Patomekanisme stroke pada infeksi human immunodeficiency virus
https://doi.org/10.22146/bns.v19i1.61893 Nur Cahyani Setiawati(1*), Paryono Paryono(2), Sekar Satiti(3)
(1) KSM Saraf, RSUD Sragen, Jawa Tengah
(2) Departemen Neurologi, Fakultas Kedokteran-Kesehatan Masyarakat dan Keperawatan Universitas Gadjah Mada, Yogyakarta
(3) Departemen Neurologi, Fakultas Kedokteran-Kesehatan Masyarakat dan Keperawatan Universitas Gadjah Mada, Yogyakarta
(*) Corresponding Author
Abstract
Stroke is one of cerebrovascular disease that may occur with or as a result of infection by human immunodeficiency virus (HIV). Direct mechanisms of HIV-related stroke include chronic inflammation associated with atherosclerosis, hypercoagulable state and vasculopathy, while the indirect mechanisms are HIV-related opportunistic infections, the effect of using highly active antiretroviral therapy (HAART), and cardioembolism.
Stimulation of the inflammatory response is estimated to be the predominant mechanism in the relationship between stroke and infections. Inflammatory cascade causing arteriosclerosis, plaque rupture, and thrombosis could result in ischemic stroke while the injury to vascular endothelial cells predisposes hemorrhagic stroke.
The characteristics of HIV infection such as viral load, duration of the disease, therapy with protease inhibitor (PI) and metabolic syndrome parameters (blood sugar, cholesterol and triglycerides, as well as blood pressure measurements) seem to influence the pathogenesis of vascular changes. Combination therapy of antiretrovirals can directly cause arterial tissue injury in which the metabolic complications such as dyslipidemia and insulin resistance may indirectly cause endothelial dysfunction, thus accelerating the occurrence of arteriosclerosis. Provision of HAART also resulted in increased levels of cytokines such as tumour necrosis factor-a (TNF-a), interleukin-1 (IL-1), interleukin-6 (IL-6), and interferon-a that induce apoptosis of subcutaneous adipose tissue in lipodystrophy in HIV patients.
Abstrak
Stroke adalah salah satu penyakit serebrovaskular yang mungkin terjadi bersamaan atau sebagai akibat dari infeksi human immunodeficiency virus (HIV). Mekanisme langsung stroke terkait HIV antara lain peradangan kronis yang berhubungan dengan aterosklerosis, hiperkoagulasi dan vaskulopati, sementara mekanisme tidak langsung adalah infeksi oportunistik terkait HIV, efek penggunaan highly active antiretroviral therapy (HAART) dan kardioemboli.
Stimulasi respons inflamasi diperkirakan menjadi mekanisme predominan hubungan antara stroke dan infeksi. Kaskade inflamasi menyebabkan aterosklerosis, ruptur plak, dan trombosis yang mengakibatkan stroke iskemia, sedangkan perlukaan pada sel endotel vaskular menjadi predisposisi stroke perdarahan.
Karakteristik infeksi HIV sendiri seperti viral load, durasi penyakit, pemberian terapi dengan protease inhibitor (PI) maupun parameter sindrom metabolik (gula darah, kolesterol dan trigliserida, serta pengukuran tekanan darah) nampaknya mempengaruhi patogenesis dari perubahan vaskular yang terjadi. Kombinasi terapi antriretroviral dapat secara langsung menyebabkan perlukaan jaringan arteri di mana komplikasi metabolik seperti dislipidemia dan resistensi insulin secara tidak langsung menyebabkan disfungsi endotel sehingga mempercepat terjadinya aterosklerosis. Pemberian HAART juga mengakibatkan peningkatan level sitokin seperti tumour necrosis factor-a (TNF-a), interleukin-1 (IL-1), interleukin-6 (IL-6), dan interferon-a yang menginduksi apoptosis jaringan adiposa subkutaneus pada lipodistrofi pada pasien HIV.
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DOI: https://doi.org/10.22146/bns.v19i1.61893
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