Purpose To estimate the incidence of herpes zoster (HZ) and rates of post-zoster pain in both the total study population and separately in patients with selected conditions/treatments associated with altered immune function.MethodsThe health administrative claims databases for commercially insured, Medicare, and Medicaid populations, together accounting for approximately 51 million insured individuals, were analyzed between 2005 and 2009 in a retrospective cohort study. Incidence of HZ episodes per 1,000 person-years (PY) was estimated in all study populations as well as within nine potentially immune-altering conditions. Among patients with HZ, the 6-month rate of persistent post-zoster pain was estimated.ResultsAnalysis of 90.2 million PY at risk revealed that the incidence of HZ in the total study population was 4.82/1,000 PY. The incidence of HZ was highest among patients with bone marrow or stem cell transplant (43.03 %) followed by solid organ transplant, human immunodeficiency virus infection, and systemic lupus erythematosus [95 % confidence interval (CI) 15.19–17.41 %]. HZ incidence rates were higher among persons on immunosuppressants/chemotherapy than among non-users. In the total study population, HZ incidence increased with age (18–49 years: 3.37/1,000 PY; 65+ years: 8.43/1,000 PY; P < 0.01) and female gender (incidence ratio vs. male 1.39, 95 % CI 1.38–1.40 %). The 6-month rate of persistent post-zoster pain was 4.29 % (95 % CI 4.22–4.36 %), which was higher in patients with the selected conditions.ConclusionsDespite providing a relatively small fraction of overall HZ cases, persons with immune function-altering conditions make a large contribution to the societal healthcare burden because they have a higher risk of developing HZ and persistent post-zoster pain. These risk factors should be considered in HZ prevention efforts.

Compared with patients with normal renal function, patients with renal impairment were older, shorter, weighed less, had been postmenopausal longer, and had lower baseline lumbar spine and femoral neck BMD. Compared with placebo, teriparatide significantly increased PINP and lumbar spine and femoral neck BMD within each renal function subgroup, and there was no evidence that these increases were altered by renal insufficiency (each treatment-by-subgroup interaction p>0.05). Similarly, teriparatide-mediated vertebral and nonvertebral fracture risk reductions were similar and did not differ significantly between patients with normal or impaired renal function (treatment-by-subgroup interactions p>0.05). The incidences of treatment-emergent and renal-related adverse events were consistent across treatment assignment in the normal, mildly impaired, and moderately impaired renal function subgroups. Teriparatide induced changes in mean GFR were unaffected by baseline renal function (treatment-by-renal function interaction p>0.05 for normal, mildly impaired, or moderately impaired subgroups). Patients in all renal function categories treated with teriparatide 20 or 40 mcg had an increased incidence of 4-6-h postdose serum calcium >10.6 mg/dl (the upper limit of normal) versus placebo; however, teriparatide 20 mcg/day was not associated with significantly increased incidence of 4-6-h postdose serum calcium >11 mg/dl in any renal function category. Teriparatide therapy was associated with increased incidence of elevated uric acid, with the incidences being highest in patients with moderately impaired renal function and in those receiving teriparatide 40 mcg/day. Even so, adverse event data did not suggest an increased incidence of gout or arthralgia or of nephrolithiasis events in teriparatide-treated patients with normal, mild, or moderate renal impairment.

These findings indicate that at any given BMD T-score, the risk of incident vertebral, non-vertebral, and any fracture depended heavily on prevalent radiographic vertebral fracture status. Assessment of vertebral fracture status, in addition to BMD, provides practical and relevant clinical information to aid in predicting fracture risk in postmenopausal women.

A majority of childhood bacterial meningitis survivors with long-term sequelae that are documented in the literature have academic and behavioral limitations. While neurologic deficits may resolve over time, subtle behavioral deficits may not be appreciated initially and may continue to affect survivors for many years. Further studies are needed to quantify the true societal and economic burden of long-term sequelae as well as fully understand the breadth of types of sequelae that survivors experience.

Increases in lumbar spine BMD account for 30-41% of the vertebral fracture risk reduction with teriparatide treatment. The remaining fracture risk reduction is caused by improvements in non-BMD determinants of bone strength.Introduction: Changes in BMD account for a small percentage of the fracture risk reduction seen in patients treated with antiresorptive drugs. The relationship between changes in lumbar spine BMD and vertebral fracture risk reduction with teriparatide treatment has not been assessed. Materials and Methods:The relationship between spine BMD and the risk of new vertebral fractures after teriparatide treatment was assessed using data from the Fracture Prevention Trial. Postmenopausal women with osteoporosis (n ‫ס‬ 1637) were randomized to placebo or teriparatide 20 or 40 g/day for a median of 19 months. Spine BMD was assessed at baseline and 18 months. Vertebrae whose fracture status changed during the trial were removed from the calculation of BMD. Baseline and endpoint lateral spine radiographs were assessed using a visual semiquantitative technique. Results: Both the baseline and change in spine BMD were contributors to vertebral fracture risk. The mean spine BMD increase in teriparatide-treated patients was 0.09 g/cm 2 across tertiles of baseline spine BMD. Compared with placebo, teriparatide significantly reduced the risk of new vertebral fracture for all endpoint BMD values. Teriparatide-mediated increases in spine BMD accounted for 30% (in the low baseline spine BMD tertile) to 41% (in the high baseline spine BMD tertile) of the reduction in vertebral fracture risk. Conclusions: Increases in BMD account for approximately one third of the vertebral fracture risk reduction seen with teriparatide. The majority of the risk reduction, however, results from improvements in non-BMD determinants of bone strength.