gms | German Medical Science

10. Kongress für Infektionskrankheiten und Tropenmedizin (KIT 2010)

Deutsche Gesellschaft für Infektiologie,
Deutsche AIDS-Gesellschaft,
Deutsche Gesellschaft für Tropenmedizin und Internationale Gesundheit,
Paul-Ehrlich-Gesellschaft für Chemotherapie

23.06. - 26.06.2010, Köln

Posterior reversible encephalopathy syndrome (PRES) and HIV/tuberculosis co-infection

Posteriores Reversibles Enzephalopathie Syndrom (PRES) und HIV/Tuberkulose Koinfektion

Meeting Abstract

  • M.F. Küpper - University of Freiburg, Department of Medicine, Division of Infectious Diseases, Freiburg, Germany
  • S. Rieg - University of Freiburg, Department of Medicine, Division of Infectious Diseases, Freiburg, Germany; University of Freiburg, Department of Medicine, IFB-Centre of Chronic Immunodeficiency, Freiburg, Germany
  • N. Venhoff - University of Freiburg, Department of Medicine, IFB-Centre of Chronic Immunodeficiency, Freiburg, Germany
  • J. Thoden - University of Freiburg, Department of Medicine, IFB-Centre of Chronic Immunodeficiency, Freiburg, Germany
  • S. Usadel - University of Freiburg, Department of Medicine, Division of Infectious Diseases, Freiburg, Germany; University of Freiburg, Department of Medicine, IFB-Centre of Chronic Immunodeficiency, Freiburg, Germany; KV Specialized Medical Practice/HIV-Center Freiburg, Germany
  • B. Lange - University of Freiburg, Department of Medicine, Division of Infectious Diseases, Freiburg, Germany; University of Freiburg, Department of Medicine, IFB-Centre of Chronic Immunodeficiency, Freiburg, Germany
  • W. Kern - University of Freiburg, Department of Medicine, Division of Infectious Diseases, Freiburg, Germany
  • D. Wagner - University of Freiburg, Department of Medicine, Division of Infectious Diseases, Freiburg, Germany; University of Freiburg, Department of Medicine, IFB-Centre of Chronic Immunodeficiency, Freiburg, Germany

10. Kongress für Infektionskrankheiten und Tropenmedizin (KIT 2010). Köln, 23.-26.06.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocP140

DOI: 10.3205/10kit194, URN: urn:nbn:de:0183-10kit1948

Veröffentlicht: 2. Juni 2010

© 2010 Küpper et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Introduction: PRES encompasses a syndrome of headache, seizures, confusion, hypertensive crisis, and visual disturbance, with a pattern of predominantly posterior cerebral edema on computed tomography (CT) or MRI. Several conditions (including influenza, eclampsia, lupus, end-stage renal disease, hematologic disease, immunosuppressants) have been described as risk factors, but very few HIV-positive patients with PRES have been reported. We here present an AIDS patient with disseminated (incl. CNS) tuberculosis (TB) who developed PRES following ART and TB therapy initiation.

Case report: A 48-year old white male patient with preexisting compensated renal insufficiency was diagnosed with advanced HIV infection (CD4 count, 29/µl) and disseminated TB, including 10 cerebral lesions (up to 1 cm in diameter). Initial treatment (including corticosteroids) was successful with clinical improvement, suppression of HI-viral load, regression of pulmonary TB, lymph node and CNS lesions. There was only a slow response in CD4 counts. After 5 months, when the patient received 2-drug TB therapy, ART and was still on 20 mg prednisolone he presented with progressive headache, nausea, VZV DNAemia and keratitis, and acute renal failure with nephrotic syndrome. After few days he developed malignant hypertension and deteriorated neurologically with dysarthria, disorientation and somnolence. Imaging showed acute increase of the cerebral edema around the still apparent tuberculous lesions temporal-occipital and parietal/parasagitally while CSF did not show evidence of active central nervous system inflammation/infection. With supportive therapy, there was a cliknical improvement within a few days, when repeat imaging showed bilateral white matter lesions with decreasing size. The patient was discharged without neurological deficits 10 days later. After one year of follow-up, the patient is doing well, HI-viral load is suppressed, CD4 count has increased to 180/µl, and kidney function has improved substantially.

Conclusions: Hypertensive disorders, immunosuppressive therapies, and renal disease – as in this patient – are risk factors for PRES. The clinical presentation and radiological appearance in our patient were consistent with this diagnosis whereas we think TB-IRIS is unlikely. CNS TB lesions or VZV reactivation may have interfered with autoregulation of cerebral blood flow or cerebral endothelial function that are putatively involved in the pathogenesis of PRES.