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April 1977

Host-Defense Mechanisms in Hidradenitis Suppurativa

Author Affiliations

From the Infectious Disease Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia. Dr Root is now with the Infectious Disease Section, Yale University, New Haven, Conn. Dr Dvorak is a fellow in Infectious Disease, University of Pennsylvania School of Medicine.

Arch Dermatol. 1977;113(4):450-453. doi:10.1001/archderm.1977.01640040058008

• 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/streptodernase, and purified protein derivative antigens. No abnormality was demonstrated in any granulocyte or cellmediated 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 aprocine glands without a generalized defect in host defense.

(Arch Dermatol 113:450-453, 1977)

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