scholarly journals Subclinical atherosclerosis and endothelial dysfunction in patients with HIV infection: is there any new diagnostic test?

2021 ◽  
Author(s):  
Francisco Arnaiz de las Revillas ◽  
Vicente Gonzalez-Quintanilla ◽  
Jose Antonio Parra ◽  
Enrique Palacio ◽  
Claudia Gonzalez-Rico ◽  
...  
Keyword(s):  
Viral Load ◽  
Endothelial Dysfunction ◽  
Hiv Infection ◽  
Subclinical Atherosclerosis ◽  
Calcium Score ◽  
High Viral Load ◽  
Breath Holding ◽  
Hiv Positive ◽  
Cd4 Cells ◽  
Immunodeficiency Virus

Abstract Introduction: To analyze the association between human immunodeficiency virus (HIV) infection, and the presence of subclinical atherosclerosis and endothelial dysfunction. Methods Prospective cohort study of HIV positive patients who underwent to intimate thickness (IMT) determination and coronary artery calcium score to determine subclinical atherosclerosis. To detect endothelial dysfunction breath holding index, flow mediated dilation and concentration of endothelial progenitor cells (EPC) were measured. Results Patients with an IMT ≥ 0.9 mm had an average of 559.3 ± 283.34 CD4/µl and those with an IMT < 0.9 mm 715.4 ± 389.92 CD4/µl (p = 0.04). Patients with a low calcium score had a significantly higher average of CD4 cells value and lower zenith viral load than those with a higher score (707.7 ± 377.5 CD4/µl vs 477.23 ± 235.7 CD4/µl (p = 0.01)) and (7x104 ± 5x104 c/ml vs 23.4 x 104 ± 19 x 104 c /ml (p = 0.02). Early EPCs concentration in patients with a CD4 nadir < 350/ul was lower than concentration among those presenting a CD4 nadir ≥ 350 (p = 0.03). Conclusion In HIV positive patients low CD4 cells levels and high viral load were associated to a higher risk of developing subclinical atherosclerosis.HIV patients with less CD4 cells may have fewer early EPCs.

scholarly journals Evaluation of endothelial function and subclinical atherosclerosis in patients with HIV infection

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
F. Arnaiz de las Revillas ◽  
V. Gonzalez-Quintanilla ◽  
J. A. Parra ◽  
E. Palacios ◽  
C. Gonzalez-Rico ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Subclinical Atherosclerosis ◽  
Calcium Score ◽  
Intima Media Thickness ◽  
Breath Holding ◽  
Hiv Positive ◽  
Flow Mediated Dilation ◽  
Immunodeficiency Virus ◽  
Cd4 Cell ◽  
Breath Holding Index

AbstractThe aim of this study was to analyse the association between human immunodeficiency virus (HIV) related clinical and analytical parameters and the presence of subclinical atherosclerosis as well as endothelial dysfunction. This was a prospective cohort study of HIV-positive patients who underwent intima media thickness (IMT) determination and coronary artery calcium scoring to determine subclinical atherosclerosis. To detect endothelial dysfunction, the breath holding index, flow-mediated dilation and the concentration of endothelial progenitor cells (EPCs) were measured. Patients with an IMT ≥ 0.9 mm had an average of 559.3 ± 283.34 CD4/μl, and those with an IMT < 0.9 mm had an average of 715.4 ± 389.92 CD4/μl (p = 0.04). Patients with a low calcium score had a significantly higher average CD4 cell value and lower zenith viral load (VL) than those with a higher score (707.7 ± 377.5 CD4/μl vs 477.23 ± 235.7 CD4/μl (p = 0.01) and 7 × 104 ± 5 × 104 copies/ml vs 23.4 × 104 ± 19 × 104 copies/ml (p = 0.02)). The number of early EPCs in patients with a CD4 nadir < 350/µl was lower than that in those with a CD4 nadir ≥ 350 (p = 0.03). In HIV-positive patients, low CD4 cell levels and high VL were associated with risk of developing subclinical atherosclerosis. HIV patients with CD4 cell nadir < 350/µl may have fewer early EPCs.

scholarly journals PREDICTORS OF CHRONICKIDNEY DISEASEINHUMAN IMMUNODEFICIENCY VIRUS PATIENTS

2018 ◽  
pp. 32-37
Author(s):  
M.O. Andrushchak
Keyword(s):  
Viral Load ◽  
Hiv Infection ◽  
Clinical Stage ◽  
High Viral Load ◽  
Kidney Damage ◽  
Average Amount ◽  
Hiv Rna ◽  
Immunodeficiency Virus ◽  
The Difference ◽  
Cd4 Lymphocytes

Purpose: to determine the frequency of diagnosis and predictors of renal disease in HIV-infected patients. Patients and methods. 292 HIV-infected patients, who were on an outpatient screening at the Chernivtsi Regional AIDS Center, were screened. Results CKD was diagnosed in 153 out of292 (52.4%) of the examined patients. among which 105 (36.0%) patients were diagnosed with isolated albuminuria/proteinuria, 48 (16.4%) patients had albuminuria /proteinuria, in combination with a decrease in glomerular filtration rate. It has been established that the presence of proteinuria in HIV infection is accompanied by a significantly higher level of HIV RNA compared to patients without this symptom (p < 0.01). At the same time, the average amount of CD4+-lymphocytes in blood serum in patients with proteinuria is significantly lower than in HIV-infected individuals who did not show kidney damage. The difference between the values of the ratios of CD4+/CD8+-lymphocytes in the analyzed groups (p < 0,05) is also significant. In most patients who were in the III-IV clinical stage of HIV infection, antiretroviral therapy (ART) was effective and reduced the viral load. Therefore, it is obvious that the amount of HIV-RNA in the blood of these individuals was significantly lower compared to patients who did not receive such treatment. At the same time, the burden of HIV, as well as the number of CD4+-lymphocytes in the representatives of the comparable groups did not differ (p > 0.05). Conclusion. The main predictors of kidney damage in HIV-infected are: high viral load, decrease in absolute numbers. CD4+-lymphocytes less than 200. Co-infection with hepatitis B and/ or C viruses does not affect the level of proteinuria and GFR in HIV-infected patients.

Abstract WP426: Subarachnoid Hemorrhage in patients infected with Human Immunodeficiency Virus

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Haralabos Zacharatos ◽  
Malik M Adil ◽  
Ameer E Hassan ◽  
Sarwat I Gilani ◽  
Adnan I Qureshi
Keyword(s):  
Human Immunodeficiency Virus ◽  
Subarachnoid Hemorrhage ◽  
Blood Transfusion ◽  
Hospital Mortality ◽  
Hiv Infection ◽  
The United States ◽  
Hiv Positive ◽  
Published Data ◽  
Immunodeficiency Virus ◽  
Hiv Negative

Background: There is limited data regarding the unique attributes of ischemic stroke among patients infected with human immunodeficiency virus (HIV). There is no published data regarding the occurrence and outcomes of subarachnoid hemorrhage (SAH) among HIV infected persons. Methods: The largest all-payer Nationwide Inpatient Sample (NIS 2002-2010) data was used to identify and analyze all patients presenting with the primary diagnosis of SAH in the United States. Among this cohort, we identified the patients who were not HIV positive and those who were HIV positive. Patient demographics, medical co-morbidities, in-hospital complications, in-hospital procedures, and discharge disposition were compared between the two groups. The association between HIV infection and outcomes was evaluated in multivariate analysis after adjusting for potential confounders. Results: Of the 351,491 patients admitted with SAH, 1367 (0.39%) were infected with HIV. HIV infected patients were younger, mean age [±SD] of 45 ±14.2 years versus those who were not 58±19 years, (p<0.0001). The rate of blood transfusion [27,286 (7.8%) versus 245.6 (18%), p=0.0003], mechanical ventilation [51,199 (14.6%) versus 316.1(23.1%), p=0.008], and sepsis [14,644 (4.2%) versus 236.1 (17.3%), p<0.0001] was significantly higher among HIV infected patients. After adjusting for age, gender, hypertension, coagulopathy, atrial fibrillation, renal failure, and dyslipidemia, HIV negative patients had a significantly higher rate of discharge to home (odds ratio [OR] 1.9, 95% CI: 1.4-2.6, p<0.0001) and lower in-patient mortality (OR 0.4, 95% CI: 0.3-0.5, p<0.001). Further adjustment for blood transfusion and sepsis reduced the odds of discharge to home for the HIV negative patients, from 1.9 to 1.7 but did not affect in-hospital mortality. Conclusion: The in-hospital mortality in HIV infected patients with SAH is higher despite these patients being younger than non-HIV infected patients. We believe that this study provides a nationwide perspective which may have some important implications for early recognition and diagnosis of HIV-infection in SAH patients.

scholarly journals Neurocysticercosis and HIV Infection: what can we learn from the published literature?

2019 ◽  
Vol 77 (5) ◽  
pp. 357-365 ◽  
Author(s):  
Omar Herrera Vazquez ◽  
Matthew L. Romo ◽  
Agnès Fleury
Keyword(s):  
Hiv Infection ◽  
Immune Status ◽  
Taenia Solium ◽  
Response To Treatment ◽  
Hiv Positive ◽  
Historical Series ◽  
Immunodeficiency Virus ◽  
The Central Nervous System ◽  
Published Research ◽  
Hiv Negative

ABSTRACT Infections caused by the human immunodeficiency virus (HIV) and by the larvae of Taenia solium (i.e., cysticercosis) are still widespread in many developing countries. Both pathologies modify host immune status and it is possible that HIV infection may modulate the frequency and pathogeny of cysticercosis of the central nervous system (i.e., neurocysticercosis [NCC]). Objective: To describe published cases of NCC among HIV-positive patients and to evaluate whether the characteristics of NCC, including frequency, symptoms, radiological appearance, and response to treatment differed between HIV-positive and HIV-negative patients. Methods: Forty cases of NCC/HIV co-infected patients were identified in the literature. Clinical and radiological characteristics, as well as response to treatment, were compared with non-matching historical series of NCC patients without HIV infection. Results: Most of these patients had seizures and multiple vesicular parasites located in parenchyma. Clinical and radiological characteristics were similar between HIV-positive and HIV-negative patients with NCC, as well as between immunocompromised and non-immunocompromised HIV-positive patients. Conclusion: Our review did not reveal clear interactions between HIV and NCC. This may be partially due to the small number of cases and reliance on published research. A systematic, multi-institutional effort aiming to report all the cases of this dual pathology is needed to confirm this finding and to clarify the possible relationship between both pathogens.

scholarly journals Levels of Macrophage Inflammatory Protein 1α (MIP-1α) and MIP-1β in Intervillous Blood Plasma Samples from Women with Placental Malaria and Human Immunodeficiency Virus Infection

2003 ◽  
Vol 10 (4) ◽  
pp. 631-636 ◽  
Author(s):  
Sujittra Chaisavaneeyakorn ◽  
Julie M. Moore ◽  
Lisa Mirel ◽  
Caroline Othoro ◽  
Juliana Otieno ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Blood Plasma ◽  
Plasma Levels ◽  
Placental Malaria ◽  
Hiv Positive ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Macrophage Inflammatory Protein ◽  
Hiv Negative

ABSTRACT Macrophage inflammatory protein-1α (MIP-1α) and MIP-1β play an important role in modulating immune responses. To understand their importance in immunity to placental malaria (PM) and in human immunodeficiency virus (HIV)-PM coinfection, we investigated levels of these chemokines in the placental intervillous blood plasma (IVB plasma) and cord blood plasma of HIV-negative PM-negative, HIV-negative PM-positive, HIV-positive PM-negative, and HIV-positive PM-positive women. Compared to HIV-negative PM-negative women, the MIP-1β concentration in IVB plasma was significantly elevated in HIV-negative PM-positive women and HIV-positive PM-positive women, but it was unaltered in HIV-positive PM-negative women. Also, PM-infected women, irrespective of their HIV status, had significantly higher levels of MIP-1β than HIV-positive PM-negative women. The MIP-1α level was not altered in association with either infection. The IVB plasma levels of MIP-1α and MIP-1β positively correlated with the cord blood plasma levels of these chemokines. As with IVB plasma, only cord plasma from PM-infected mothers had significantly elevated levels of MIP-1β compared to PM-negative mothers, irrespective of their HIV infection status. MIP-1β and MIP-1α levels in PM-positive women were positively associated with parasite density and malaria pigment levels. Regardless of HIV serostatus, the IVB MIP-1β level was significantly lower in women with PM-associated anemia. In summary, an elevated level of MIP-1β was associated with PM. HIV infection did not significantly alter these two chemokine levels in IVB plasma.

scholarly journals CD8+ T lymphocytes provide helper activity for IgE synthesis in human immunodeficiency virus-infected patients with hyper-IgE.

1995 ◽  
Vol 181 (1) ◽  
pp. 423-428 ◽  
Author(s):  
R Paganelli ◽  
E Scala ◽  
I J Ansotegui ◽  
C M Ausiello ◽  
E Halapi ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
T Cell ◽  
Hiv Infection ◽  
Cd8 T Cells ◽  
Cd8 T Cell ◽  
Cd4 Cells ◽  
In Vitro Synthesis ◽  
Immunodeficiency Virus ◽  
Ige Synthesis

Increased levels of serum IgE and eosinophilia have been described in human immunodeficiency virus (HIV) infection, almost exclusively in patients with CD4+ cell count &lt; 200 cells/microliters. IgE production is regulated by CD4+ T helper type 2 (Th-2) lymphocytes, producing interleukin 4 (IL-4) and expressing a ligand for the B cell-specific CD40 molecule (CD40 ligand [L]). A shift to a Th-2-like pattern of cytokine secretion has been postulated to be associated with progression toward acquired immunodeficiency syndrome (AIDS). We studied three AIDS patients with very high levels of IgE and almost complete depletion of CD4+ lymphocytes, suggesting that IgE synthesis could not be driven by CD4+ cells. IgE in vitro synthesis by cells from such patients was, however, inhibited by anti-IL-4. We show that both CD8+ T cell lines and the majority of CD8+ T cells clones derived from these patients produce IL-4, IL-5, and IL-6 in half of the cases together with interferon gamma (IFN-gamma). 44% of CD8+ T cell clones expressed a CD40L, and the supernatants of the clones were capable of inducing IgE synthesis by normal B cells costimulated with anti-CD40. CD8+ T cells in these patients therefore functionally mimic Th-2 type cells and may account for hyper-IgE and eosinophilia in the absence of CD4+ cells. The presence of such CD8+ cells may also provide a source of IL-4 directing the development of predominant Th-2 responses in HIV infection.

scholarly journals Analysis of Total Human Immunodeficiency Virus (HIV)-Specific CD4+ and CD8+ T-Cell Responses: Relationship to Viral Load in Untreated HIV Infection

2001 ◽  
Vol 75 (24) ◽  
pp. 11983-11991 ◽  
Author(s):  
Michael R. Betts ◽  
David R. Ambrozak ◽  
Daniel C. Douek ◽  
Sebastian Bonhoeffer ◽  
Jason M. Brenchley ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Viral Load ◽  
T Cell ◽  
Hiv Infection ◽  
Highly Active Antiretroviral Therapy ◽  
T Cell Responses ◽  
T Cell Response ◽  
Cell Responses ◽  
Immunodeficiency Virus

ABSTRACT Human immunodeficiency virus (HIV)-specific T-cell responses are thought to play a key role in viral load decline during primary infection and in determining the subsequent viral load set point. The requirements for this effect are unknown, partly because comprehensive analysis of total HIV-specific CD4+ and CD8+T-cell responses to all HIV-encoded epitopes has not been accomplished. To assess these responses, we used cytokine flow cytometry and overlapping peptide pools encompassing all products of the HIV-1 genome to study total HIV-specific T-cell responses in 23 highly active antiretroviral therapy naı̈ve HIV-infected patients. HIV-specific CD8+ T-cell responses were detectable in all patients, ranging between 1.6 and 18.4% of total CD8+ T cells. HIV-specific CD4+ T-cell responses were present in 21 of 23 patients, although the responses were lower (0.2 to 2.94%). Contrary to previous reports, a positive correlation was identified between the plasma viral load and the total HIV-, Env-, and Nef-specific CD8+ T-cell frequency. No correlation was found either between viral load and total or Gag-specific CD4+ T-cell response or between the frequency of HIV-specific CD4+ and CD8+ T cells. These results suggest that overall frequencies of HIV-specific T cells are not the sole determinant of immune-mediated protection in HIV-infection.

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