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• W1974041978 abstract "Myelopathy in HIV-infected patients may result from a variety of causes, including HIV-associated vacuolar myelopathy, cytomegalovirus myelitis and spinal cord compression secondary to non-Hodgkin's lymphoma [1]. This report presents a patient with myelopathy secondary to HAART-associated lipodystrophy and spinal epidural lipomatosis (SEL). HAART-associated SEL should be considered as a differential diagnosis in HIV-infected patients presenting with myelopathy. A 43-year-old homosexual man (CDC stage C3) presented in June 2003 with bilateral leg weakness, unsteady gait and mild urinary retention, which had developed slowly during the previous 12 months. During the previous 2 years, he had developed mild lipodystrophy manifestations with visceral fat accumulation and buccal fat loss. His body status was otherwise unremarkable, with a normal body weight [weight 81 kg, height 186 cm, body mass index (BMI) 23 kg/m2]. Routine blood tests were also unremarkable. The CD4 cell count was 427 cells/μl and the viral load was less than 50 copies/ml. Non-fasting total cholesterol and triglyceride values were 198 and 283 mg/dl, respectively, while he was on 400 mg bezafibrate per day. The patient was diagnosed with HIV infection in 1992 when he presented with oral thrush and recurrent anal herpes (CD4 cell count 17 cells/μl). He has received antiretroviral treatment since January 1993, with a total of 10 regimens, including various nucleoside analogue reverse transcriptase inhibitors (didanosine, zidovudine, lamividine, stavudine, and abacavir), non-nucleoside analogue reverse transcriptase inhibitors (delavirdine, viramune), and protease inhibitors (ritonavir, saquinavir, nelfinavir, amprenavir). He experienced virological failure on some of these regimens as a result of non-compliance and the development of resistance. At the time of his presentation in June 2003 the patient was on a HAART regimen (started in March 2000) of 400 mg lopinavir/100 mg ritonavir (Kaletra) plus 300 mg zidovudine/150 mg lamivudine (Combivir) twice a day. The neurological evaluation in June 2003 revealed myelopathic syndrome, including mild paraparesis, proprioceptive deficits, a positive Romberg's test, decreased vibration sense without gradient, increased muscle tone of the lower extremities, brisk patella tendon and adductor reflexes, and a negative Babinski sign. Lumbar puncture, as well as electromyography and nerve conduction studies, was unremarkable. Sensory evoked potentials from the tibialis nerve revealed a significant bilateral disturbance at the spinal level and established the diagnosis of myelopathy. Magnetic resonance imaging (MRI) documented compression of the spinal cord at the C4–T5 level by extensive epidural lipomatosis (Fig. 1). Other causes of myelopathy, including vitamin B12 and folic acid deficiencies, were excluded [1].Fig. 1: Magnetic resonance imaging of the spine. (a) Sagittal, T1-weighted view demonstrating an epidural fat pad (white arrow) along the C4–T5 level of the cord (open arrow). (b) Axial, T1-weighted image demonstrating epidural fat (white arrow) at T2–T3, which fills almost one third of the spinal canal and leads to displacement of the cord (open arrow).As SEL was considered to be HAART associated, the antiretroviral regimen was switched in July 2003 to a protease inhibitor-sparing regimen consisting of zidovudine/lamivudine/abacavir plus nevirapine. After regimen failure in December 2003 (CD4 cell count 204 cells/μl, viral load 35 300 copies/ml), the medications were switched to a ritonavir-boosted double protease inhibitor regimen consisting of 400 mg lopinavir/100 mg ritonavir (Kaletra) twice a day plus 300 mg atazanavir once a day. After the initial presentation and discontinuation of the Kaletra plus Combivir regimen in July 2003 there were no signs or symptoms of the progression of myelopathy and lipodystrophy. A follow-up evaluation in May 2005 showed findings, including physical status, BMI, neurological examination, sensory evoked potentials and magnetic resonance imaging of the spine, to be stable. Routine blood tests were again unremarkable. The CD4 cell count was 498 cells/μl and the viral load was less than 50 copies/ml. Non-fasting total cholesterol and triglyceride values were 205 and 330 mg/dl, respectively, while he was on 400 mg bezafibrate per day. SEL is a rather rare condition, with approximately 100 cases discussed in the literature [2]. It is associated with a variety of conditions, including long-term steroid use and endocrinopathies such as Cushing's syndrome or hypothyroidism. Idiopathic SEL occurs almost exclusively in the obese population (BMI > 27.5) and in younger patients (average age 35 years) [3]. We concluded that SEL might be a manifestation of HAART-associated lipodystrophy because our patient revealed typical features of lipodystrophy and other causes of SEL did not apply. Lipodystrophy manifesting with reduced insulin sensitivity, hyperlipidemia and fat accumulation appears to be primarily caused by the use of protease inhibitors [4,5]. Nucleoside analogue reverse transcriptase inhibitors can also contribute to fat accumulation; although these drugs are primarily associated with subcutaneous fat loss [5]. Fat accumulation usually manifests with visceral fat accumulation, dorsocervical fat pads (buffalo hump) and supraclavicular fat pads [4,5]. Symptomatic HAART-associated SEL appears to be a rare event, and to our knowledge only two cases have been reported so far in the literature. The first patient received long-term steroids together with ritonavir and required subsequent surgical decompression [6]. The second patient received indinavir treatment, with SEL resolving upon the discontinuation of indinavir and continuation of treatment with a protease inhibitor-sparing regimen [7]. Our patient was treated with a variety of protease inhibitors. We speculate that he developed lipodystrophy and SEL mainly as a result of taking Kaletra. It should be noted that there was no further progression during treatment with Kaletra plus atazanavir over an 18-month follow-up period. Whether the combination of Kaletra with atazanavir, and its favorable metabolic characteristics [8], together with the omission of nucleoside analogues, may have reduced the risk of progression of SEL remains unclear. An alternative explanation might be that fat accumulation is often known to increase for some time and to then remain stable for years thereafter in spite of the continuation of HAART [5]." @default.
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• W1974041978 title "Spinal epidural lipomatosis: a manifestation of HAART-associated lipodystrophy" @default.
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