The effect of perinatal HIV and antiretroviral therapy on vascular structure and function in young people: A systematic review and meta-analysis

Majonga, Edith; Ferrand, Rashida A; Deanfield, John; Chiesa, Scott T

doi:10.1016/j.atherosclerosis.2022.05.013

Cited by 4 publications

(2 citation statements)

References 54 publications

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“…Previous studies have found that HIV infection can aggravate arterial stiffness, atherosclerosis, and endothelial disfunction though HIV-related inflammation and immune activation, increasing reactive oxygen species production and reducing nitric oxide bioavailability [ 8 – 12 ]. However, there was large heterogeneity between HIV and vascular pathologies in previous reviews, and the results were often contradictory [ 13 , 14 ]. In our case, the comorbidity, AIDS, aggravated the infection and may accelerate vascular damage, expanding the extent of ADF.…”

Section: Discussionmentioning

confidence: 99%

A secondary abdominal aorta-duodenal fistula accompanied with acquired Immune Deficiency Syndrome presented with recurrent sepsis: a case report

Hu,

Yan

2024

BMC Infect Dis

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Background Abdominal aorta-duodenal fistulas are rare abnormal communications between the abdominal aorta and duodenum. Secondary abdominal aorta-duodenal fistulas often result from endovascular surgery for aneurysms and can present as severe late complications. Case presentation A 50-year-old male patient underwent endovascular reconstruction for an infrarenal abdominal aortic pseudoaneurysm. Prior to the operation, he was diagnosed with Acquired Immune Deficiency Syndrome and Syphilis. Two years later, he was readmitted with lower extremity pain and fever. Blood cultures grew Enterococcus faecium, Salmonella, and Streptococcus anginosus. Sepsis was successfully treated with comprehensive anti-infective therapy. He was readmitted 6 months later, with blood cultures growing Enterococcus faecium and Escherichia coli. Although computed tomography did not show contrast agent leakage, we suspected an abdominal aorta-duodenal fistula. Esophagogastroduodenoscopy confirmed this suspicion. The patient underwent in situ abdominal aortic repair and received long-term antibiotic therapy. He remained symptom-free during a year and a half of follow-up. Conclusions This case suggests that recurrent infections with non-typhoidal Salmonella and gut bacteria may be an initial clue to secondary abdominal aorta-duodenal fistula.

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Section: Discussionmentioning

confidence: 99%

A secondary abdominal aorta-duodenal fistula accompanied with acquired Immune Deficiency Syndrome presented with recurrent sepsis: a case report

Hu,

Yan

2024

BMC Infect Dis

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“…Certain antiretrovirals can stimulate components of the RAAS 164 though the specific effects depend on the class and mechanism of the antiretroviral. HIV PIs, in particular, are associated with increased blood pressure, 147 potentially mediated by endothelial dysfunction, 242 vascular stiffness, 243 and renal damage. 241 Long-term ART use has also been associated with metabolic changes that can affect the RAAS, including lipid abnormalities 244 and insulin resistance, 245,246 which are risk factors for hypertension.…”

Section: Raas Activationmentioning

confidence: 99%

HIV-Associated Hypertension: Risks, Mechanisms, and Knowledge Gaps

Prakash,

Swami Vetha,

Chakraborty

et al. 2024

Circulation Research

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HIV type 1 (HIV-1) is the causative agent of AIDS. Since the start of the epidemic, HIV/AIDS has been responsible for ≈40 million deaths. Additionally, an estimated 39 million people are currently infected with the virus. HIV-1 primarily infects immune cells, such as CD 4+ (cluster of differentiation 4 + ) T lymphocytes (T cells), and as a consequence, the number of CD 4+ T cells progressively declines in people living with HIV. Within a span of ≈10 years, HIV-1 infection leads to the systemic failure of the immune system and progression to AIDS. Fortunately, potent antiviral therapy effectively controls HIV-1 infection and prevents AIDS-related deaths. The efficacy of the current antiviral therapy regimens has transformed the outcome of HIV/AIDS from a death sentence to a chronic disease with a prolonged lifespan of people living with HIV. However, antiviral therapy is not curative, is challenged by virus resistance, can be toxic, and, most importantly, requires lifelong adherence. Furthermore, the improved lifespan has resulted in an increased incidence of non-AIDS–related morbidities in people living with HIV including cardiovascular diseases, renal disease, liver disease, bone disease, cancer, and neurological conditions. In this review, we summarize the current state of knowledge of the cardiovascular comorbidities associated with HIV-1 infection, with a particular focus on hypertension. We also discuss the potential mechanisms known to drive HIV-1–associated hypertension and the knowledge gaps in our understanding of this comorbid condition. Finally, we suggest several directions of future research to better understand the factors, pathways, and mechanisms underlying HIV-1–associated hypertension in the post-antiviral therapy era.

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Endothelial dysfunction, a predictor of cardiovascular disease in HIV patients on antiretroviral therapy: A systematic review and meta-analysis

Strauss,

Phoswa,

Lebelo

et al. 2024

Thrombosis Research

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The effect of perinatal HIV and antiretroviral therapy on vascular structure and function in young people: A systematic review and meta-analysis

Cited by 4 publications

References 54 publications

A secondary abdominal aorta-duodenal fistula accompanied with acquired Immune Deficiency Syndrome presented with recurrent sepsis: a case report

A secondary abdominal aorta-duodenal fistula accompanied with acquired Immune Deficiency Syndrome presented with recurrent sepsis: a case report

HIV-Associated Hypertension: Risks, Mechanisms, and Knowledge Gaps

Endothelial dysfunction, a predictor of cardiovascular disease in HIV patients on antiretroviral therapy: A systematic review and meta-analysis

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