Validation of Noninvasive Methods for Detecting Hepatic Steatosis in Patients With Human Immunodeficiency Virus Infection

Siddiqui, Mohammad Shadab; Patidar, Kavish R.; Boyett, Sherry; Smith, Paula G.; Sanyal, Arun J.; Sterling, Richard K.

doi:10.1016/j.cgh.2014.06.027

Cited by 16 publications

(14 citation statements)

References 13 publications

(19 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were significantly higher in LTRs versus both lean and obese controls ( P < 0.001). The liver fat scores for the lean and obese controls were −2.31 and −1.33, respectively, and this made the presence of undiagnosed fatty liver disease in the control groups unlikely . A majority of the LTR cohort consisted of Caucasians (75.8%) and African Americans (17.4%), whereas other ethnicities accounted for the remaining 6.8% of the cohort.…”

Section: Resultsmentioning

confidence: 99%

“…The liver fat scores for the lean and obese controls were 22.31 and 21.33, respectively, and this made the presence of undiagnosed fatty liver disease in the control groups unlikely. 14,15 A majority of the LTR cohort consisted of Caucasians (75.8%) and African Americans (17.4%), whereas other ethnicities accounted for the remaining 6.8% of the cohort. The mean follow-up after LT was 68 6 60 weeks, with a median of 48 weeks and a range of 6 to 264 weeks.…”

Section: Resultsmentioning

confidence: 99%

“…The control groups had blood work done as part of their annual wellness visits, and both control groups had normal serum alanine aminotransferase (ALT) levels (<19 IU/L for women and <31 IU/L for men). The control groups did not have any known chronic medical or liver disease, and underlying nonalcoholic fatty liver disease was ruled out via the liver fat score, which is a well‐validated marker of hepatic steatosis . Additionally, any control subjects who met the criteria for either diabetes (on the basis of fasting serum glucose or HbA1C) or dyslipidemia (on the basis of fasting serum HDL, LDL, total cholesterol, and TGs) were excluded.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Evolution of serum atherogenic risk in liver transplant recipients: Role of lipoproteins and metabolic and inflammatory markers

Chhatrala

Siddiqui²,

Stravitz

et al. 2015

Liver Transpl

Self Cite

View full text Add to dashboard Cite

Although cardiovascular disease (CVD) is the leading cause of long-term mortality in liver transplant recipients (LTRs), the role of recently identified biomarkers of CVD risk in liver transplantation is unknown. We aimed to evaluate an extensive CVD risk profile in LTRs. Markers of CVD risk in 65 LTRs with no known history of diabetes mellitus (DM), dyslipidemia, or ischemic heart disease were compared to age-, sex-, and body mass index (BMI)-matched controls with no chronic medical disease. LTRs on corticosteroids or those with graft cirrhosis (GC) were excluded. The effect of calcineurin inhibitors on the CVD risk profile was separately analyzed in LTRs receiving either tacrolimus (Tac) or cyclosporine A (CsA). To evaluate the impact of GC, a comparison was made between LTRs with and without GC. Non-DM LTRs were matched to controls with respect to age, sex, and BMI. LTRs had similar serum high-density lipoprotein-cholesterol (HDL-C), low-density lipoproteincholesterol (LDL-C), and total cholesterol in comparison with BMI-matched controls. Proatherogenic small-dense (sd) LDL-C (33.6 6 14 versus 25.9 6 9.9 mg/dL; P < 0.001) and %sdLDL-C (30% 6 10% versus 26.4% 6 9%; P 5 0.02) were significantly higher in LTRs. In comparison with controls, LTRs had higher apolipoprotein B (apoB; 98 6 37 versus 88 6 24 mg/dL; P < 0.01), very low density lipoprotein-particle concentration (VLDL-P; 7.7 6 6.7 nmol/L versus 3.2 6 9.1 nmol/L; P < 0.001), and VLDL size (51.1 6 6.6 versus 46.5 6 6.9 nm; P < 0.001). In LTRs, VLDL size and VLDL-P were directly related to serum CsA levels (r 5 0.53, P 5 0.09, and r 5 0.63, P < 0.01, respectively) but not to Tac levels. In comparison with controls, LTRs had significantly lower total serum high-density lipoprotein-particle concentration. In comparison with those with preserved graft function, LTRs with GC had lower levels of serum atherogenic markers characterized by low sdLDL-C, apoB, triglycerides, LDL-C, and total cholesterol. In conclusion, LTRs have a proatherogenic lipoprotein profile that is not captured with a traditional lipid panel, and this suggests that a detailed serum atherogenic profile is needed to truly assess CVD risk in LTRs. Liver Transpl 21:623-630, 2015. V C 2015 AASLD. Received November 20, 2014 accepted January 28, 2015. Improvements in the medical and surgical care of liver transplant recipients (LTRs) have increased long-term survival rates and have shifted the causes of mortality from surgical and infectious complications to cardiovascular disease (CVD). 1,2 In comparison with an ageand sex-matched general population, LTRs have a much higher rate of cardiovascular events, which ranges from 9% at 5 years to 25% at 10 years after transplant. [3][4][5] The increased CVD mortality is likely multifactorial and results from a combination of

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Evolution of serum atherogenic risk in liver transplant recipients: Role of lipoproteins and metabolic and inflammatory markers

Chhatrala

Siddiqui²,

Stravitz

et al. 2015

Liver Transpl

Self Cite

View full text Add to dashboard Cite

show abstract

“…The control group consisted of subjects with no known liver disease and normal serum aminotransferase levels (AST/ALT < 19 IU/L in women and <30 IU/L in men) (23). In controls, the presence of underlying hepatic steatosis was additionally ruled out via use of liver fat score, which now has been further validated as a robust marker of detecting NAFLD even when compared to those with HCV (24, 25). Subjects with known diagnosis of diabetes, fasting blood sugar of >100 mg/dL, use of oral hypoglycemic agents or insulin were excluded from the study.…”

Section: Methodsmentioning

confidence: 99%

Nonalcoholic Steatohepatitis (NASH) Is Associated with a Decline in Pancreatic Beta Cell (β-Cell) Function

et al. 2015

Self Cite

View full text Add to dashboard Cite

Background Nonalcoholic fatty liver disease (NAFLD) is a common cause of abnormal liver tests in the U.S. population. NAFLD represents a histological spectrum ranging from benign hepatic steatosis (NAFL) to nonalcoholic steatohepatitis (NASH). NAFLD is closely associated with features of metabolic syndrome, particularly insulin resistance (IR). Although the role of IR in NAFL and NASH has been an area of intense investigation, there is limited evaluation of pancreatic β-cell in NASH, particularly in the United States. Aim The aim of the current study was to evaluate the status of pancreatic β-cell function in NAFLD using the homeostatic model assessment-β (HOMA-β) and β-cell index (BI). Method HOMA-β was measured in ninety-nine non-diabetic subjects with histologically confirmed NAFLD and compared to lean (age and gender matched) and obese (age-, gender-, and BMI-matched) controls. Using the values from an oral glucose tolerance test β-cell index (BI) was compared in 31 subjects with non-diabetic, non-cirrhotic subjects with NASH and gender- and BMI matched controls. Results The subjects with NAFLD had higher HOMA- β compared to both lean and obese controls (43.1% vs. 9% vs. 22.1, respectively, P<.05). HOMA-β was directly related to serum alkaline phosphate, total bilirubin, weight and inversely to age. There was no difference in HOMA-β between subjects with NAFL and NASH. Subjects with NASH had lower pancreatic β-cell function as measured by a lower BI (2.09±1.64 vs. 7.74±25.12; P = .04). In patients with NASH, BI was inversely associated with fibrosis independent of age, BMI, and serum ALT levels. In contrast, HOMA-β was directly associated with fibrosis stage. Conclusion NASH is associated with strained pancreatic β-cell function in non-diabetic subjects. Future studies are necessary to evaluate the temporal relationship between β-cell function and hepatic histology.

show abstract

“…liver fat score (LFS) and lipid accumulation product (LAP), which have been assessed in HIV patients. 72 Management HIV patients have comorbidities including DM (diabetes mellitus) and obesity, and similar to the rest of the US population, they are increasing in prevalence. 73,74 At present, there are no therapeutic interventions to treat NASH that have been studied in the HIV-infected patient.…”

Section: Box 1 Pathogenesis Of Nafld In Hivmentioning

confidence: 99%

Chronic Liver Disease in the Human Immunodeficiency Virus Patient

Acharya

Dharel

Sterling

2015

Clinics in Liver Disease

Self Cite

View full text Add to dashboard Cite

Validation of Noninvasive Methods for Detecting Hepatic Steatosis in Patients With Human Immunodeficiency Virus Infection

Cited by 16 publications

References 13 publications

Evolution of serum atherogenic risk in liver transplant recipients: Role of lipoproteins and metabolic and inflammatory markers

Evolution of serum atherogenic risk in liver transplant recipients: Role of lipoproteins and metabolic and inflammatory markers

Nonalcoholic Steatohepatitis (NASH) Is Associated with a Decline in Pancreatic Beta Cell (β-Cell) Function

Chronic Liver Disease in the Human Immunodeficiency Virus Patient

Contact Info

Product

Resources

About