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Severe septicaemia in a patient with polychondritis and Sweet’s syndrome after initiation of treatment with infliximab
  1. F G Matzkies1,
  2. B Manger1,
  3. M Schmitt-Haendle1,
  4. T Nagel1,
  5. H-G Kraetsch1,
  6. J R Kalden1,
  7. H Schulze-Koops1,2
  1. 1University of Erlangen-Nuremberg, Department of Internal Medicine III and Institute for Clinical Immunology, Krankenhausstrasse 12, 91054 Erlangen, Germany
  2. 2Nikolaus Fiebiger Centre for Molecular Medicine, Clinical Research Group III, University of Erlangen-Nuremberg, Glueckstrasse 6, 91054 Erlangen, Germany
  1. Correspondence to:
    Dr H Schulze-Koops, Nikolaus Fiebiger Centre for Molecular Medicine, Clinical Research Group III, University of Erlangen-Nuremberg, Glueckstrasse 6, 91054 Erlangen, Germany;
    Schulze-Koops{at}med3.imed.uni-erlangen.de

https://doi.org/10.1136/ard.62.1.81

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    RD Sweet first described an acute febrile neutrophilic dermatosis in 1964 characterised by acute onset, fever, leucocytosis, and erythematous plaques.1 Skin biopsy specimens show infiltrates consisting of mononuclear cells and neutrophils with leucocytoclasis, but without signs of vasculitis. Sweet’s syndrome is frequently associated with solid malignancies or haemoproliferative disorders, but associations with chronic autoimmune connective tissue disorders have also been reported.2 The aetiology of Sweet’s syndrome is unknown, but evidence suggests that an immunological reaction of unknown specificity is the underlying mechanism.

    CASE REPORT

    A 51 year old white man with relapsing polychondritis (first diagnosed in 1997) was admitted to our hospital in June 2001 with a five week history of general malaise, fever, recurrent arthritis, and complaints of morning stiffness. Besides autoimmune polychondritis, he had insulin dependent diabetes mellitus that was diagnosed in 1989.

    On admission, he presented with multiple small to medium, sharply demarked, raised erythematous …

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