Reversible drug-induced antiphospholipid syndrome.

We report an original case of reversible antiphospholipid syndrome (APS) due to minocycline in a young male patient who experienced recurrent strokes while taking minocycline. He started minocycline therapy (50 mg twice daily) at 15 years old for acne. After three years of treatment, the patient experienced a lateral medullary syndrome. He was treated with aspirin while minocycline was continued. Eighteen months later, the patient complained about horizontal binocular diplopia. MRI revealed an infarct of the oculomotor nerve nucleus. Laboratory investigations revealed high titers of anti-beta 2 glycoprotein 1 (antiß2GP1) antibodies of 470 U/ml (normal range <15 U/ml) and antiphosphatidylethanolamine antibodies of 137.4 U/ml (normal range <18 U/ml). Other laboratory tests were normal. Six weeks after discontinuation of minocycline, anti-ß2GP1 antibodies decreased to 335 U/ml and to 36 U/ml at six months and then remained negative for six years. Many drugs have been considered as possibly causing APS but only in a limited number of patients. To our knowledge this is the first case of drug-induced APS with complete disappearance of high titers of anti-ß2GP1 antibodies after minocycline withdrawal. This case also illustrates the need to monitor the levels of antiphospholipid antibodies, even though initial values are high and confirmed after 12 weeks.

Subtentorial cerebral nocardiosis in immunocompetent patients: CT and MR imaging findings.

PURPOSE: To describe the clinical presentation and computed tomography (CT) and magnetic resonance imaging (MRI) appearances of subtentorial nocardia cerebral abscesses developing in immunocompetent patients. PATIENTS AND METHODS: The clinical findings and the results of CT and MRI examinations of three immunocompetent patients with nocardiosis located initially only in the subtentorial region were studied. Three patients underwent CT examination and two patients had MRI. RESULTS: Clinically, two patients had cerebellar syndrome and the third had meningism with fever. The diagnosis of nocardiosis was bacteriologically confirmed by demonstrating the organism in lumbar puncture fluid in one patient and by an aspiration biopsy of the abscess in the other two. Two of the patients improved under targeted antibiotic therapy whereas the third patient died. The main imaging features of the lesions were a multiloculated appearance with peripheral enhancement after intravenous administration of iodinated contrast material on CT and a multicystic appearance on MRI, with a peripheral hypointense rim on T2-weighted images, a relatively minor mass effect and a multiloculated appearance on gadolinium-chelate enhanced T1-weighted images. CONCLUSION: The clinical presentation of cerebral nocardiosis is relatively non-specific. A microcystic lesion surrounded by hypointensity on T2-weighted MR images with a multiloculated pattern after gadolinium chelate administration on T1-weighted MR images in association with a relatively minor mass effect should suggest this diagnosis even if the lesion is single and in the absence of immunosuppression.