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Transaminase [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)] Activity of HIVFemale Patients on Drugs and Female Patients Not on Drugs
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... In accordance with our results, the elevation of transaminases in patients with HIV has been reported in several studies. [35][36][37] Furthermore, our results revealed that the serum levels of ALT in both ART-experienced groups were higher than those observed in patients who were ART-naïve or healthy control patients, which is in accordance to those reported by Odiba, Onosakponome, et al 35 ; Usman et al 36 ; Agbecha and Ikyernum 37 ; and Adiga and Malawadi. 38 In contrast, Osakunor et al 39 conducted a case-control study on 2 groups of patients with HIV who were receiving ART and who were ART-naïve in Ghana and found that ART had minimal effects on hepatotoxicity and ALT activity. ...
... 38 In contrast, Osakunor et al 39 conducted a case-control study on 2 groups of patients with HIV who were receiving ART and who were ART-naïve in Ghana and found that ART had minimal effects on hepatotoxicity and ALT activity. In line with the current results, the elevation of ALT in patients with HIV who were ART-naïve has also been reported by some authors [35][36][37]40 ; however, this finding was not the case in Indian patients with HIV who were ART-naïve. 38 The differences can be attributed to population genetics, different demographic and lifestyle factors, and the number of participants enrolled in the studies. ...
... In this study, elevated ALT level was present in 32% of patients with HIV, including 146 (33%) and 20 (26.7%) patients in the ART-experienced and ART-naïve groups, respectively. The rate of ALT abnormality in the current study was lower than that observed in patients with HIV who had received ART in Nigeria (74.2%) 35 and similar to that in Cameroonian patients (22.6%). 41 On the other hand, the elevation of ALT level in our patients with HIV who were ART-naïve (26.7%) was higher than that observed in patients who were ARTnaïve in Tanzania (13%) 42 and North America (15%). ...
Objective
To investigate hepatotoxicity in Iranian patients with HIV to assess the association between virologic response to HIV treatment and serum alanine aminotransferase (ALT).
Methods
This study was conducted with 200 control patients, 75 patients with HIV naïve to antiretroviral therapy (ART), and 443 patients who received ARTs with virologic response (≤1000 copies/mL) or virologic treatment failure (>1000 copies/mL). Serum ALT level and HIV viral load were determined in all patients.
Results
Patient ALT levels were significantly higher than those of control patients (45.1 ± 44.4 IU/L vs 23.8 ± 5.4 IU/L). Compared to patients who were ART-naïve, patients with ART experience had significantly higher ALT levels (38.2 ± 26.2 IU/L vs 46.3 ± 46.7 IU/L), and severe hepatotoxicity was only detected in those with ART experience (8 patients, 1.8%). Mean ALT had no significant difference between virologic response/failure groups. The ALT activity and HIV load had a negative correlation coefficient, but it was not significant.
Conclusion
Periodic monitoring for the possibility of hepatotoxicity is highly recommended in all patients with HIV, especially in those receiving ART treatment.
... Hydroxyproline content further confirmed that Antrodin C inhibited CCl 4 induced collagen production in mice ( Figure 6C). ALT (alanine transaminase) and AST (aspartate aminotransferase) have been recognized as indicators of liver function (Odiba et al., 2014). The elevated serum ALT and AST revealed that CCl 4 treatment FIGURE 5 | Effects of Antrodin C on the PDGF-BB-induced signaling pathway. ...
Hepatic stellate cells (HSCs) play an essential role in the development of liver fibrosis. Antrodia camphorata ( A. camphorata ) is a medicinal fungus with hepatoprotective effect. This study investigated whether Antrodin C, an A. camphorata -fermented metabolite, could exert a protective role on liver fibrosis both in vitro and in vivo . The anti-fibrotic effect of Antrodin C was investigated in CFSC-8B cell (hepatic stellate cell) stimulated by transforming growth factor-β1 (TGF-β1) or platelet-derived growth factor-BB (PDGF-BB) in vitro and in CCl 4 induced liver fibrosis in mice. Antrodin C (50 μM) inhibited TGF-β1 or PDGF-BB stimulated CFSC-8B cell activation, migration and extracellular matrix (ECM) accumulation (all p < 0.05). Antrodin C (3, 6 mg/kg/d) oral administration reduced the degree of liver fibrosis induced by CCl 4 in mice. Antrodin C down-regulated the expression of α-smooth muscle actin (α-SMA) and collagen I in fibrotic livers. Furthermore, Antrodin C ameliorated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation in serum (all p < 0.05). Mechanistically, Antrodin C executes its anti-fibrotic activity through negatively modulate TGF-β1 downstream SMAD Family Member 2 (Smad2), AKT Serine/Threonine Kinase 1 (AKT), extracellular signal-regulated kinase (ERK), and P38 MAP Kinase (P38), as well as PDGF-BB downstream AKT and ERK signaling pathways. Antrodin C ameliorates the activation, migration, ECM production in HSCs and CCl 4 -induced liver fibrosis in mice, suggesting that Antrodin C could serve as a protective molecule against liver fibrosis.
... ɣ-glutamyltranspeptidase, a membrane enzyme found in the hepatobiliary system, that is essential for synthesis of glutathione, which is the main antioxidant molecule in cells, is controlled by GGT.in the presence of cholestasis in viral hepatitis, GGT increases more than 10 folds, whereas in absence of cholestasis, it increases upto 5 times [15].ALT is the most reliable biochemical value to show the of liver injury in patients with acute and chronic viral hepatitis, this is due to the distribution of cytoplasmic exclusively of ALT and longer half-life in the blood (about 50 hours) than for AST (about 16 hours) [16,17]. The possible mechanisms include Excretion of ALP is reduced in bile Will cause the in regurgitation of enzyme into circulation by the hepatic sinusoid [18,19]. ALP increased in disease resembles the ALP which can be removed from liver. ...
Hepatitis B infection is a worldwide healthcare problem, especially in developing areas. The current study was to evaluate the alterations in different biochemical parameters including paraoxonase (PON), 5′-Nucleotidase (5NT), total bilirubin, direct bilirubin, indirect bilirubin, Prothrombin time (PT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), Total serum protein (TSP), albumin (Alb), Superoxide dismutase (SOD) and ɣ-glutamyl transpeptidase (GGT) in the serum samples of the viral hepatitis patients (n=100) compared with healthy controls(n=100). This study shown that there were significant increase (p<0.05) in the TSB, D. Bilirubin, In. Bilirubin, AST, ALT, PT, GGT, 5-NT, and ALP in viral hepatitis patients compared to their respective normal controls and there were significant decrease (p<0.05) in the serum (PON, SOD) activities, TSP and albumin concentration. It can be concluded that PON, 5-NT, SOD, ALT, AST, ALP and GGT may be specific method for making a diagnosis of viral hepatitis and also in distinguishing it with other kinds of hepatitis.
Diabetes mellitus is a metabolic disease affecting various body organs and systemscausing several complications such ascardiovascular diseases, stroke, nephropathy, retinopathy, neuropathy, erectile dysfunction and diabetic foot ulcer development. Diabetic patients are under oxidative stress and inflammation that play crucial role in complications development.Pomegranate, containingvarious phytochemicals with antioxidant, anti-inflammatory, antihyperglycemic, antihyperlipidemic, antihypertensive, antiatherogenic, antimicrobial, cardioprotective, neuroprotective, regenerative, wound healing andimmuno modulatory bioactivities, at the same time is sufficiently treating diabetesand its’ complications without any side effects as safety tests have shown. Pomegranate treatment improves antioxidant status of the patients, reduces inflammation, ameliorates diabetes improving insulin sensitivity, increasing insulin production and secretion,reducing blood glucose levels, inhibiting hemoglobin glycosylation, protecting pancreas and is contributing to pancreatic islets regeneration and stimulation. It also ameliorates cardiovascular complications decreasing total cholesterol, triglycerides, LDL, lipid peroxidation, atherosclerosis, increasing the beneficial HDL. Pomegranate alsoenhances wound healing byreducing bacterial count, inhibiting quorum sensing and biofilm formation, increasing collagen production, upregulating the EGF, VEGF and TGF-β1 levelsand leading to excellent epithelialization and neovascularization. Besides, pomegranate treatment ameliorates nephropathy reducing serum creatinine, urine albumin, blood urea nitrogen, urine albumin to creatinine ratio,renal fibrosis, glomerular sclerosis, hypertrophyand interstitial hyperplasia. Pomegranate treatment is preventing or ameliorating neuropathy and alsoimproving erectile function by increasingintracavernosal blood flow and MICP/MAP percentage in patients with atherosclerosis. Moreover, pomegranate ameliorates retinopathy reducing the oxidative stress biomarker 8-OHdG, decreasing the levels of sialic acid, malondialdehyde, improving retina cell layers and delaying cataract onset. Is important to be mentioned that while in diabetic individuals the values of several biochemical parameters were significantly improved, at the same time there were not changes on thehealthy individuals’ biochemical parameters which were normal, indicatingexcept its’ excellent pharmaceutical properties alsoa regulatory role of pomegranate as it is acting only whenever it is needed for health achievement and maintenance.These results indicate that pomegranate can offer an alternative,safe, holistic treatment for diabetes and its’ complications, improving the general health and quality of life of the patient.
Lamivudine is a nucleoside analog with activity against human immunodeficiency virus (HIV) and hepatitis B virus (HBV). Patients
coinfected with HIV and HBV may have hepatitis flares when lamivudine therapy is discontinued or when resistance of HBV to
lamivudine emerges. This retrospective, descriptive study conducted in three tertiary care medical centers describes patients
coinfected with HIV type 1 and HBV who presented with a spectrum of clinical and subclinical hepatitic responses to lamivudine
withdrawal or resistance. One patient had fulminant hepatic failure and a second patient had subclinical hepatitis when lamivudine
therapy was discontinued and a more efficacious antiretroviral regimen was substituted. Three patients had flares of hepatitis
after 13 to 18 months of lamivudine therapy. Lamivudine withdrawal or emergence of lamivudineresistant mutants in patients
coinfected with HIV and HBV may result in severe hepatitis. Clinicians caring for patients with coinfection with HIV and HBV
should be aware of the possibility that a hepatitis B flare may occur in previously asymptomatic carrier patients.
Highly active antiretroviral therapy has decreased human immunodeficiency virus (HIV)-associated mortality; other comorbidities,
such as chronic liver disease, are assuming greater importance. We retrospectively examined the causes of death of HIV-seropositive
patients at our institution in 1991, 1996, and 1998–1999. In 1998–1999, 11 (50%) of 22 deaths were due to end-stage liver
disease, compared with 3 (11.5%) of 26 in 1991 and 5 (13.9%) of 36 in 1996 (P = .003). In 1998–1999, 55% of patients had nondetectable plasma HIV RNA levels and/or CD4 cell counts of>200 cells/mm3 within the year before death. Most of the patients that were tested had detectable antibodies to hepatitis C virus (75% of
patients who died in 1991, 57.7% who died in 1996, and 93.8% who died in 1998–1999; P = NS). In 1998–1999, 7 patients (31.8%) discontinued antiretroviral therapy because of hepatotoxicity, compared with 0 in
1991 and 2 (5.6%) in 1996. End-stage liver disease is now the leading cause of death in our hospitalized HIV-seropositive
population.
Objective: To study hepatic cytolysis in patients treated by highly active antiretroviral therapy (HAART) with protease inhibitor or with two nucleoside reverse transcriptase inhibitors (NRTIs).
Methods: We selected patients of the Aquitaine Cohort who initiated HAART or two NRTIs before 1 January 1998, had alanine amino-transferase (ALT) ≤ 200 IU/l at baseline and at least one follow-up measure. Cox model was used to study the association between occurrence of severe hepatic cytolysis (ALT>200 IU/l) and age, gender, HIV transmission group, baseline CD4 and CD8 cell count, history of hepatic cytolysis, antiretroviral drug, baseline liver enzymes (WHO classification level 0: ≤?50 IU/l, level 1: 51 to 100, level 2: 101 to 200), hepatitis B and C co-infection.
Results: Sixty-four of 748 (8.5%) patients treated with HAART and 71 of 1249 (5.7%) treated with two NRTIs developed cytolysis. The probability of occurrence was 7.9% after 1 year [95% confidence interval (CI), 5.9-10.4] for patients treated with HAART and 4.8% (95% CI, 3.6-6.4) for patients treated with two NRTIs (log-rank test, P = 0.01). The median time to occurrence was 164 days for HAART-treated patients and 252 days for those treated with two NRTIs. In multivariate analysis, the history of cytolysis [hazard ratio (HR) = 2.3; 95% CI, 1.2-4.4], baseline value of ALT (HR = 2.4; 95% CI, 1.2-4.8 and HR = 3.3; 95% CI, 1.4-7.4 for levels 1 and 2, respectively), hepatitis B (HR = 3.0; 95% CI, 1.4-6.2) and C co-infections (HR = 3.2; 95% CI, 1.7-6.2) remained significantly associated with the occurrence of severe hepatic cytolysis among HAART-treated patients. History of cytolysis, hepatitis B and C were associated with cytolysis in patients treated with two NRTIs (HR = 14.8, 2.6 and 2.7, respectively).
Conclusion: Hepatic cytolysis is more frequent among patients treated with HAART than with two NRTIs. Hepatitis B and C are the major risk factors after initiation of HAART or treatment with NRTIs. Co-infections with hepatitis B virus or hepatitis C virus may modify the management of HIV-infected patients treated by HAART.
This report updates and combines earlier versions of guidelines for the prevention and treatment of opportunistic infections (OIs) in HIV-infected adults (i.e., persons aged >/=18 years) and adolescents (i.e., persons aged 13--17 years), last published in 2002 and 2004, respectively. It has been prepared by the Centers for Disease Control and Prevention (CDC), the National Institutes of Health (NIH), and the HIV Medicine Association (HIVMA) of the Infectious Diseases Society of America (IDSA). The guidelines are intended for use by clinicians and other health-care providers, HIV-infected patients, and policy makers in the United States. These guidelines address several OIs that occur in the United States and five OIs that might be acquired during international travel. Topic areas covered for each OI include epidemiology, clinical manifestations, diagnosis, prevention of exposure; prevention of disease by chemoprophylaxis and vaccination; discontinuation of primary prophylaxis after immune reconstitution; treatment of disease; monitoring for adverse effects during treatment; management of treatment failure; prevention of disease recurrence; discontinuation of secondary prophylaxis after immune reconstitution; and special considerations during pregnancy. These guidelines were developed by a panel of specialists from the United States government and academic institutions. For each OI, a small group of specialists with content-matter expertise reviewed the literature for new information since the guidelines were last published; they then proposed revised recommendations at a meeting held at NIH in June 2007. After these presentations and discussion, the revised guidelines were further reviewed by the co-editors; by the Office of AIDS Research, NIH; by specialists at CDC; and by HIVMA of IDSA before final approval and publication. The recommendations are rated by a letter that indicates the strength of the recommendation and a Roman numeral that indicates the quality of evidence supporting the recommendation, so that readers can ascertain how best to apply the recommendations in their practice environments. Major changes in the guidelines include 1) greater emphasis on the importance of antiretroviral therapy for the prevention and treatment of OIs, especially those OIs for which no specific therapy exists; 2) information regarding the diagnosis and management of immune reconstitution inflammatory syndromes; 3) information regarding the use of interferon-gamma release assays for the diagnosis of latent Mycobacterium tuberculosis (TB) infection; 4) updated information concerning drug interactions that affect the use of rifamycin drugs for prevention and treatment of TB; 5) the addition of a section on hepatitis B virus infection; and 6) the addition of malaria to the list of OIs that might be acquired during international travel. This report includes eleven tables pertinent to the prevention and treatment of OIs, a figure that pertains to the diagnois of tuberculosis, a figure that describes immunization recommendations, and an appendix that summarizes recommendations for prevention of exposure to opportunistic pathogens.
This report outlines recommendations for postexposure interventions to prevent infection with hepatitis B virus, hepatitis C virus, or human immunodeficiency virus, and tetanus in persons wounded during bombings or other events resulting in mass casualties. Persons wounded during such events or in conjunction with the resulting emergency response might be exposed to blood, body fluids, or tissue from other injured persons and thus be at risk for bloodborne infections. This report adapts existing general recommendations on the use of immunization and postexposure prophylaxis for tetanus and for occupational and nonoccupational exposures to bloodborne pathogens to the specific situation of a mass-casualty event. Decisions regarding the implementation of prophylaxis are complex, and drawing parallels from existing guidelines is difficult. For any prophylactic intervention to be implemented effectively, guidance must be simple, straightforward, and logistically undemanding. Critical review during development of this guidance was provided by representatives of the National Association of County and City Health Officials, the Council of State and Territorial Epidemiologists, and representatives of the acute injury care, trauma and emergency response medical communities participating in CDC's Terrorism Injuries: Information, Dissemination and Exchange (TIIDE) project. The recommendations contained in this report represent the consensus of U.S. federal public health officials and reflect the experience and input of public health officials at all levels of government and the acute injury response community.
Although coinfection with HIV-1 and hepatitis B virus (HBV) is common, few long-term studies on liver-disease mortality in coinfected people have been undertaken. Our aim was to examine liver-related mortality among people at risk for HIV-1 and HBV infections.
We used data from a multicentre, prospective cohort study to classify 5293 men who had sex with men, according to their HIV-1 antibody status, ascertained semiannually, and their hepatitis-B surface antigen status (HBsAg), which we ascertained at baseline. Mortality rates were estimated in terms of person-years and Poisson regression methods were used to test for significance of relative risks.
326 (6%) men were HBsAg positive, of whom 213 (65%) were HIV-1 positive. Of the 4967 HBsAg negative men, 2346 (47%) were infected with HIV-1. The liver-related mortality rate was 1.1/1000 person years, and was higher in men with HIV-1 and HBsAg (14.2/1000) than in those with only HIV-1 infection (1.7/1000, p<0.001) or only HBsAg (0.8/1000, p<0.001). In coinfected individuals, the liver-related mortality rate was highest with lower nadir CD4+ cell counts and was twice as high after 1996, when highly active antiretroviral therapy (HAART) was introduced.
Individuals coinfected with HIV-1 and HBV, especially those with low CD4+ nadir counts, are at increased risk for liver-related mortality, underscoring the importance of prevention, identification, and comprehensive management of hepatitis B in people infected with HIV-1.
Coinfection with hepatitis B virus (HBV) is common in the human immunodeficiency virus-1 (HIV)-infected patient because of shared modes of transmission. HBV does not appear to alter HIV disease progression; however, HBV infection is more frequent and more severe in the HIV-infected population, emphasizing the importance of preventing HBV infection. The goal of anti-HBV therapy is prevention of cirrhosis because therapy does not eradicate the hepatic reservoirs (cccDNA). The approved therapies-interferon-alfa, lamivudine, and adefovir-each have a niche in the treatment of chronic hepatitis B in the HIV-infected population, but none has been well-studied in this setting. As new drugs currently in clinical trials become available, therapy for chronic hepatitis B will enter the promising era of combination therapy.
To examine the prevalence and incidence of hyperglycemia among HIV-infected patients by hepatitis C virus (HCV) infection and type of highly active antiretroviral therapy (HAART). DESIGN Retrospective cohort analysis of 1230 persons on their first HAART regimen who had at least 1 random glucose measurement before and during antiretroviral therapy.
The prevalence of hyperglycemia and the incidence of hyperglycemia were compared among persons with and without HCV infection while on a protease inhibitor (PI)-containing HAART regimen, a nonnucleoside reverse transcriptase inhibitor (NNRTI)-containing regimen, or a regimen that contained both a PI and an NNRTI. Hyperglycemia was defined as either 2 random glucose levels > 11.1 mM (200 mg/dL) or documentation of the diagnosis of diabetes in the medical record.
The prevalence of hyperglycemia was significantly higher in HCV-coinfected (5.9%) than HCV-uninfected persons (3.3%, P = 0.02). Among persons receiving HAART, both HCV coinfection (adjusted relative hazard [ARH], 2.28; 95% CI, 1.23-4.22) and PI use (ARH, 5.02; 95% CI, 1.39-18.16) were independent risk factors of developing hyperglycemia. The incidence of hyperglycemia was highest among HCV-coinfected persons receiving a PI (5.6 cases per 100-person years) and only 1 person who was neither HCV-infected nor receiving a PI developed hyperglycemia.
In this urban HIV cohort, the risk of hyperglycemia was increased in HCV-coinfected patients and those prescribed a PI.
To determine whether hepatitis C virus (HCV) infection status affected hospitalization rates, intensive care utilization rates, and discharge diagnoses between 1995 and 2000 in patients with HIV.
We conducted a prospective cohort study of 3730 HIV patients who were longitudinally followed between 1995 and 2000. All hospitalizations of these patients were classified as an opportunistic illness (OI) using the 1993 indicator diagnoses in the case definition of AIDS, complication of injection drug use (IDU) (abscess, cellulitis, osteomyelitis, bacteremia, endocarditis, and poisoning by analgesics), liver-related complication (acute and subacute necrosis of the liver, chronic liver disease and cirrhosis, liver abscess, hepatic coma, portal hypertension, hepatorenal syndrome, hepatocellular carcinoma, and gastrointestinal bleed), or other. Negative binomial regression was used to assess for risk factors for hospitalization.
Inpatient hospitalization and intensive care utilization rates and discharge diagnoses.
Nearly half (42.8%) of our cohort was infected with HCV. Between 1995 and 2000, hospitalization rates for HCV-negative patients decreased from 61.9 to 33.9 per 100 patient-years (PY) of follow-up (P = 0.007). Hospitalization rates decreased between 1995 and 1997 for HCV-positive patients from 55.4 to 43.5 per 100 PY but increased between 1997 and 2000 from 43.5 to 62.9 per 100 PY (P = 0.001). When stratified by diagnostic category, IDU-related complications increased from 13.6 to 18.4 admissions per 100 PY and liver-related complications increased from 5.4 to 26.7 admissions per 100 PY between 1995 and 2000 in HCV-positive patients (P < 0.001); however, OIs remained relatively unchanged from 1995 to 2000, with 14.6 to 13.0 hospitalizations per 100 PY. In multivariate analysis, HCV infection (incidence rate ratio [IRR] = 1.75, 95% confidence interval [CI]: 1.47, 2.07), female gender (IRR = 1.56, 95% CI: 1.32, 1.85), age <37 years (IRR = 1.19, 95% CI: 1.01, 1.41), African American ethnicity (IRR = 1.30, 95% CI: 1.05, 1.61), and CD4 cell count <50 cells mm3 (IRR = 2.20, 95% CI: 1.72, 2.83) were predictive of hospitalization.
Our data indicate that hospitalization rates decreased significantly between 1995 and 2000 for HCV-negative patients but increased significantly for HCV-positive patients. Hospitalization rates for IDU- and liver-related complications increased during this time interval in coinfected patients. In the era of highly active antiretroviral therapy, HIV/HCV-coinfected patients are more likely to suffer from higher hospitalization rates, which will require more health care resources.
Chronic hepatitis B and C represent a leading cause of morbidity and mortality among human immunodeficiency virus (HIV)-infected patients worldwide. New treatment options against both hepatitis B (HBV) and C (HCV) viruses have prompted us to update previous recommendations for the management of coinfected individuals. Fifteen topics (nine related to HCV, five to HBV and one to both viruses) were selected for this purpose. A panel of Spanish experts in the field was invited to review these areas and propose specific recommendations, which were scored according to the Infectious Disease Society of America (IDSA) grading system. These guidelines represent a comprehensive and updated overview on the management of hepatitis B and C in HIV-infected patients.