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Fulminant Candida albicans peritonitis and ascites in a HIV-HCV co-infected patient,
possibly prompted by a prolonged self-administration of nimesulide
Roberto Manfredi, Sergio Sabbatani
Infectious Diseases, University of Bologna, Italy
Introduction
The mortality rate of HIV-infected patients (p) with concurrent liver disease is steadily
increasing.
Case Report
An exceedingly rare case of Candida albicans fulminant peritonitis and ascites in a p with
HIV-HCV-coinfection, but no prior history of liver cirrhosis, which was possibly related to
exaggerated self-administered nimesulide,is reported. A 46-year-old p with HIV infection
recognized since 14 years received isolated lamivudine-stavudine therapy since six years
with a favorable laboratory response, as expressed by a plasma viremia of 480 HIV-RNA
copies/mL, and a CD4+ lymphocyte count of 428 cells/µL. Neither liver biopsy nor
specific treatment were performed for a concurrent stable HCV infection. Two months
before admission, our p suffered from a shoulder fracture, and uncontrolled nimesulide
self-medication was performed during six consecutive weeks. A rapidly worsening ascites
and oliguria led to hospital admission. Slightly increased serum ALT, amylase, and
bilirubin were detected, but a rapidly increasing ascites and diffuse edema occurred,
paracentesis, and diuretic-albumin administration failed to improve the clinical picture, and
the worsening ascites and anuria evolved into hyperacute kidney failure. One day later our
p deceased, and necropsy studies showed a diffuse polyvisceritis and hepatitis with
abundant ascites, in absence of kidney and urinary tract abnormalities, and liver cirrhosis.
After patient's death, multiple ascites cultures yielded isolated Candida albicans.
Conclusions
HIV-infected p have increased risks of liver toxicity. Non-steroideal anti-inflammatory
drugs (NSAID) are implicated in severe, sometimes lethal hepatotoxicity. The exceedingly
rapid-severe evolution towards a Candida-infected ascites associated with refractory
anuria, in absence of decompensated cirrhosis, acute hepatotoxicity, and kidney
involvement at autopsy, was never observed after NSAID/nimesulide use. Animal models
showed a NSAID-induced increased enteric vascular permeability causing infectious
peritonitis. In conclusion, clinicians who face p with chronic hepatitis but no
decompensated cirrhosis, should remind that NSAID may act on liver-bowel function, and
could prompt a liver-kidney damage, possibly complicated with infectious ascites.
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