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Elevated PTH concentrations are associated with a five-year cognitive decline in a general aged population, independently of Ca2+ and renal function. The role of vitamin D deficiency, the most common cause of elevated PTH in the elderly, needs to be further investigated.

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Objective: Short-term studies on selected patients have indicated that elevated serum parathyroid hormone (PTH) is an independent risk factor of death. However, long-term data on unselected populations are lacking, thus far. In order to evaluate the predictive value of elevated serum PTH during the last years of life, random persons of age cohorts of 75, 80 and 85 years were followed for 17 years. Design: A prospective cohort study. Methods: Subjects (nZ567) were investigated for calcaemic status including serum intact PTH, serum total calcium (CaT) and ionized calcium (Ca 2C ). Thorough clinical examinations included an assessment of co-morbidity. Mortality data were collected from National Census Records. Results: Up to 93% of the subjects died within the follow-up. In contrast to Ca 2C levels, high serum PTH (R63 ng/l, IV quartile cut point) was associated with significant over-mortality (HRZ1.56, 95% CI: 1.29-1.88) and a 2.3-year reduction of median life expectancy. After controlling for age, gender, co-morbidity and creatinine, the prognostic impact of elevated serum PTH was still significant (HRZ 1.24, 95% CI: 1.01-1.53). The tendency for over-mortality was consistent in both genders, in all age groups as well as in subjects with varying co-morbidity, renal function, body mass index categories and Ca 2C levels. Conclusions: Elevated serum PTH level is an independent predictor of impaired long-term survival prognosis in unselected aged population. Serum Ca 2C did not emerge as a significant prognostic indicator. The long-term prognostic impact of vitamin D deficiency, the most common cause of elevated PTH levels in the elderly, remains to be investigated. European Journal of Endocrinology 158 749-753

Background: The concentration of N-terminal propeptide of type I procollagen (PINP) in the serum reflects the rate of type I collagen formation. Intact PINP assay measures the trimeric propeptide while total P1NP assay measures both trimeric and monomeric forms. In this study we compared these two assays emphasizing the possible differences. Methods: Intact and total PINP were measured from serum in healthy Finnish blood donors (n ¼ 34) and in the patients with chronic renal failure before and after haemodialysis (n ¼ 39). In addition, the serum of a normal man, pooled hospital serum samples and the serum of a patient with haemodialysis treatment were fractioned by gel filtration and trimeric and monomeric forms were located. Fractions were lyophilized and intact and total PINP were measured in each fraction. Samples from bedridden geriatric patients (n ¼ 173) were also measured using intact and total PINP assays and a degradation marker of type I collagen (ICTP). Results: The correlation between intact and total PINP in controls was 0.89 and their PINP concentrations were similar. In haemodialysis or bedridden geriatric patients, the PINP methods gave significantly different results. In gel filtration studies, intact PINP hardly measured monomeric form even if its concentration was disproportionately increased in haemodialysis patients. In bedridden geriatric patients, the difference of total and intact PINP correlated significantly to degradation marker ICTP. Conclusions: Difference between total and intact assays for PINP seem to reflect degradation of pN-collagen rather than denaturation of intact propeptide.