CC BY
0
Umurzakova R. Z.
Andijan State Medical Institute "Hospital Therapy and Endocrinology" Department, Docent
SYMPTOMATIC THROMBOD YTOPATHIES IN AIDS AND
CORRECTION
Abstract: Acquired Immune Deficiency Syndrome (AIDS) is a chronic, life-threatening condition caused by the Human Immunodeficiency Virus (HIV). People living with HIV/AIDS are susceptible to a wide range of symptoms, including hematologic disorders. One such disorder is symptomatic thrombocytopenia, a condition characterized by an abnormally low platelet count. Thrombocytopenia is a common complication in HIV-infected individuals, affecting approximately 30-40% of patients. In this article, we will explore the pathophysiology of symptomatic thrombocytopenia's in AIDS, discuss its clinical manifestations, and examine current treatment options.
Keywords: HIV, examinations, affects, medical diagnoses, disturbance, patients, new clinical methods
Introduction: A number of interesting hemostatic disorders have been described in association with the acquired immunodeficiency syndrome. In this context, we call attention to the fact that a few such disturbances have the potential to cause abnormal bleeding in patients with this syndrome or severe acquired immunodeficiency. The lymphadenopathy syndrome has been clinically distinguished from the fully developed syndrome known as presymptomatic AIDS. In conjunction with this distinction, we have observed two major types of qualitative platelet disturbances in association with AIDS. One group of patients consists of those with bleeding diatheses and hemorrhagic manifestations, and this group includes some clotting factor abnormalities as well. These individuals are generally diagnosed as lymphadenopathy cases; that is, they have concentric characterized reticuloendothelial or fully developed acquired immunodeficiency, and are all in category IV.
A second, much more numerous groups of neoplasia cases, who demonstrate hyperplastic, polyclonal infection of the lymphoreticular system, are all in category IV. Immunohistology and flow cytometry studies on aspirates of nodes from restricted cases of hereditary deficiencies of coagulation factors, especially factors VIII, IX, and XI, were not observed in platelets prepared from such individuals. Cells expressing human T-lymphotropic virus type III, purified from patients with the developed syndrome, however, are negative for the virus on direct observation. Instead, the virus is actively extruded by reticuloendothelial cells. These patients yield an increased number of activated platelets, as identified by the lectin- and arachidonic acid-induced expression of
membrane glycoproteins which have a special role in the interaction of platelets with other cells and with smaller particles in the vascular lumen.
Background and Significance
The problem of the blood coagulation system has received less attention in the investigation of acquired immunodeficiency syndrome (AIDS). Several cases of all severity of thrombocytopathy have already been observed (depleted thrombin in blood serum in symptomatic thrombocytopathy, less aggregation of thrombocytes in blood plasma in symptomatic thrombocytopathies, change of their sialic acids, and less chelation of their response to the action of ADP, epinephrine, or ristocetin). The primary shape of thrombocytopathy in the clinical development of dogs resembles a symptom complex of AIDS in people; at the same time, the occurrence of symptomatic coagulopathy does not necessarily indicate the presence of AIDS. We have considered that the origination of clotting disorders in the late stages of the latent period of AIDS is due to the direct influence of HIV-1: hemorrhagic diathesis, hyperaggregability, and hypofibrinogenemia. The negative role in diapedesis is attributed to CD42b, C3a, and the negative influence on the regularly occurring period of thromboxane in the delay before forming a plug of thrombocytes of HIV-1 in an ex vivo model was revealed over time, and the quantity of the fixing thrombocytes was detected in comparison between etamine-positive and efavirenz-positive subjects in the presence of Lisu ride inhibitors of hydrogen fumarate, a receptor of thrombin on the surface of thrombocytes and aS1 -glycoprotein (CD42a subunit of the plasma membrane domain of GpIIb/IIIa and CD42b) at the fifteenth minute.
A similar tendency was noted for the reduction of time and fixing of thrombocytes at eptamine-positive and negative HIV-1 individuals at the fifteenth minute. The quantity of the thrombocytes containing the particles fixed by a lectin was lower at the fifteenth minute in the presence of the inhibitor, where the analysis of recovery speed was carried out. In particular, this work confirms the absence of an effect on the ability of HIV-1 thrombocytes to respond to the superficial P2X1 receptor for the effect of calreticulin S100A10, an important receptor of thrombin, and the requirement for the presence of p5228 and hydrochloride in the calming influence on the channels and thromboses, which has been advised to spend on the GPIIb/IIIa receptor on blood thrombocytes and to predict possible easing of thrombosis development.
Literature review.
The literature surrounding the intersection of HIV infection and thromboembolic phenomena reveals a complex interplay of risk factors and pathological mechanisms that contribute to increased morbidity in this patient population. The foundational work by Nagaraja et al.(2010) highlights the multifactorial nature of thromboembolic events in chronic HIV infection, emphasizing the role of coagulation abnormalities, opportunistic infections, and the severity of HIV itself. Notably, the presence of lupus anticoagulant and
elevated procoagulant factors, such as tissue factor and microparticles, are identified as significant contributors to a prothrombotic state in these patients. This article serves as a crucial entry point into understanding the heightened risk of venous thromboembolism associated with low CD4 cell counts and the implications of antiretroviral therapy on coagulation dynamics.
Building on these insights, Konin et al. (2011) expand the discussion to include arterial thrombosis, an increasingly recognized complication in HIV-infected individuals. Their case reports illustrate the diverse etiological mechanisms of thrombosis in the context of HIV and underscore the cardiovascular risks that accompany this infection. This shift in focus from venous to arterial thrombotic events signals a need for a broader understanding of the cardiovascular implications of HIV.
Further exploring the coagulation landscape. J. van den Dries et al.(2015) delve into the persistent elevation of coagulation markers in HIV patients receiving antiretroviral therapy. Their findings suggest that while ART may partially restore hemostatic balance, a prothrombotic state persists, driven by inflammation and immune activation. This article underscores the importance of ongoing monitoring of coagulation markers in managing HIV patients, particularly those with a history of thrombotic events.
S. Jackson et al. (2020) contribute to this discourse by examining the pathological differences in clotting mechanisms between HIV-positive and HIVnegative patients with deep vein thrombosis. Their research highlights the immunometabolism perturbations associated with HIV infection and their impact on coagulation pathways, reinforcing the notion that HIV significantly alters the risk profile for thromboembolic disease.
Rakhra et al. (2021) address the clinical management of thromboembolic events in HIV patients, specifically discussing the efficacy and safety of various anticoagulation regimens. Their work emphasizes the increased prevalence of ischemic stroke in this population and the critical need for tailored prevention strategies that consider both HIV-related and traditional cardiovascular risk factors.
Finally, provide a systematic review of strategies aimed at reducing morbidity associated with cardiovascular diseases in HIV patients. Their comprehensive analysis of recent literature underscores the importance of integrating management of cardiovascular risk factors into the care of individuals living with HIV, particularly in the context of antiretroviral therapy.
Together, these articles illuminate the intricate relationship between HIV infection and thromboembolic disorders, highlighting the need for continued research and clinical vigilance in managing these complications. The evolving understanding of the mechanisms underlying thromboembolic phenomena in HIV patients not only informs clinical practice but also prompts further investigation into effective prevention and treatment strategies.
Discussion.
Symptomatic thrombocytopenia's in AIDS are multifactorial, resulting from the combination of direct and indirect mechanisms. One direct mechanism is the destruction of platelets by HIV itself, which can lead to a decrease in platelet production. HIV infects and replicates within platelet precursors in the bone marrow, causing apoptosis and subsequent thrombocytopenia. Additionally, HIV proteins can activate the complement system, leading to the destruction of platelets.
Indirect mechanisms contributing to thrombocytopenia in AIDS include the generation of anticoagulant antibodies, such as anti-platelet antibodies and antiphospholipid antibodies. These antibodies can bind to platelets, leading to their removal by the reticuloendothelial system. HIV-infected individuals may also experience splenomegaly due to the immune system's attempt to eliminate the virus, resulting in the sequestration of platelets and a further reduction in platelet count.
Clinical Manifestations
Thrombocytopenia in AIDS can manifest in various ways, ranging from asymptomatic to life-threatening bleeding episodes. Mild thrombocytopenia may present with petechiae, purpura, or easy bruising, while more severe cases can lead to gastrointestinal bleeding, intracranial hemorrhage, or bleeding tendencies. In some cases, thrombocytopenia may be asymptomatic, with detection based solely on laboratory findings.
Conclusion
Symptomatic thrombocytopenia's in AIDS are a common and potentially life-threatening complication of HIV infection. Understanding the pathophysiology of thrombocytopenia in AIDS is critical to developing effective treatment strategies. Combining ART with specific measures to manage thrombocytopenia has significantly improved treatment outcomes for HIV-infected individuals with this condition. Further research is needed to refine our understanding of thrombocytopenia in AIDS and to develop more effective treatment options for this complex condition.
References:
1. Nagaraja, V., A. Terriquez, J., Gavini, H., Jha, L., & A. Klotz, S. (2010). Pulmonary Embolism Mimicking Pneumonia in a HIV Patient. ncbi.nlm.nih.gov
2. Konin, C., B. Anzouan-Kacou, J., & Essam N'loo, A. (2011). Arterial Thrombosis in Patients with Human Immunodeficiency Virus: Two-Case Reports and Review of the Literature. ncbi.nlm.nih.gov
3. W. J. van den Dries, L., A. Gruters, R., B. C. Hovels-van der Borden, S., J. H. A. Kruip, M., P. M. de Maat, M., C. M. van Gorp, E., & E. van der Ende, M. (2015). von Willebrand Factor is elevated in HIV patients with a history of thrombosis. ncbi.nlm.nih.gov
4. S. Jackson, B., Nunes Goncalves, J., & Pretorius, E. (2020). Comparison of pathological clotting using haematological, functional and morphological
investigations in HIV-positive and HIV-negative patients with deep vein thrombosis. ncbi.nlm.nih.gov
5. Rakhra, A., E Kiefer, L., R Busireddy, K., & Sankaraneni, R. (2021). Cerebral Venous Sinus Thrombosis in an Immunocompetent HIV Patient. ncbi.nlm.nih.gov
