Human immunodeficiency virus type 1 infection in Oman: antiretroviral therapy and frequencies of drug resistance mutations.

Highly active antiretroviral therapy (HAART), consisting mainly of two nucleoside reverse transcriptase inhibitors (NRTIs) and one protease inhibitor (PI), is offered to < 10% of HIV-infected subjects in Oman. The aims of the present study were to determine the frequency of resistance-associated mutations in these patients, and to assess the contribution of drug resistance to treatment outcome. Among 29 patients on HAART for > or =6 months, virological, failure was observed in 27 (93%). Genotypic analysis indicated that in five of these 27 patients, there were no mutations that confer resistance to reverse transcriptase inhibitors (RTIs). The genotypes of 17 other patients carried one or two RTI mutations, mainly the lamivudine-associated resistance mutation M184V. Three or more RTI mutations were found in only five (14.7%) patients with virological failure, including three patients on the nonnucleoside RTI efavirenz. Major PI mutations were infrequent, and were detected in seven (26%) of 27 patients failing HAART, mainly as single mutation at codons 82 or 90. In contrast, accessory mutations in the protease gene were present in all patients. However, there were significant differences in the prevalence of accessory mutations at codons 36 and 77 among clade B and non-B viruses. When genotypic data of this study were used to change therapy of seven patients whose isolates had multiple resistance mutations, adequate viral suppression was observed in five. Our results indicate that the high rate of treatment failure among patients in Oman is mainly due to factors other than resistance to antiretroviral drugs. These factors, which may include nonadherence to therapy and treatment interruptions, need to be investigated.

Frictional amyloidosis in Oman--a study of ten cases.

Macular amyloidosis is an important cause for cutaneous pigmentation, the aetiology of which is poorly understood. Friction has recently been implicated the causation of early lesions, referred to as frictional amyloidosis. Confirmation of diagnosis by the detect on of amyloid using histochemical stains is inconsistent. Ten patients with pigmentation suggestive of macular amyloidosis were studied with detailed history, clinical examination, biopsy for histochemistry and electron microscopy. Nine out of ten patients had a history of prolonged friction with various objects such as bath sponges, brushes, towels, plant sticks and leaves. Amyloid was demonstrated by histochemical staining in only six out of ten cases. In the remaining four cases, amyloid was detected by electron microscopy. These consisted of aggregates of non-branching, extracellular, intertwining fibres measuring between 200-500 nm in length and between 20-25 nm in diameter. The study confirms the role of friction in the causation of this condition. Histochemical stains are not always successful in the detection of amyloid and electron microscopy is helpful for confirming its presence. The term frictional amyloidosis aptly describes the condition.