Antiretrovirals
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Avascular osteonecrosis: 3 case reports Three men developed Ficat stage II-III avascular osteonecrosis (AVON) during antiretroviral therapy [ART, dosages not stated] for HIV infections. All three men had other risk factors for developing AVON including smoking, alcohol use, hypertriglyceridaemia, heterozygote sickle cell disease, and lipodystrophy. [Patient outcomes not stated.] A 33-year-old man with HIV-1 infection was hospitalised in February 2005 with a 4-month history of right hip pain and impaired mobility. He had commenced ART with zidovudine and didanosine in October 1998, and saquinavir was added in December 1998. He was switched to stavudine, lamivudine and nelfinavir in October 1999. Nelfinavir-related digestive intolerance developed and, in January 2002, his ART was changed to zidovudine, lamivudine and efavirenz. In March 2003, he was switched again to tenofovir disoproxil fumarate, lamivudine and lopinavir/ritonavir. He developed AVON 23 months later. A CT scan demonstrated right femoral head AVON, and haemoglobin electrophoresis revealed 41% of haemoglobin S. Right hip arthroplasty was performed in August 2005. Tenofovir was withdrawn, and abacavir was started; lopinavir/ritonavir was continued. A 44-year-old man was hospitalised in February 2005 with a 2-month history of bilateral hip pain, and impaired mobility. He had started ART with stavudine, lamivudine and nelfinavir in October 2000 for HIV-2 infection. He was switched to zidovudine, didanosine and lamivudine in August 2002, then to abacavir, lamivudine and lopinavir/ ritonavir. AVON developed 19 months later. A CT scan revealed bilateral femoral head AVON, and 45% of haemoglobin S was observed on haemoglobin electrophoresis. Abacavir and lamivudine were continued, and lopinavir/ritonavir was switched to indinavir/ritonavir. A 45-year-old man with HIV-1/2 infection was hospitalised with a 4-month history of right hip pain and impaired mobility in May 2005. He had commenced ART in November 1999 with stavudine, didanosine and nelfinavir. He developed stavudine-related peripheral neuropathy and, in July 2001, stavudine was switched to zidovudine. His ART was changed to zidovudine, didanosine and indinavir in July 2002, then abacavir, lamivudine and ritonavir/saquinavir in October 2003. He subsequently developed pulmonary tuberculosis and, in July 2004, ritonavir/saquinavir was switched to lopinavir/ritonavir. Ten months later, he developed symptoms of AVON. A CT scan demonstrated AVON of his right femoral head. Haemoglobin electrophoresis revealed 50% of haemoglobin S, and he had lipodystrophy. Lamivudine and abacavir were continued, and lopinavir/ritonavir was switched to indinavir/ritonavir. Author comment: "Physicians should be aware of the symptoms of AVON and of its potential risk factors, including HIV infection, ART, steroids, alcohol and dyslipidaemia." Eholie SP, et al. Avascular osteonecrosis of the femoral head in three West African HIV-infected adults with heterozygous sickle cell disease. Antiviral Therapy 14: 1011-1014, No. 7,
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