Short Communication, J Pharm Sci Emerg Drugs Vol: 9 Issue: 12

A study of thyroid function cardiac risk assessment profile and hematological changes in HIV infected patients and AIDS patients

The Human Immunodeficiency Virus (HIV) causes acquired immunodeficiency syndrome (AIDS), which a deadly sickness is caused by a retrovirus known as the Human Immunodeficiency Virus (HIV). HIV attacks CD4 cells and leads to AIDS. In India, 2.47 million people are infected with HIV, accounting for 0.36% of the adult population. The updated national estimate reflects improved data rather than a significant reduction in real HIV prevalence in India. The most common mode of transmission is still sexual (87.4%); other modes of transmission, in order of proportion, are prenatal (4.7%), unsafe blood and blood products (1.7%), infected needles and syringes (1.8%), and unspecified (1.7%). (4.1%). Three HIV-positive men were found to have hypercholesterolemia as well as hypertriglyceridemia. In people with AIDS, a link has been discovered between plasma triglyceride and circulating interferon levels. The mechanism of hypercholesterolemia in HIV and other diseases, on the other hand, is unknown. In individuals treated with protease inhibitors, a pattern of hyperlipidaemia has been reported (i.e., higher total cholesterol, low-density lipoprotein cholesterol, and triglycerides, with a decreased level of highdensity lipoprotein cholesterol). Infection can raise plasma triglyceride levels by slowing the clearance of circulating lipoproteins, which is thought to be due to a lack of Lipoprotein Lipase (LPL), or by promoting hepatic lipid synthesis. Increased hepatic fatty acid synthesis or re-esterification of lipolytic fatty acids. Materials and Methods The initial dyslipidaemia reported in HIV patients was hypertriglyceridemia, although additional lipid abnormalities such as hypercholesterolemia and hypo HDL cholesterolaemia have also been reported. Because of the virus's affinity for the CD4 surface marker, the CD4+ lymphocyte is the primary target of HIV infection. HIV infection causes a progressive degradation of cellular functioning, characterised by a steady decrease in peripheral blood CD4+ lymphocyte numbers, which increases vulnerability to a wide range of opportunistic, viral, bacterial, protozoal, and fungal infections, as well as certain cancers. As a result, HIV can replicate its genome as DNA in the host's cells, such as human T4-helper lymphocytes, resulting in the production of large numbers of viral particles. Although all AIDS patients have immune dysfunction, the clinical spectrum of HIV infection is heterogeneous, and multiple organ involvement is prevalent. With more experience with this illness, a range of HIVrelated endocrine disorders that occur in both the early and late phases of the disease have been identified. Previous cross-sectional investigations have found a high frequency of abnormalities in thyroid function tests among these illnesses. Lambert et al. discovered unusual thyroid function test anomalies. They described a rise in serum thyroxin binding globulin but no other binding proteins like Cortisol Binding Globulin (CBG) that accompanied a drop in CD4 count as HIV infection progressed. FeldtRasmussen found that an increase in sr. TSH and s. TBG concentrations, as well as a decrease in FT-4, occurred often in AIDS patients and is linked to CD4 cell depletion. 10 Furthermore, thyroid dysfunction was linked to immunosuppression and viral replication, and it occurred before the condition worsened. Thyroid function tests (TFT) changes are more common with HIV infection and can occasionally be detected in the early stages of the disease. Thyroid function tests show abnormalities that are specific to HIV and are consistent with an aberrant response to acute illness. A variety of explanations have been proposed to explain such TFT anomalies. Direct infection of the thyroid gland by opportunistic organisms such as Pneumocystis carinii, infiltration of the gland by tumours such as Kaposi sarcoma, effect of humoral factors such as IL-1 and TNF-, side effects of HIV drugs such as rifampicin, ketoconazole, steroids, and direct infection of the gland by HIV are some of these. As a result, we looked at a wide range of newly diagnosed HIV+ patients, from asymptomatic to AIDS, who were not on HAART. The goal of this study was to look at how HIV infection, AIDS, and HIV-negative controls affected lipid, CD4+ T cell counts, and thyroid hormone levels. Discussion The current study discovered that the lipid profile of HIV and AIDS patients was altered. The lipid profile changed even in the early stages of HIV infection, and it changed significantly more as the disease advanced. This large number of AIDS cases and the absence of patients in clinical phases in our study could be related to the fact that patients with HIV infection only seek hospital admission when they have opportunistic infections in the late stages of their illness. Patients with AIDS have substantially aberrant total lipid contents in their plasma, according to previous investigations. A few authors determined the levels of plasma triglycerides, total cholesterol, and HDL cholesterol in HIV infected individuals based on the level of immunological deficiency as determined by the CD4+ cell count, and came to the same conclusion that, as immunological deficiency and clinical development of HIV infection increased, lipid profile disorders, as indicated by an increase in triglyceride levels and decreased HDL cholesterol concentrations, intensified. Our findings were similar to those reported before, in that a decrease in CD4 count due to disease progression was accompanied by a decrease in total cholesterol, HDL, and LDL, as well as an increase in triglyceride and VLDL levels.

Abstract

Keywords: thyroid