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Caballero-Granado FJ, Viciana P, Cordero E, Gomez-Vera MJ, del Nozal M, Lopez-Cores LF. 
“Ergotism related to concurrent administration of ergotamine tartrate and ritonavir in an AIDS patient”. 
Antimicrob Agents Chemother. 1997 May;41(5):1207.
Ritonavir is a potent protease inhibitor recently approved by the U.S. Food and Drug Administration and the European Agency for the Evaluation of Medical Products for the treatment of human immunodeficiency virus (HIV) infecton. Its mechanism of action is well-known, but its pharmacokinetics are still uncertain. Ritonavir interacts with many drugs due to its hepatic metabolism (1, 5). We report a case of ergotism in a patient in whom treatment with ritonavir was recently begun.

The patient, a 63-year-old man, had long suffered from migraines and had taken ergotamine tartrate over the last 5 years (1 to 2 mg/day). He had HIV infection (B3 stage) and was being treated with zidovudine (200 mg/8 h), zalcitabine (0.75 mg/8 h), and co-trimoxazole. In April 1996, zalcitabine was withdrawn due to tingling and burning in both the patient’s hands. The patient began treatment with zidovudine (250 mg/12 h), didanosine (200 mg/12 h), and ritonavir (600 mg/12 h). Ten days after beginning this treatment, he began having severe symptoms characterized by subacute pain, paresthesias, skin paleness alternating with areas of cyanosis, and coldness in both arms. He was admitted to Hospital Universitario Virgen del Rocı´o 1 week later. Physical examination revealed an absence of axillary, brachial, radial, and ulnar pulses in both arms, paresis and semiflexion of fingers of both hands, and a few petechial lesions on the dorsum of the left hand. An arterial doppler test was performed, and it revealed the absence of flow in both radial and ulnar arteries. Treatment with prostaglandin E1 (500 mg/12 h intravenously for 3 days) and calcic nadroparin (15,000 U/12 h subcutaneously) was begun promptly. Ritonavir and ergotamine were withdrawn. Pain, paleness, cyanosis, and coldness disappeared 3 days later. Paresis of interosseous, thenar, and hypothenar musculature and long flexors of fingers of both hands remained as sequels.
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