Host-defense mechanisms in hidradenitis suppurativa.
Host-defense mechanisms were studied in seven patients with active hidradenitis suppurativa (HS). Granulocyte phagocytic function was measured by ingestion of Staphylococcus aureus labeled with radioactive carbon 14 and intracellular killing was determined by bactericidal pour plate method. Chemotaxis was measured by radioactive counting of sodium chromate Cr 51 granulocytes migrating in modified Boyden chambers. Granulocyte adherence was estimated in vitro by filtering blood samples through nylon fiber columns. Cell-mediated immunity was measured by intradermal delayed hypersensitivity responses to Candida, mumps. streptokinase/streptodornase, and purified protein derivative antigens. No abnormality was demonstrated in any granulocyte or cell-mediated immune function tests. Moreover, all patients had normal immunoglobulin levels and elevated total hemolytic complement. Therefore, we conclude that HS is a localized chronic infection of apocrine glands without a generalized defect in host defense.[1]References
- Host-defense mechanisms in hidradenitis suppurativa. Dvorak, V.C., Root, R.K., MacGregor, R.R. Archives of dermatology. (1977) [Pubmed]
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