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Increased plasma chemoattractant in Sweet's syndrome.

S S Kaplan, H L Wechsler, R E Basford

Journal of the American Academy of Dermatology

|June 1, 1985

Summary

This study investigated neutrophil function in a patient with Sweet's syndrome and acne, finding increased chemoattractant activity. Isotretinoin therapy reduced this activity, but aspirin only managed symptoms, not the underlying chemoattractant.

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Area of Science:

Dermatology
Immunology

Background:

Sweet's syndrome is an inflammatory condition characterized by fever, neutrophilia, and tender skin lesions.
Acne vulgaris, particularly the severe cystonodular form, can also involve inflammatory processes.

Observation:

Neutrophil function, including chemotaxis, phagocytosis, metabolic activation, and bacterial killing, was evaluated over 2.5 years in a patient with Sweet's syndrome and cystonodular acne.
Plasma leukotactic activity and serum chemoattractant levels were specifically monitored.
The patient received isotretinoin therapy and aspirin for symptom management.

Findings:

Neutrophil chemotaxis was frequently elevated, particularly during Sweet's syndrome exacerbations, and decreased during isotretinoin treatment.
A heat-stable, nonlipid chemoattractant was consistently present in the patient's serum, except during isotretinoin therapy.
While aspirin alleviated symptoms, it did not eliminate the plasma chemoattractant.

Implications:

These findings support the hypothesis that elevated chemoattractant levels drive neutrophil recruitment and inflammation in Sweet's syndrome.
Isotretinoin may modulate neutrophil activity and chemoattractant levels in this context.
Aspirin offers symptomatic relief but does not address the core chemoattractant abnormality in Sweet's syndrome.