Kenneth S. Babe

PYODERMA GANGRENOSUM ASSOCIATED WITH ANTIPHOSPHOLIPID ANTIBODIES

An otberwise healthy 67-year-old man was seen for evaluation and treatment of painful right ankle skin ulcers. Physical examination revealed two closely situated cutaneous ulcerations measuring 2.0 by 3.0 cm^ and 1.7 by 2.0 cm^ in tbe region of tbe right medial malleolus (Fig. 1). Tbe border of the lesions appeared undermined, and tbe skin between and surrounding them was violaceous in color and infiltrated in texture. Abnormal laboratory values included tbe following: WBC 1780/mm^ Hgb 9.6 g/dL, platelets 81,000/mm^ PTT 40.8 s, Westergren ESR 102 mm/b, C-reactive protein 3.7 mg/dL (NV, 0-0.8), weakly positive RPR, and ANA 1:320 dilutions witb a homogeneous pattern. Anticardiolipin IgG antibodies were detected by ELISA and were quantitated at 33 g/L (0-15). The following were negative or normal: serum chemistries, urinalysis, PT, direct and indirect Coombs test, serum protein electrophoresis, and rheumatoid factor. Biopsy of perilesional skin revealed thrombosis of small and medium sized dermal blood vessels witbout accompanying inflammation or vasculitis {Fig. 2). The patient was treated with oral prednisone 15 mg twice daily, dapsone 100 mg daily, and cephradine 500 mg four times daily. Topical tberapy consisted of normal saline rinses followed by application of silver sulfadiazine cream and a telfa dressing. Over the course of several montbs, tbe skin lesions resolved slowly and completely, wbile tbe patients wbite blood cell counts returned to normal. Tbe patient continues to do well on a maintenance dose of oral aspirin 325 mg daily.

The pathogenesis of Munchausen syndrome. A review and case report.

The authors present a case of Munchausen syndrome notable for an extended premorbid length and lack of early identifiable antisocial behavior. The patients life history has been reconstructed, and an integrated psychobiological evaluation of the patient is given including neuroanatomical, neurohormonal, and neuropsychological assessments. Frontotemporal cerebral atrophy and lack of thyroid-stimulating hormone response to thyroid-releasing hormone infusion were found. Although self-object losses did appear to precipitate the Munchausen syndrome in a step-wise fashion, it appears that central nervous system deterioration might have been related to the development of the disorder.