These results indicate that GH attenuates the decrease in muscle strength and bone mass as well as the gain of abdominal fat with ageing in elderly women. The present data provide useful information about the application of GH treatment in elderly women.
Although there is clinical evidence showing that combined therapy with parathyroid hormone (PTH) and estrogen is additively effective in increasing the bone mass of patients with osteoporosis, the mechanism of the interaction between these hormones remains unclear. The present study was performed to determine whether estrogen would affect osteoblast proliferation and function modulated by PTH in human osteoblastic SaOS-2 cells. Human PTH-(1-34) significantly inhibited [3 H]thymidine (TdR) incorporation, which was attenuated by 24 h pretreatment with 10 10 to 10 7 M 17 -estradiol (17 -E 2 ) in a concentration-dependent manner. PTH significantly stimulated alkaline phosphatase (ALP) activity, collagen synthesis and type-1 procollagen mRNA expression after pretreatment with 17 -E 2 in these cells. Tamoxifen, an anti-estrogen, antagonized these 17 -E 2 -induced effects. Pretreatment with insulin-like growth factor-I (IGF-I) mimicked estrogen action, and coincubation of 3 µg/ml anti-IGF-I antibody antagonized the effects of 17 -E 2 as well as those of IGF-I. In the presence of 17 -E 2 pretreatment, PTH strongly stimulated IGF-binding protein (IGFBP)-5 mRNA expression in these cells, and recombinant IGFBP-5 increased type-1 procollagen mRNA expression and ALP activity. In conclusion, estrogen attenuates PTH-induced inhibition of osteoblast proliferation and PTH stimulates osteoblast function in the presence of estrogen pretreatment. IGF-I and/or IGFBP-5 seemed to be involved in the estrogen-induced modulation of PTH action on osteoblast proliferation and function.
The present study was performed to examine the effect of natural menopause on serum levels of IGF-I, IGF-binding protein (IGFBP)-2 and -3 as well as on bone mass and lipid metabolism in perimenopausal women. One hundred and twenty-one healthy Japanese women, who were 45-55 years old, were studied (71 premenopausal and 50 postmenopausal women 1-9 years after menopause). Bone mineral density (BMD) was measured at the middle third of the radius by using dual energy X-ray absorptiometry. Serum levels of IGF-I, but not those of IGFBP-2 or -3, were significantly reduced in the postmenopausal group compared with the premenopausal group. One year after menopause, serum IGF-I levels were significantly lower, and the biochemical markers of bone turnover, such as serum total alkaline phosphatase level and urinary calcium to creatinine ratio, were significantly higher than the premenopausal levels. Serum levels of IGF-I, but not those of IGFBP-2 or -3, were positively correlated with BMD. Serum levels of IGFBP-2, but not those of IGF-I or IGFBP-3, were negatively correlated with body mass index and body weight. Finally, serum levels of IGFBP-3, but not those of IGF-I, were positively correlated with serum levels of total cholesterol and triglyceride. The present findings suggest that a rapid decrease in serum IGF-I levels after menopause might be partly involved in bone loss following gonadal failure and that IGFBP-2 and -3 might be related to the regulation of body mass and lipid metabolism during perimenopause respectively, although the mechanisms remain unknown.
Cytomegalovirus (CMV)-associated gastric ulcers can be found not only in immunocompromised hosts but also in normal individuals. The accurate endoscopic diagnosis of CMV ulcers is not easy because of the absence of characteristic morphological features. We present a case of CMV-associated gastric ulcer in an immunocompetent patient. He was a 33-year-old male with epigastralgia. Upper gastrointestinal endoscopy showed multiple erupted papules and a large irregularly shaped shallow ulcer. We did not find intracellular inclusion bodies characteristic of CMV in hematoxylin-eosin-stained gastric biopsy specimens, while CMV antigens corresponding to intracellular inclusion bodies were confirmed using an immunoperoxidase method with the monoclonal CMV antibody. If CMV ulcers are suspected, it is important to examine for inclusion bodies using not only hematoxylin-eosin staining, but also CMV immunohistochemistry for a sensitive diagnosis.
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