent Test; D017455:Receptors, IgE / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology
D000906:Antibodies; D015703:Antigens, CD; D019013:CD40 Antigens; D016756:Immunoglobulins, Intravenous; D017455:Receptors, IgE; D015847:Interleukin-4; D007073:Immunoglobulin E; D011241:Prednisone