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العنوان
Neurological Complications of HIV Infection/
المؤلف
Esmail,Lobna Abu Bakr
هيئة الاعداد
باحث / لبنى أبو بكر إسماعيل
مشرف / محمد أسامة عبد الغني
مشرف / نجلاء محمد الخياط
مشرف / هيثم حمدي سالم
الموضوع
Neurological Complications- HIV Infection-
تاريخ النشر
2012
عدد الصفحات
208.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب النفسي والصحة العقلية
تاريخ الإجازة
1/1/2012
مكان الإجازة
جامعة عين شمس - كلية الطب - Neuropsychiatry
الفهرس
Only 14 pages are availabe for public view

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from 16

Abstract

HIV is a lentivirus, and like all viruses of this type, it attacks the immune system. Lentiviruses are in turn part of a larger group of viruses known as retroviruses. There are two types of HIV: HIV-1 and HIV-2. Worldwide, the predominant virus is HIV-1, and generally when people refer to HIV without specifying the type of virus they will be referring to HIV-1.
Initial HIV infection causes an acute phase of HIV specific humoral and cell-mediated immune responses. However, these responses do not completely eliminate HIV, and the immune system remains in a state of chronic activation. HIV primarily infects cells expressing the CD4 receptor molecule, although it can also bind to other cell surface molecules such as the CXCR4 coreceptor on T cells, and CCR5 receptor on macrophages.
The most remarkable immunological feature of HIV disease is the fall in the number of CD4 cells .During the late stages of HIV infection in the setting of declining systemic immunity, patients develop more debilitating and morbid complications relating either to HIV infection itself or to opportunistic infections, which are conditions related to suppressed immunity.
In approximately 50% of cases primary HIV-1 infection remains asymptomatic, whereas 50% of the patients develop flu-like symptoms within the first four weeks after infection. During primary infection, virus titres are extremely high in peripheral blood (up to 108 HIV-1 RNA copies/ml plasma) and the number of CD4+ T lymphocytes decreases significantly. The onset of HIV-1 specific cellular immune response and the subsequent synthesis of HIV-1 specific antibodies lead to the decline of plasma viral load to a patient-specific level and chronification of HIV-1 infection.
Neurological diseases affecting either the CNS or PNS occur in the majority of infected individuals and are the initial presenting illnesses of AIDS in 7–20% of patients. Stages are most frequently defined: primary HIV infection, latent stage/early symptomatic disease, and AIDS. The latter is heralded by the development of an AIDS-defining illness such as opportunistic infections and malignancies.
The spectrum of neurocognitive impairment, now termed HAND, includes asymptomatic neurocognitive impairment, varying degrees of HIV associated mild neurocognitive disorders and the sever form. HAD is diagnosed when the patient presents with acquired moderate-to-severe cognitive impairment, with scores that are at least two standard deviations below the demographically corrected norms in at least two different areas associated with marked difficulties in daily functioning.
HIV-associated neuropathy occurs in several patterns, with DSPN as the most frequently occurring type; other patterns of peripheral neuropathy include IDP, progressive polyradiculopathy, mononeuropathy multiplex and autonomic neuropathy. It was found that DSPN is a complex symptom that occurs across HIV disease and may be related to exposure to neurotoxic ART, disease duration, viral load, and mitochondrial toxicity.
As regard opportunistic infections, among bacterial infections, there has been a very significant increase in the incidence of TB in the developed world, largely related to the increasing numbers of AIDS patients. Also viral infections include CMV, herpes group, JCV of PML and EBV. Parasitic infections are common, mostly toxoplasma.
Patients infected with HIV have an increased risk of developing malignancy in comparison to the general population, Impaired cellular immunity against oncogenic viruses is believed to be the main mechanism leading to the development of some cancers associated with HIV infection. PCNSL is the second most common mass lesion in AIDS.
Movement disorders are common among HIV infected individuals, with both hypokinetic and hyperkinetic syndromes that may manifest themselves at all stages of the disease and occasionally appear as the first clinical manifestations of HIV infection. Also vacuolar myelopathy is the most common spinal cord disease in AIDS, found in up to 30% of patients.
Also vascular disorders are very common among infected patients; a few studies support direct deleterious effect of HIV infection on vascular properties through immunodepression and studies performed during the pre- HAART era reported the presence of atherosclerotic lesions in HIV-infected patients, even in the absence of traditional risk factors.
So, we have to early detect HIV with HIV specific protocol and suspecting HIV in neurologically ill persons. The goal of most HIV diagnostic tests is to detect HIV infection as early as possible, thereby decreasing the length of the diagnostic window. In addition to facilitating detection of HIV infection, serologic tests also allow for the determination of HIV viral type (HIV-1 or HIV-2), viral subtype, viral load (as measured by viral RNA levels in the blood), HIV drug resistance.
CSF analysis can directly identify the underlying etiological agent and it can also characterize specific local immune responses that establish etiology and predict Prognosis. In the context of HIV-1 infection, CSF analysis has proved useful in the diagnosis of opportunistic infections and tumors. Both traditional microbiological methods (e.g. CSF culture or antigen detection for diagnosis of CNS cryptococcosis), and more recent nucleic acid amplification techniques (primarily PCR), enable a rapid and certain etiological diagnosis of most of these complications. HIV reaches the CNS, or at least the meninges and perivascular spaces, at the time of primary infection, subsequently; the virus is almost always detected in the CSF during the neurologically asymptomatic stages of infection, both in early and late disease. CSF examination done for detection and quantification of HIV-1 virus, for HIV genetic studies, detection of anti-HIV antibodies and detection of host markers
Also neuroimmages are of high diagnostic value, including CT scan, MRI, and MRS.
The advent of ART, however, has significantly changed the landscape of HIV neuropathogenesis. Illicit drug usage and lack of ART availability may also influence neurological disease manifestations. Of these, the most feared long-term complication of HIV disease is cognitive dysfunction. Present antiretroviral drugs span six classes that target steps in the HIV life cycle.
More recently, efforts are being made to develop nano ART. Much effort has been placed in finding long-acting forms of injectable antiretrovirals to circumvent the challenges of therapy adherence currently faced by HIV-1-infected individuals. ART is also known to decrease PAF activity when used in combination with PAF antagonists, HIV-1-associated neurodegeneration could be substantially decreased.
Also we should be aware of the regimens of ART, when to start treatment, treatment to start with, when to switch to another treatment and testing and monitoring the response of these drugs. also the serious side effects of these drugs including IRIS which is a group of syndromes characterized by paradoxic clinical worsening that usually occurs within the first 4 to 8 weeks after starting cART.