PubMed Health⌕ Search

Biomedical subjects

Y Weisman

Publications and source records attributed to Y Weisman.

At least 73 records · Page 4Linked to original sources
PubMed1993

Sex-specific response of bone cells to gonadal steroids: modulation in perinatally androgenized females and in testicular feminized male rats.

We have found previously that rat diaphyseal bone in vivo, as well as rat embryo calvaria cells in culture, show a sex-specific response to gonadal steroids in stimulation of creatine kinase (CK)-specific activity, and the rate of [3H]thymidine incorporation into DNA; male-derived cells responded only to testosterone or to dihydrotestosterone (DHT), whereas female-derived cells were stimulated exclusively by estradiol (E2). In this study, we tested whether developmental hormone manipulation could alter this sex specificity. We showed that diaphyseal bone of prenatally or neonatally androgenized female rats responds to a single injection of either E2 (5 micrograms/rat) or DHT (50 micrograms/rat) at 3-4 weeks postandrogenization. This response of androgenized female diaphyseal bone to androgen gradually declines; 3 months posttreatment, diaphyseal bone no longer responds to DHT and reverts to its original sex specificity. Rat embryo calvaria cell cultures prepared from female fetuses androgenized in utero showed the same lack of hormonal specificity, that is, the cells responded to both E2 (30 nM) or DHT (300 nM). Cells derived from the male siblings of the prenatally androgenized rats were not affected and responded only to DHT. In contrast to experiments in utero, in vitro administration of testosterone (1 microM) or E2 (1 microM) to calvaria cells from female embryos failed to cause the cells to respond to DHT. Androgen receptor-deficient (Tfm) male rats, which have approximately 10% of the normal response to androgens, also showed a response to both testosterone and E2 in comparison to their normal male siblings, whose bones responded only to androgens.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgen-Insensitivity Syndrome↗
PubMed1993

Decreased bone density in elderly men treated with the gonadotropin-releasing hormone agonist decapeptyl (D-Trp6-GnRH).

Administration of GnRH agonist analogs to women may result in a hypoestrogenic state and bone mass reduction. In the present study we examined bone mineral density (BMD) and parameters of mineral metabolism in elderly men with benign prostatic hyperplasia before and during a hypoandrogenic state induced by the long-acting GnRH agonist D-Trp6-LHRH (decapeptyl). Our results showed that decapeptyl treatment caused a significant decrease in serum testosterone concentrations in all patients and resulted in a significant decrease in individual vertebral BMD in 10 of 17 patients. A significant decrease in BMD was observed in 5 patients after 6 months of treatment. Another 5 patients showed a decreased BMD only after 12 months. The mean serum concentrations of osteocalcin, phosphorus, and alkaline phosphatase activity increased after 6-12 months of treatment with decapeptyl. Serum calcium, vitamin D metabolites, and PTH concentrations remained unchanged during treatment. Urinary calcium excretion was slightly, but not significantly, increased after 6 months of treatment. These results demonstrate that long-acting GnRH agonist treatment may cause high turnover accelerated bone loss in some men during the first year of GnRH agonist treatment, as has been previously shown in women.

Aged↗
PubMed1993

Effect of 1,25-dihydroxyvitamin D3 on interleukin 1 beta actions and cell growth in human synovial fibroblast cultures.

OBJECTIVE: To investigate the effects of vitamin D3 [1,25-(OH)2D3] metabolites on interleukin 1 beta (IL-1 beta) stimulated secretory activities and on the proliferation of human synovial fibroblasts in culture. METHODS: Dose dependent effects on IL-1 beta actions were determined in nonproliferating cultures containing 1% fetal calf serum (FCS) in the culture medium. Production of prostaglandin E (PGE), collagenase and hyaluronic acid (HA) was measured respectively by radioimmunoassay, enzymatic degradation of radiolabelled collagen gels after collagenase activation and 14C-glucosamine incorporation. Effects on cell growth in 10% FCS were monitored colorimetrically, by staining cells with crystal violet. RESULTS: 1,25-(OH)2D3 inhibited the effects of IL-1 beta on PGE production by up to 90%, with half maximal inhibition at 2.0 x 10(-10) M. Inhibitory effects on stimulated collagenase and HA production and cell growth were also found but were less marked. At 10(-7) M 1,25-(OH)2D3 inhibition was 50, 21 and 50%, respectively. 24,25-dihydroxyvitamin D3 was a less potent inhibitor than 1,25-(OH)2D3. Neither metabolite influenced IL-1 beta effects on PGE or sulfated glycosaminoglycan production in human articular cartilage in tissue culture. CONCLUSION: Our results suggest that the active metabolites of vitamin D3 may modulate the behavior of synovial fibroblasts in articular inflammatory processes.

24,25-Dihydroxyvitamin D 3↗
PubMed1992

Polymerase chain reaction for differentiation between pathogenic and non-pathogenic serotype 1 Marek's disease viruses (MDV) and vaccine viruses of MDV-serotypes 2 and 3.

A polymerase chain reaction (PCR) test based on primers flanking the 132 bp tandem repeat in pathogenic MDV-1 DNA was developed. These primers amplify a dimer or a trimer 132 bp repeat in pathogenic MDV-1 DNA from blood and organs of commercial chickens with Marek's disease (MD) symptoms. Using the same primers in a radioactive PCR test, it was possible to distinguish between vvMDV-1 and the non-pathogenic MDV-1 CVI-988 vaccine in which the 132 bp repeats in the DNA were increased up to 9 repeats. The MDV-1 specific primers did not amplify MDV-2 (SB1) and MDV-3 (HVT) DNA. Primers prepared according to the nucleotide sequence of MDV-1 antigen A gene amplified MDV-1 DNA only. Specific primers prepared according to the nucleotide sequence of MDV-3 (HVT) antigen A gene amplified MDV-3 DNA but not MDV-1 nor MDV-2 DNA. The results of the present study show that the PCR tests can be used for the early identification of vvMDV-1 DNA in pathological samples from diseased commercial chickens and to distinguish between the vvMDV-1 and the three types of virus vaccines used to immunize chickens. The tests are accurate and can be performed in the presence of vaccine virus DNA in the sample.

Animals↗
PubMed1992

Effect of iron on serum 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D concentrations.

In 13 of 17 infants (aged 10.5 +/- 4.3; mean +/- SD mo) with iron-deficiency anemia, the serum 24,25-dihydroxyvitamin D concentration was below the normal range and in 9 of these 13 the serum 25-hydroxyvitamin D concentration was below the normal range despite the fact that these infants received 10 micrograms vitamin D/d from the age of 1 mo. The infants were treated with intramuscular iron dextran (Imferon). The iron-dextran treatment increased the hemoglobin and serum iron concentrations as well as 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D concentrations. It is known that iron deficiency impairs fat and vitamin A intestinal absorption. Therefore, it is suggested that absorption of vitamin D may also be impaired. This may contribute to the development of vitamin D deficiency. Iron supplementation may have improved the absorption of vitamin D in the small intestine and hence increased the vitamin D concentration in the plasma.

25-Hydroxyvitamin D 2↗
PubMed1992

Prolonged treatment with finasteride (a 5 alpha-reductase inhibitor) does not affect bone density and metabolism.

OBJECTIVE: Since it is not clear whether testosterone or dihydrotestosterone is the active hormone in bone metabolism, we wished to assess the effect of finasteride, a 5 alpha-reductase inhibitor, or vertebral bone mineral density and parameters of bone and mineral metabolism. DESIGN: Patients were treated in a randomized, double-blind controlled study with either placebo, 1 or 5 mg/day finasteride. PATIENTS: Twenty-three men with benign prostatic hyperplasia (BPH) were included in this study; eight received placebo, seven were allocated to treatment with 1 mg/day, and eight to 5 mg/day finasteride for 12 months. MEASUREMENTS: Vertebral bone mineral density was measured at the lumbar spine by dual energy X-ray bone densitometry. Serum calcium, phosphorus, parathyroid hormone, osteocalcin and vitamin D metabolites were measured regularly. Urinary calcium and creatinine excretion were monitored as well. RESULTS: Finasteride caused a significant decrease in serum dihydrotestosterone after 6 and 12 months, but no effect on serum testosterone. Vertebral bone mineral density remained unaltered. None of the other parameters monitored were affected except for a small unexplained increase in 1.25-dihydroxyvitamin D in the group receiving 5 mg finasteride/day. CONCLUSIONS: Testosterone is probably the active hormone in bone metabolism. However, oestradiol, the product of testosterone aromatization (which remains unaltered under finasteride) may yet be another possible responsible steroid in the maintenance of bone density. We can also not rule out that the small amount of dihydrotestosterone remaining under finasteride administration is sufficient for maintaining normal bone metabolism.

5-alpha Reductase Inhibitors↗
PubMed1991

Regulation of proliferation of rat cartilage and bone by sex steroid hormones.

We have demonstrated previously that 17 beta-estradiol (E2) stimulates proliferation of skeletal tissues, both in vivo and in vitro, as measured by increased DNA synthesis and creatine kinase (CK) specific activity. The effect of E2 on bone is sex specific. E2 is active only in females and androgens only in males. By contrast, in cartilage of both sexes, dihydrotestosterone (DHT) as well as E2 stimulates CK specific activity and DNA synthesis. In bone, we find that sex steroids stimulate skeletal cell proliferation in gonadectomized as well as in immature rats. Ovariectomized (OVX) rats, between 1 and 4 weeks after surgery, show stimulation of CK by E2. The basal activity and response of CK changes with the varying endogenous levels of E2 in cycling rats, in which the highest basal activity is at proestrus and estrus and the highest response is in diestrus. In rats of all ages tested, both the basal and stimulated specific activity of CK is higher in diaphysis and epiphysis than in the uterus, or in the adipose tissue adjacent to the uterus, which has a response similar to that of the uterus itself. The effect of E2 in vivo, and in chrondroblasts and osteoblasts in vitro, is inhibited by high levels of the antiestrogen tamoxifen which, by itself, in similar high concentrations, shows stimulatory effects. In addition to the sex steroids, skeletal cells are also stimulated by secosteroid and peptide calciotrophic hormones. The interactions of the sex steroids with these hormones modulate the response of cartilage and bone cells to both sex steroids and the other calciotrophic hormones. These results provide the first steps towards understanding the regulation of bone cell proliferation and growth by the concerted action of a variety of hormones and growth factors.

Animals↗
PubMed1991

Effects of high concentrations of dietary vitamin E and ethoxyquin on the performance of laying hens.

1. Three experiments were carried out with light strain laying hens to evaluate the effects of relatively high doses of dietary vitamin E (125 mg/kg food) or ethoxyquin (EQ) (250 mg/kg food) on their laying performance. The control diet contained 5 and 125 mg/kg vitamin E and EQ, respectively. The experimental diets were fed either from one or 32 weeks until 88 or 89 weeks of age. 2. The two antioxidants did not affect the growth of the pullets, age at first egg, final body weight, average egg weight or relative abdominal fat pad size and liver weight at the termination of the experiments. In two out of three experiments, vitamin E and EQ did not affect egg production, food efficiency or mortality; in the third experiment vitamin E significantly (P less than 0.05) improved egg production and food efficiency after an outbreak of Newcastle disease which occurred at 34 weeks of age. EQ significantly reduced mortality during the course of this experiment, but did affect the variables of performance. In two experiments vitamin E consistently improved shell density, although a significant effect was observed in only one of the eight determinations carried out. EQ did not affect this variable. 3. The uterine muscle was more susceptible to oxidation than the drumstick meat, as evaluated by TBA values. In both tissues, vitamin E significantly and consistently decreased TBA values and restricted their increase during incubation, while EQ was less effective, particularly in the drumstick meat. 4. It is concluded that increasing vitamin E and EQ concentrations in diets of laying hens have no effect on the decrease in egg production due to aging. However, vitamin E may minimize the decline in egg production and food efficiency following the outbreaks of some diseases and slightly improve--under certain yet undefined conditions--shell density.

Adipose Tissue↗
PubMed1991

Hepatitis in a family infected by Chlamydia psittaci.

Hepatic involvement is considered a rare complication of psittacosis. Occurrence of icteric hepatitis as the cardinal manifestation of the disease has been rarely reported. We describe two members of a family infected by psittacosis, in whom icteric hepatitis was the prominent expression of the disease. The diagnosis of psittacosis was confirmed by isolation of the pathogen and by detection of serum antibodies to Chlamydia species. No serological evidence for acute TWAR infection was found. Chlamydia psittaci was also isolated from the family's parrot.

Adolescent↗
PubMed1990

Reciprocal modulation by sex steroid and calciotrophic hormones of skeletal cell proliferation.

We have demonstrated previously that 17 beta-estradiol (E2) stimulates cell proliferation in skeletal tissues, as measured by increased DNA synthesis and creatine kinase (CK) specific activity, and that calciotrophic hormones modulate E2 activity in rat osteoblastic sarcoma cells (ROS 17/2.8). Moreover, E2 failed to stimulate DNA synthesis in vitamin D-depleted female rat bone in the absence of prior i.p. injections of 1.25(OH)2D3. We have, therefore, studied the effects of pretreatment of cells by one hormone on their response to challenge by a second hormone. We now report reciprocal interactions of sex steroids and other hormones modulating bone formation on cell proliferation parameters in primary bone and cartilage cell cultures: these interactions can selectively augment or diminish cell responsiveness to a given hormone. Pretreatment of rat epiphyseal cartilage cell cultures with 1.25(OH)2D3, 24.25(OH)2D3 or parathyroid hormone (PTH) for 5 days, followed by E2 treatment for 24h, resulted in increased DNA synthesis compared to cultures pretreated with vehicle. Prostaglandin (PGE2) pretreatment blocked further response to E2. In the reciprocal case, rat epiphyseal cartilage cells, pretreated with E2, showed an increased response to PTH, a loss of the response to PGE2 or 24.25(OH)2D3 and an inhibition of CK activity and DNA synthesis by 1.25(OH)2D3, similar to the characteristic inhibitory action of 1.25(OH)2D3 in osteoblasts. By contrast, rat epiphyseal cartilage cells pretreated with testosterone showed no changes in response to PTH, 24.25(OH)2D3 or PGE2 and a decreased response to E2, but were stimulated by 1.25(OH)2D3. Rat embryo calvaria cell cultures behaved similarly to epiphyseal cartilage cultures except that 24.25(OH)2D3 pretreatment did not increase the response to E2. Reciprocally, pretreatment with E2 before exposure to calciotrophic hormones did not change the responses of rat embryo calvaria cell cultures to 1.25(OH)2D3 or 24.25(OH)2D3. These findings suggest that the mutual interactions between calciotrophic hormones and E2, demonstrated here in vitro, could selectively affect the responses of bone and cartilage cells to E2 by several mechanisms. These possibilities include increased E2 receptors and E2-stimulated differentiation of cartilage cells to more E2 responsive cells showing some characteristics of osteoblasts.

24,25-Dihydroxyvitamin D 3↗
PubMed1990

Hormonal stimulation of bone cell proliferation.

The recent demonstration of estrogen receptors in bone derived cells has stimulated the study of direct effects of sex steroids on bone. We have shown direct stimulation of proliferation by 17 beta-estradiol (E2) of ROS 17/2.8 rat osteogenic osteosarcoma cells, and other bone-derived cells in culture, as well as sex-specific stimulation of diaphyseal bone in vivo by estrogen and testosterone, using [3H]thymidine incorporation into DNA and stimulation of the specific activity of creatine kinase as markers. ROS 17/2.8 cells were used as models of osteoblast-like cells to study the reciprocal modulation of stimulation of bone cell proliferation by sequential treatment by sex steroid and calciotrophic hormones. Pretreatment with 1,25(OH)2D3 and PTH augmented stimulation by E2, while pretreatment with PGE2 followed by E2 resulted in no additional stimulation. Reciprocally, pretreatment with E2 significantly reduced the response to PGE2 while showing an insignificant effect on the response to the other hormones. Gonadectomized Wistar-derived rats provided a useful model system for study of postmenopausal osteoporosis. In diaphyseal bone, [3H]thymidine incorporation and creatine kinase activity decreased 4 weeks after gonadectomy. At that time, a single i.p. injection of E2 in females, and testosterone in males, resulted in a highly significant increase in both these parameters within 24 h.

Animals↗
PubMed1990

Long-term physical exercise retards trabecular bone loss in lumbar vertebrae of aging female mice.

The present study examined the effect of long-term, moderate physical exercise on trabecular bone volume (TBV), calcium content, 3H-proline uptake, and the activities of alkaline and acid phosphatases in lumbar vertebrae of aging and senescent mice. It became apparent that if physical activity starts at an early stage of life, i.e., prior to middle age and is extended until old age, it exerts beneficial effects on trabecular bone mass and mineralization. Such a positive effect is not obtained if the training program is initiated after middle age. The training-induced reduction in bone loss was accompanied by a significant decrease in acid phosphatase activity whereas no changes took place with regard to the activity of alkaline phosphatase. Long-term physical exercise also enhanced the uptake of 3H-proline by lining cells along the bone trabecules. In spite of its moderate nature, the endured training program served as a stress factor for the involved animals, a fact that was manifested by an increase in the serum levels of corticosterone. Thus, it seems that whereas young animals respond favorably to such a stimulatory stress, older animals lose this ability of adaptation.

Acid Phosphatase↗
PubMed1990

Prenatal diagnosis of vitamin D-dependent rickets, type II: response to 1,25-dihydroxyvitamin D in amniotic fluid cells and fetal tissues.

Vitamin D-dependent rickets type II (VDDR-II; hereditary resistance to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]), an autosomal recessive genetic disease that results from a failure to respond to 1,25-(OH)2D3, is characterized by severe rickets, hypocalcemia, growth retardation, and high prevalence of alopecia. We used amniotic fluid cells in the 17th week of gestation to detect VDDR-II in fetuses at risk for the defect. First, we demonstrated in cells obtained from 15 control pregnancies the presence of a specific high affinity 1,25-(OH)2D3 receptor (Kd = 0.3 x 10(-11) mol/L; maximal number of binding sites, 6.1 fmol/mg protein) and 1,25-(OH)2D3-induced 25-hydroxyvitamin D3-24-hydroxylase activity (up to 30-fold increase). Amniotic fluid cells from a woman who had already given birth to a child with VDDR-II contained receptors that bound [3H]1,25-(OH)2D3 normally and responded to 1,25-(OH)2D3 stimulation with a 10-fold increase in 24-hydroxylase activity. The fetus was, therefore, judged unaffected, and a normal baby girl was born. At the age of 16 months she did not demonstrate clinical or biochemical features of VDDR-II. Amniotic fluid cells from another mother of a child with VDDR-II were unable to bind [3H]1,25-(OH)2D3, and the hormone failed to stimulate 24-hydroxylase activity. VDDR-II in this fetus was confirmed after termination of pregnancy by the total inability of 1,25-(OH)2D3 to stimulate 24-hydroxylase activity in tissue explants and cell cultures prepared from the fetus's kidney and skin. In contrast, tissues from dead control fetuses responded to stimulation by 1,25-(OH)2D3 with a 3- to 10-fold increase in 24-hydroxylase activity. Fetal kidney and skin explants and cell cultures also synthesized a [3H]1,25-(OH)2D3-like metabolite from [3H]25-OHD3 as early as the 17th week of gestation. 1,25-(OH)2D3 (10 nM) decreased the in vitro synthesis of the [3H]1,25-(OH)2D3-like metabolite in tissues from dead control fetuses, but not from the affected fetus. Thus, human fetuses at midgestation already have the regulatory mechanisms responsive to 1,25-(OH)2D3 present postnatally. The prenatal diagnosis of VDDR-II is now possible and is indicated in a high risk family.

Adult↗
PubMed1989

Direct and sex-specific stimulation by sex steroids of creatine kinase activity and DNA synthesis in rat bone.

A direct in vitro effect of 17 beta-estradiol (E2) was demonstrated on bone and cartilage cell energy metabolism. Sex-specific stimulation by E2 and testosterone was shown in diaphyseal bone of weanling rats. E2 (30 nM) caused, within 24 hr, a 70-200% increase in creatine kinase (CK; ATP:creatine N-phosphotransferase, EC 2.7.3.2) specific activity in ROS 17/2.8 rat osteogenic sarcoma cells, MC3T3-E1 mouse calvaria-derived cells, and rat fetal calvaria cells, and a 40% increase in rat epiphyseal cartilage cells. Stimulation of CK activity by E2 was dose and time dependent: in ROS 17/2.8 cells, a highly significant increase was found at 3 nM E2 and a greater than 100% increase in CK activity was found 1 hr after E2 administration. In female 20-day-old Wistar-derived rats, E2 (5 micrograms per rat) increased CK activity in diaphyseal bone by 82% within 1 hr of i.p. injection, with a maximal increase of 200% after 24 hr; neither the weakly estrogenic agonist 17 alpha-estradiol, testosterone, nor progesterone showed this effect. Conversely, in male rat diaphyseal bone, testosterone or dihydrotestosterone increased CK activity after 24 hr by approximately 100%, while E2 was ineffective. In epiphyseal cartilage, both E2 and testosterone increased CK activity. Stimulation of CK activity by sex hormones was paralleled by significant increases in [3H]thymidine incorporation into DNA. Therefore, it is possible that direct sex-specific actions of gonadal steroids may contribute to stimulating bone growth and maintaining balanced bone turnover.

Animals↗
PubMed1989

Vitamin D deficiency in elderly patients in a general hospital.

Serum 25-hydroxyvitamin D (25-OHD) levels were measured in 338 elderly patients admitted to the Geriatric Medicine Departments of a general hospital in Israel in the course of one year. The mean (+/- SD) serum 25-OHD levels were significantly lower (P less than .01) in the elderly patients (13.5 +/- 8.9 ng/mL) than in healthy young controls (24.7 +/- 6.1 ng/mL). One hundred ten patients (35.5%) were either vitamin D deficient (25-OHD less than 5 ng/mL) or had borderline serum levels of 25-OHD (5-9 ng/mL). The mean (+/- SD) serum 25-OHD concentration of patients who were completely mobile before hospitalization was 15.5 +/- 8.8 ng/mL (n = 239). In patients mainly immobilized but able to leave the house occasionally, it was 10.2 +/- 6.3 ng/mL (n = 84) and of bed-ridden patients, it was 5.2 +/- 3.2 ng/mL (n = 15). No correlation was found between serum 25-OHD levels and the patients' age or serum calcium, phosphorus, alkaline phosphatase, and albumin values. Thus, in order to detect vitamin D deficiency in the elderly, it is necessary to measure serum 25-OHD concentration. The results demonstrate that vitamin D deficiency is common among elderly patients even in sunny climates and indicate the need for development of effective programs of prevention and treatment.

Adult↗
PubMed1989

Modulation by vitamin D status of the responsiveness of rat bone to gonadal steroids.

We have previously demonstrated that gonadal steroids stimulate [3H]thymidine incorporation and creatine kinase specific activity in skeletal tissues. In the present study we report that in 20-day-old vitamin D-deficient Wistar-derived rats, 17 beta-estradiol (E2; 5 micrograms/rat) or testosterone (50 micrograms/rat) failed to stimulate [3H]thymidine incorporation into diaphyses of long bones and that the response to these hormones in terms of increased creatine kinase specific activity was less than half the value in normally fed rats. Two daily ip injections of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3; 0.5 ng/g BW], but not 24,25-(OH)2D3 (5 ng/g BW), partially restored the biological responses to E2 in bone of 21-day-old vitamin D-deficient female rats. Vitamin D deficiency did not impair the responsiveness to gonadal steroids in the epiphysis of long bones, uterus, or prostate, in contrast to its effect on diaphysis. In 21-day-old normally fed female rats, neither vitamin D metabolite enhanced the response to E2. When cultures of rat epiphyseal cells were treated daily for 5 days with either 1,25-(OH)2D3 (1 nM) or 24,25-(OH)2D3 (10 nM), followed by E2 (30 nM) for 24 h, creatine kinase activity was significantly higher than in cultures treated daily for 5 days with vehicle alone, and then with E2. The same treatment of rat embryo calvaria bone cells showed that 1,25-(OH)2D3, but not 24,25-(OH)2D3, significantly increased the creatine kinase activity response to E2. These findings suggest that vitamin D metabolites selectively affect the biological responses of skeletal tissues to gonadal steroids.

Animals↗
PubMed1989

Bone biopsies and serum vitamin-D levels in patients with hip fracture.

To assess the correlation between osteoid and vitamin D in patients with a proximal femoral fracture, bone biopsies of the fracture site and the iliac crest were studied; and vitamin-D levels were measured in fasting blood taken on the day of admission. No osteomalacia was found at either site in any of the 95 patients investigated. In 65/95 patients, levels of 25-hydroxy-vitamin D (25-OHD) and 24,25-dihydroxy-vitamin D (24, 25-OH2D) were within the normal range, whereas 30/95 patients were deficient. Because there was no correlation between the amount of osteoid and vitamin-D metabolites in our patients, we concluded that osteomalacia was not a contributory factor in the pathogenesis of the hip fracture.

24,25-Dihydroxyvitamin D 3↗