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• W3146045613 abstract "Keith Henry and colleagues (May 2, p 1328)1Henry K Melroe H Huebsch J et al.Severe premature coronary artery disease with protease inhibitors.Lancet. 1998; 351: 1328Summary Full Text Full Text PDF PubMed Scopus (485) Google Scholar report two cases of HIV-protease-inhibitor-induced hyperlipidaemia leading to premature coronary artery disease. A similar case of a 41-year old man with ritonavir-induced hypercholesterolaemia and myocardial infarction was reported to the Swiss pharmacovigilance centre. These cases clearly show that drug-induced hyperlipidaemia, a well-known adverse drug reaction (ADR) of ritonavir,2Danner SA Carr A Leonard JM et al.A short-term study of the safety, pharmacokinetics, and efficacy of ritonavir, an inhibitor of HIV-1 protease.N Engl J Med. 1995; 333: 1528-1533Crossref PubMed Scopus (526) Google Scholar can have important clinical consequences. The other implicated protease inhibitor was indinavir, which is known to cause lipodystrophy associated with metabolic abnormalities. As far as we are aware, however, lipid alterations have not been recorded with the use of saquinavir and nelfinavir.We extracted all reports from the national and international database of spontaneous ADR reporting that included one of the terms hyperlipidaemia, hypertrigliceridaemia, hypercholesterolaemia, or HDL decrease as the suspected ADR for protease inhibitors. For comparison we also obtained the corresponding reports for zidovudine. The table summarises the reports for lipid alterations and other ADRs and shows clearly that lipid alterations have been reported substantially more often for all protease inhibitors than for zidovudine. Since five of the seven cases associated with saquinavir use did not receive any other drug known to affect serum lipids (for example, other protease inhibitors or didanosine), confounding by comedication can be excluded. The only case on nelfanivir was reported recently from Switzerland in a 51-year old man who developed hyper-cholesterolaemia 3 months after starting the drug.TableComparison between spontaneously reported ADRs of lipid alterations for protease inhibitors and zidovudineNumber of ADRsNumber of patientsLipid alterationsOtherLipid alterationsHyperchole-sterolaemiaRitonavir11518808240Saquinavir1061175Indinavir4033703015Nelfinavir11511Zidovudine154037133ADR-reporting odds ratios3Egberts AC Meyboom RH De Koning FH et al.Non-puerperal lactation associated with antidepressant drug use.Br J Clin Pharmacol. 1997; 44: 277-281Crossref PubMed Scopus (71) Google Scholar are: ritonavir vs zidovudine 16·5 (95% CI 9·6–28·3); saquinavir vs zidovudine 4·4 (2·0–9·8); indinavir vs zidovudine 3·2 (1·8–5·8). Open table in a new tab Plasma cholesterol was raised in 50% of the patients with protease-inhibitor-induced lipid alteration, irrespective of the protease-inhibitor used. Lipid disorders were diagnosed after a median exposure time of 8 (range 1–40) weeks. 13 patients on ritonavir recovered without sequelae after stopping this drug and one positive rechallenge was reported. For the other protease inhibitors no follow-up data were available.The ADR reporting odds ratio for saquinavir and indinavir is lower than for ritonavir. A possible explanation for these differences is that plasma lipids are checked more frequently in ritonavir-treated patients and reporting is more complete, because physicians are aware of this effect only for ritonavir.The fact that plasma cholesterol fell to normal values after changing from ritonavir to nelfinavir in one of the Swiss cases, and that one other patient was successfully switched from ritonavir to indinavir, suggests that changing the protease inhibitor could prevent lipid alterations despite the fact that they can occur with all protease inhibitors. If treatment with a lipid-lowering drug is necessary, it is important to consider that most protease inhibitors strongly inhibit cytochrome P450 3A4 and that severe ADRs have been reported for fibrates and most statins in combination with CYP 3A4 inhibitors.4Aursens I Drugs effecting lipid metabolism.in: Dukes MNG Meyler's side effects of drugs. 13th edn. Elsevier, Amsterdam1996: 1324-1335Google Scholar Hence, by contrast with Henry and colleagues, a statin that is not exclusively metabolised by CYP3A4 such as, for example, pravastatin or fluvastatin, should be chosen for the safe treatment of protease-inhibitor-induced hyper-lipidaemia.KEF was supported by a fellowship from the Swiss National Science Foundation (32–51955.97). Keith Henry and colleagues (May 2, p 1328)1Henry K Melroe H Huebsch J et al.Severe premature coronary artery disease with protease inhibitors.Lancet. 1998; 351: 1328Summary Full Text Full Text PDF PubMed Scopus (485) Google Scholar report two cases of HIV-protease-inhibitor-induced hyperlipidaemia leading to premature coronary artery disease. A similar case of a 41-year old man with ritonavir-induced hypercholesterolaemia and myocardial infarction was reported to the Swiss pharmacovigilance centre. These cases clearly show that drug-induced hyperlipidaemia, a well-known adverse drug reaction (ADR) of ritonavir,2Danner SA Carr A Leonard JM et al.A short-term study of the safety, pharmacokinetics, and efficacy of ritonavir, an inhibitor of HIV-1 protease.N Engl J Med. 1995; 333: 1528-1533Crossref PubMed Scopus (526) Google Scholar can have important clinical consequences. The other implicated protease inhibitor was indinavir, which is known to cause lipodystrophy associated with metabolic abnormalities. As far as we are aware, however, lipid alterations have not been recorded with the use of saquinavir and nelfinavir. We extracted all reports from the national and international database of spontaneous ADR reporting that included one of the terms hyperlipidaemia, hypertrigliceridaemia, hypercholesterolaemia, or HDL decrease as the suspected ADR for protease inhibitors. For comparison we also obtained the corresponding reports for zidovudine. The table summarises the reports for lipid alterations and other ADRs and shows clearly that lipid alterations have been reported substantially more often for all protease inhibitors than for zidovudine. Since five of the seven cases associated with saquinavir use did not receive any other drug known to affect serum lipids (for example, other protease inhibitors or didanosine), confounding by comedication can be excluded. The only case on nelfanivir was reported recently from Switzerland in a 51-year old man who developed hyper-cholesterolaemia 3 months after starting the drug. ADR-reporting odds ratios3Egberts AC Meyboom RH De Koning FH et al.Non-puerperal lactation associated with antidepressant drug use.Br J Clin Pharmacol. 1997; 44: 277-281Crossref PubMed Scopus (71) Google Scholar are: ritonavir vs zidovudine 16·5 (95% CI 9·6–28·3); saquinavir vs zidovudine 4·4 (2·0–9·8); indinavir vs zidovudine 3·2 (1·8–5·8). Plasma cholesterol was raised in 50% of the patients with protease-inhibitor-induced lipid alteration, irrespective of the protease-inhibitor used. Lipid disorders were diagnosed after a median exposure time of 8 (range 1–40) weeks. 13 patients on ritonavir recovered without sequelae after stopping this drug and one positive rechallenge was reported. For the other protease inhibitors no follow-up data were available. The ADR reporting odds ratio for saquinavir and indinavir is lower than for ritonavir. A possible explanation for these differences is that plasma lipids are checked more frequently in ritonavir-treated patients and reporting is more complete, because physicians are aware of this effect only for ritonavir. The fact that plasma cholesterol fell to normal values after changing from ritonavir to nelfinavir in one of the Swiss cases, and that one other patient was successfully switched from ritonavir to indinavir, suggests that changing the protease inhibitor could prevent lipid alterations despite the fact that they can occur with all protease inhibitors. If treatment with a lipid-lowering drug is necessary, it is important to consider that most protease inhibitors strongly inhibit cytochrome P450 3A4 and that severe ADRs have been reported for fibrates and most statins in combination with CYP 3A4 inhibitors.4Aursens I Drugs effecting lipid metabolism.in: Dukes MNG Meyler's side effects of drugs. 13th edn. Elsevier, Amsterdam1996: 1324-1335Google Scholar Hence, by contrast with Henry and colleagues, a statin that is not exclusively metabolised by CYP3A4 such as, for example, pravastatin or fluvastatin, should be chosen for the safe treatment of protease-inhibitor-induced hyper-lipidaemia. KEF was supported by a fellowship from the Swiss National Science Foundation (32–51955.97)." @default.
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• W3146045613 title "“Buffalo hump” in HIV-1 infection" @default.
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