jules levin, NATAP: research notes on HIV/AIDS, viral hep, HCV & bone density studies (039)


richardkearns.awo.shadow-light-moi-0309091540from Jules: 60% with HIV have osteopenia, 15% osteoporosis, at the average ages of 45. Fracture rates likely to be increased for HIV+ vs HIV- as patients age. Bone loss can contribute to frailty and mortality.

“BMD [bone mineral density —rk] is a predictor of both fragility fractures [15] and all-cause mortality”

“We found that viral hepatitis increased the risk of low BMD among HIV-infected patients. Future studies should evaluate fracture rates and examine risk factors and potential mechanisms for low bone mass among HIV/viral hepatitis-coinfected patients.”

“Regardless of sex, coinfected patients had lower intact PTH concentrations but similar 25-hydroxyvitamin D and octeocalcin levels compared with patients with HIV alone.”

from Jules: The literature is full of studies finding HCV is associated with bone loss so it’s reasonable that coinfected patients might have more bone loss than HIV-negative individuals. There is every reason to think that BMD in HIV+ men is as serious if not more serious in men than women. In this study perhaps menopause played a role. Several studies suggest that HIV+ men have perhaps more of a problem with bone loss than HIV+ women, the reasons are unclear but lipoatrophy and lifestyle may play a role. The finding in this study was after they adjusted for BMI, of course, because men suffer more with lipoatrophy in HIV than women and have other risk factors.

“Among viral hepatitismonoinfected patients, the prevalence of reduced lumbar or femoral BMD, or both has been reported to range from 10 to 56% [8,24–28]. However, these studies are difficult to interpret given their small sample sizes, inclusion of predominantly male patients, and use of different BMD outcomes.”

“Men also had lower mean Z-scores at the femoral neck than women”

Differences in lumbar spine bone mineral density Z-scores

Overall, men had lower mean Z-scores at the lumbar spine than women [ 0.50 versus +0.06; difference= – 0.56 (95% CI – 0.42 to – 0.69); P<0.001]. However, viral hepatitis-coinfected women had significantly lower mean lumbar spine Z-scores compared with HIVmonoinfected women [ 0.15 versus +0.29; difference= – 0.44 (95% CI 0.65 to – 0.23); P<0.001]. After adjustment for age, BMI, duration of HIV infection, use of ART, physical activity, and smoking, deficits in lumbar BMD remained greater among coinfected women [difference1/4 0.51 (95% CI 0.75 to -0.27); P<0.001; Table 2]. In contrast, coinfected men had similar mean Z-scores at the lumbar spine compared with monoinfected men [- 0.52 versus – 0.47; difference= – 0.05 (95% CI 0.22 to +0.12); P1/40.5]. Adjustment for confounders (Table 2) yielded little change in the difference in lumbar BMD between these two groups [difference1/4 0.12 (95% CI – 0.32 to +0.08); P1/40.2]. When we performed adjusted analyses excluding HBsAgpositive patients, mean lumbar Z-scores remained lower in HCV-coinfected compared with HIV-monoinfected women [ 1.31 versus – 0.82; difference1/4 0.49 (95% CI – 0.74 to – 0.25); P<0.001] but not between coinfected and monoinfected men [ 1.24 versus 1.14; difference1/4 0.10 (95% CI – 0.32 to – 0.12); P1/40.4].

Viral hepatitis is associated with reduced bone mineral density in HIV-infected women but not men — see attached pdf

published ahead of print



Lo Re, Vincent III; Guaraldi, Giovanni; Leonard, Mary B; Localio, Anthony R; Lin, Jennifer; Orlando, Gabriella; Zirilli, Lucia; Rochira, Vincenzo; Kostman, Jay R; Tebas, Pablo


Objective: Few studies have examined the impact of viral hepatitis on bone mineral density (BMD), and none have done so among HIV-infected patients. Our objective was to determine whether viral hepatitis was associated with low BMD in HIV.

Design: A cross-sectional study among 1237 HIV-infected patients (625 with viral hepatitis).

Methods: Dual-energy X-ray absorptiometry scans of the lumbar spine and femoral neck were obtained. Clinical data, hepatitis B and C status, and markers of bone metabolism were determined at dual-energy X-ray absorptiometry scanning. Multivariable logistic regression examined the association between hepatitis and low BMD (Z-score <=-2.0 at the lumbar spine, femoral neck, or both).

Results: Mean BMD Z-scores were lower among hepatitis-coinfected women at the lumbar spine {-0.15 versus +0.29; difference = -0.44 [95% confidence Interval (CI) -0.65 to -0.23]; P < 0.001} and femoral neck [-0.64 versus -0.39; difference = -0.25 (95% CI -0.44 to -0.06); P = 0.009] compared with HIV-monoinfected women. No differences in mean BMD Z-scores were observed between coinfected and monoinfected men. After adjustment for age, BMI, duration of HIV, antiretroviral use, physical activity, and smoking, viral hepatitis was associated with low BMD among women (adjusted odds ratio 2.87, 95% CI 1.31-6.29) but not men (adjusted odds ratio 1.19, 95% CI 0.74-1.91). Coinfected women had lower mean parathyroid hormone (60.1 versus 68.1 pg/ml; P = 0.02) but similar mean 25-hydroxyvitamin D (19.1 versus 19.6 ng/ml; P = 0.6) and osteocalcin (3.0 versus 3.2 ng/ml; P = 0.8) concentrations than HIV-monoinfected women.

Conclusion: Viral hepatitis was associated with a higher risk of low BMD among HIV-infected women but not men.


Although advances in antiretroviral therapy (ART) have led to a substantial decline in AIDS-related opportunistic infections and increased longevity of HIV-infected patients, complications of chronic viral hepatitis have now emerged as a major cause of morbidity in the HIV population [1]. Existing studies among HIV-infected patients have mainly examined the impact of viral hepatitis coinfection on liver-related complications (e.g., cirrhosis, end-stage liver disease, and hepatocellular carcinoma) [2–4], but the effect of viral hepatitis on nonhepatic outcomes, in particular abnormalities in bone mineral density (BMD) and bone metabolism (termed ‘hepatic osteodystrophy’), remains unclear. Viral hepatitis has been associated with reduced BMD among HIV-uninfected individuals [5,6], and a number of factors related to chronic viral hepatitis have been hypothesized to contribute to low BMD (Fig. 1). Prior studies have suggested that elevated serum levels of cytokines associated with viral hepatitis [e.g., tumor necrosis factor-a, interleukin (IL)-1, and IL-6] could inhibit bone formation and increase bone resorption, leading to low BMD [7,8]. In addition, progressive hepatitis-induced liver dysfunction may be associated with reduced hepatic hydroxylation of vitamin D [9], hypogonadism [10], and impaired hepatic production of insulin-like growth factor-1 and osteoprotegerin, both of which promote bone formation [6], and these conditions can also contribute to low BMD. Moreover, HIV itself is associated with reduced BMD and increased fracture risk [11–13]. However, to date, no study has yet examined whether viral hepatitis is an independent risk factor for low BMD in HIV. Evaluating the association between viral hepatitis and low BMD in HIV-infected patients is important because viral hepatitis is prevalent in HIV [14] and low BMD is a predictor of both fragility fractures [15] and all-cause mortality [16,17]. We therefore examined whether viral hepatitis coinfection was associated with reduced BMD among HIV-infected patients.

bone density chart

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