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Biomedical subjects

S Shany

Publications and source records attributed to S Shany.

At least 55 records · Page 3Linked to original sources
PubMed1990

Calcitonin in Ghanaians and Israelis.

Calcitonin (CT) in serum was measured in a group of (black) Ghanaian traumatic fracture patients (GFP) and in two healthy control groups, (black) Ghanaian (GMS) and (white) Israeli (IMS) medical students. CT (mean +/- SD) in GFP, GMS and IMS was, respectively, 17.2 +/- 6.4, 15.5 +/- 2.8 and 7.6 +/- 3.3 pmol/l. The mean difference between the GFP and GMS was not significant, but that between the Ghanaian groups combined and IMS was 8.8 pmol/l, 95% CI 4.1-13.7, P less than 0.001. Observations elsewhere that CT levels in adult blacks in the tropics are higher than those in whites are confirmed.

Adult↗
PubMed1990

Diversity in peritoneal macrophage response of CAPD patients to 1,25-dihydroxyvitamin D3.

A major complication of continuous ambulatory peritoneal dialysis (CAPD) is peritonitis. Increasing the activity of the peritoneal macrophages, the predominant cell type found in the peritoneal cavity, may be a promising treatment for this infection. The effect of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] on the activity of peritoneal macrophages from CAPD patients and nonuremic controls was studied. 1,25(OH)2D3 had a biphasic effect on superoxide generation in the concentration range of 2.5 10(-9) M to 5 x 10(-6) M with a peak at 2 x 10(-8) M. The addition of 2 x 10(-8) M 1,25(OH)2D3 to nonuremic control macrophages for 24 hours caused a significant twofold increase in superoxide generation in response to phorbol myristate acetate (PMA), from 2.21 + 0.2 to 4.1 + 0.2 nmol/10(6) mac (P less than 0.001), and enhanced the bactericidal activity from 60 + 7% to 85 + 9% (P less than 0.005). CAPD patients were divided into two groups: Group A, patients with high peritonitis incidence (HPI); group B, patients with low peritonitis incidence (LPI). Macrophages from HPI patients show a lower bactericidal activity (37 +/- 5%) and were not affected by 1,25(OH)2D3 after 24 hours of treatment. The increase in macrophage activity was seen only after three days of incubation with the hormone. Macrophages from this group generated a high amount of prostaglandin E2 (PGE2) during the first 24 hours in culture (7.8 +/- 0.52 ng/ml as compared with 0.35 +/- 0.03 ng/ml in the controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol↗
PubMed1990

Effect of cimetidine on hepatic vitamin D metabolism in humans.

Cimetidine inhibits the action of vitamin D-hydroxylase (a hepatic mixed-function oxidase) in the rat. Therefore, the hypothesis was tested that this H2 receptor antagonist would affect vitamin D metabolism in humans. Nine adult patients were treated with 400 mg cimetidine orally twice daily during a period from winter to summer, when days were becoming longer. Serum levels of 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D were monitored before treatment, after 4 weeks of treatment, and 1 month after cessation of treatment. No seasonal increase in the level of 25-hydroxyvitamin D was observed during the period of treatment, but the level rose significantly after withdrawal of the drug. The other hydroxylates of vitamin D were not affected. Levels of albumin, total calcium, phosphorus and alkaline phosphatase remained normal. The data suggest that short-term treatment with cimetidine could potentially perturb vitamin D metabolism in man.

Cimetidine↗
PubMed1990

1,25-Dihydroxyvitamin D3 enhances cytosolic free calcium in HL-60 cells.

1,25-Dihydroxyvitamin D3 (1,25[OH]2D3) caused a rise in the concentration of intracellular free calcium ions ([Ca2+]i) in HL-60 cells. This effect of 1,25(OH)2D3 parallels its suppression of cell proliferation and its induction of cell differentiation into monocyte-like cells. The changes in [Ca2+]i are dose and time dependent. The concentration of 1,25(OH)2D3 (10(-7) M) that induced maximal differentiation also caused the maximal increase in intracellular Ca2+. The rise in cytoplasmic free Ca2+ concentration was not immediate and reached statistical significance only after 24 h. The [Ca2+]i reached its peak at 48 h (134 +/- 4 nM vs 101 +/- 3 nM in controls) and remained stable at this level. The increase in intracellular Ca2+ was found to be related to new protein synthesis, because it was inhibited in the presence of specific RNA and protein synthesis inhibitors. The rise in [Ca2+]i was not observed during incubation of HL-60 cells with 24,25-dihydroxyvitamin D3 (24,25[OH]2D3), a vitamin D metabolite that does not induce the differentiation of HL-60 cells. In contrast, 25-hydroxyvitamin D3 (25-OH-D3) and phorbol 12-myristate 13-acetate (TPA), both of which induce differentiation in this cell line, also increase [Ca2+]i. In conclusion, the present study emphasizes that a significant increase in intracellular free Ca2+ occurs in the effect of 1,25(OH)2D3 on HL-60 cells.

Calcitriol↗
PubMed1990

Acromegaly and proximal femoral fracture in an aged person: bone histomorphometry, vitamin D metabolites and parathormone.

Osteoporosis and fractures are rare in acromegaly. An 84-year-old acromegalic woman sustained a fractured neck of femur in a fall. Histomorphometric analysis of an iliac crest biopsy showed marked osteoporosis and augmented resorption parameters. Cortical plates were very thin and bone volume was 8.5%; 12.5% is the reference value for women at this age. The total resorption surfaces were 23.7% compared with the reference value of 8%. We conjecture that postmenopausal and involutional osteoporosis were far advanced before the development of acromegaly, explaining the coexistence of the two conditions. Parathormone (65 pmol/l) and 24,25-dihydroxyvitamin D (1.34 ng/ml) levels were within normal limits, but those of 25-hydroxyvitamin D (5.6 ng/ml) and 1,25-dihydroxyvitamin D (15 pg/ml) were markedly decreased.

Acromegaly↗
PubMed1989

Involvement of intracellular pH elevation in the effect of 1,25-dihydroxyvitamin D3 on HL-60 cells.

Besides its effect in inhibiting proliferation and inducing differentiation of HL-60 to monocyte-like cells, 1,25-dihydroxyvitamin D3 also causes a rise in intracellular pH (pHi) from 7.17 +/- 0.02 to 7.3 +/- 0.05, as measured by the fluorescence of 2',7'-bis(carboxyethyl)-5-(6)-carboxy-fluorescein. The effect of 1,25-dihydroxyvitamin D3 on pHi is dose dependent in a parallel manner to its effect on the proliferation and differentiation processes. The elevation of pHi by 1,25-dihydroxyvitamin D3 is gradual but precedes the differentiation process. A significant increase in pHi was obtained after 16 h of incubation with the hormone and reached its maximum level after 48 h. pHi then dropped back to its initial level, which is also similar to that of peripheral normal blood monocytes. A rise in pHi was not observed during incubation of HL-60 cells with 24,25-dihydroxyvitamin D3, a metabolite which does not promote their differentiation. In contrast, other agents such as phorbol 12-myristate 13-acetate known to induce differentiation in this cell line do cause an increase in pHi. Moreover, alkalinization of HL-60 cells by NH4Cl causes induction of differentiation to monocytes. The results suggest that a rise in pHi plays a role in regulating the molecular mechanism of the inhibition of proliferation and the induction of differentiation in HL-60 cells.

Ammonium Chloride↗
PubMed1989

Serum and bone vitamin D metabolites in elective patients and patients after fracture.

Vitamin D metabolite levels were measured in serum and bone samples obtained from 27 patients undergoing elective bony procedures and from 28 patients operated on after a fracture. Serum 25 hydroxyvitamin D3 (25-OH-D3) and 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) did not differ significantly between the elective and fracture patients, but serum 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) was significantly reduced in the fracture patients. Very little 25-OH-D3 was found in bone, although it was the major vitamin D metabolite in serum (90%). In elective patients bone levels of 24,25(OH)2D3 and 1,25(OH)2D3 were similar to those in serum; however, in bone from around pertrochanteric fractures, but not from subcapital or patellar fractures, the concentrations of these compounds were considerably increased. These findings may shed light on the mechanism of callus formation and on the role of vitamin D metabolites in bone healing.

24,25-Dihydroxyvitamin D 3↗
PubMed1988

The involvement of calcium ions in the effect of 1,25-dihydroxyvitamin D3 on HL-60 cells.

1,25-Dihydroxyvitamin D3 (1,25[OH]2D3) was found to suppress growth of human leukemic cells (HL-60), and to induce the differentiation of these cells to monocyte-like cells. The purpose of the present study was to examine the role of calcium ions in the effects of 1,25(OH)2D3 on HL-60 cells. Incubation of the HL-60 cells with 1,25(OH)2D3 (10(-7) M) for 4 days caused a significant inhibition of 50% of cell growth. The number of differentiated cells increased simultaneously from 24 x 10(3) +/- 2 x 10(3) in the controls to 658 x 10(3) +/- 32 x 10(3) in the 1,25(OH)2D3 (10(-7) M)-treated cells. The role of calcium ions in the effects of 1,25(OH)2D3 on HL-60 cells was first studied by changing the available calcium in the medium and by measuring the effect of 1,25(OH)2D3 on intracellular Ca2+ levels. Limitation of the available Ca2+ by means of ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) or verapamil enhanced the inhibitory effect on proliferation and decreased the number of differentiated cells obtained by 1,25(OH)2D3 alone. These effects could be abolished by restoring the Ca2+ levels. The role of the intracellular free Ca2+ ions in the effect of 1,25(OH)2D3 was further illustrated by measuring the intracellular Ca2+ levels. The intracellular free Ca2+ concentration in 1,25(OH)2D3 (10(-7) M)-treated HL-60 cells rose significantly from 117.0 +/- 6.3 nM in the untreated HL-60 cells to 145.0 +/- 7.5 nM in the treated cells (p less than 0.02). Addition of verapamil moderated the increase in intracellular free Ca2+ (125.0 +/- 5.2 nM) obtained by 1,25(OH)2D3 alone. Thus the elevation of intracellular free Ca2+ caused by 1,25(OH)2D3 treatment may be involved in the effect of the hormone on the HL-60 cells.

Calcitriol↗
PubMed1988

Vitamin D-deficiency in the elderly: treatment with ergocalciferol and hydroxylated analogues of vitamin D3.

The purpose of the present work was to study the effect of vitamin D and its metabolites in correcting hypovitaminosis D in the elderly. Thirty elderly people (mean age 78.4 years) participated in this study. They all had low serum levels of 25-hydroxyvitamin D (25-OH-D), of 24,25-dihydroxyvitamin D [24,25(OH)2D] and of 1,25-dihydroxyvitamin D [1,25(OH)2D]. These low levels did not increase in nine subjects after oral administration of vitamin D2 (3,000 IU/day for 12 weeks). However, administration of 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3) to 12 other subjects (0.5 micrograms/day for 8 weeks) led to a significant increase in the serum levels of 1,25(OH)2D. The other vitamin D metabolite levels remained unchanged. A significant increase in the levels of all three main vitamin D metabolites was obtained following administration of 25-hydroxyvitamin D3 (25-OH-D3) to a third group of nine subjects (25 micrograms/day for 1 week). These results suggest that vitamin D nutrition in elderly people insufficently exposed to the sun could be maintained by regular administration of 25-OH-D, whereas the administration of native vitamin D (ergocalciferol) in the doses used was inadequate for vitamin D nutrition.

24,25-Dihydroxyvitamin D 3↗
PubMed1987

1,25-Dihydroxyvitamin D-3 alters membrane phospholipid composition and enhances calcium efflux in HL-60 cells.

1,25-Dihydroxyvitamin D-3 (1,25(OH)2D3) had direct effects on the HL-60 cell membrane. Treatment of HL-60 cells with 1,25(OH)2D3 for short time periods (2-4 hours) caused an increase in calcium efflux. This phenomenon was found to be unrelated to new protein synthesis since it was not inhibited in the presence of RNA and protein synthesis inhibitors. The treatment of the HL-60 cells with 1,25(OH)2D3 for four hours caused changes in their membrane phospholipid composition. The phosphatidylcholine:phosphatidylethanolamine ratio increased from 1.2 to 1.5. Thus the alteration in the phospholipid composition in the membrane induced by 1,25(OH)2D3 may be responsible for the changes in the permeability of the membrane to calcium ions.

Calcitriol↗
PubMed1987

Bile salt deficiency and the absorption of vitamin D metabolites. In vivo study in the rat.

We studied the effect of the absence of bile salts on the absorption of vitamin D metabolites in vivo, in the biliary duct-ligated rat. The mesenteric, lymphatic absorption of the metabolites studied (vitamin D3, 25-hydroxyvitamin D3, and 1,25-dihydroxyvitamin D3) was almost completely abolished in the experimental animals. These results differed significantly (P less than 0.001) from those of the control rats. The 1,25-dihydroxyvitamin D3 absorption into the portal vein system was unaffected by the lack of biliary salts. The absorption of 25-hydroxyvitamin D3 was decreased and that of vitamin D3 was negligible, under the same experimental conditions. These data show that the more polar vitamin D metabolites, like 1,25-dihydroxyvitamin D3 and to some extent 25-hydroxyvitamin D3, are absorbed directly into the portal blood without the involvement of bile salts and micelle formation. Thus, the use of polar vitamin D metabolites should be considered in correcting hypovitaminosis D and osteomalacia in cases of chronic biliary salt depletion.

Animals↗
PubMed1986

Enhancement of 24,25-dihydroxyvitamin D levels in patients treated with continuous ambulatory peritoneal dialysis.

We measured 24,25-dihydroxyvitamin D [24,25(OH)2D] levels in patients treated with chronic ambulatory peritoneal dialysis (CAPD), before and after receiving vitamin D2 or 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3). Vitamin D2 administration led to an increase in 25-hydroxyvitamin D (25-OH-D) and a concomitant rise in 24,25(OH)2D. No change was observed in 1,25-dihydroxyvitamin D [1,25(OH)2D]. Administration of 1 alpha-OH-D3 resulted in an increase in 1,25(OH)2D3, and a concomitant rise in 24,25(OH)2D, but no change in 25-OH-D3. Thus, 24,25(OH)2D levels may be increased in CAPD patients by raising 25-OH-D levels, or by raising 1,25(OH)2D3 levels. Since the latter enhances specifically the renal 24-hydroxylase enzyme, we conclude that this enzyme is present in CAPD patients with kidneys in situ, and may be stimulated by adequate 1,25(OH)2D3 levels. Thus, administration of 1 alpha-OH-D3 to CAPD patients with kidneys in situ seems to be sufficient to obtain normal levels of 1,25(OH)2D3 and 24,25(OH)2D3. However, anephric patients require vitamin D2 in addition as a source of 25-OH-D, the substrate for extrarenal production of 24,25(OH)2D.

Calcifediol↗
PubMed1986

Seasonal variation in serum levels of vitamin D metabolites and parathormone in geriatric patients with fractures in Southern Israel.

In 41 geriatric patients with long bone fractures, a seasonal variation was observed in the serum levels of 25-hydroxyvitamin D (25-OH-D), 1,25-dihydroxyvitamin D [1,25(OH)2D], 24,25-dihydroxyvitamin D [24,25(OH)2D] and parathormone (PTH). The serum concentrations of vitamin D metabolites correlate positively, while that of PTH correlates negatively with day length and global solar radiation in southern Israel. Our data suggest that the higher serum levels of vitamin D metabolites during the summer suppress PTH secretion. During the winter, the reduction of serum levels of vitamin D metabolites due to decreased endogenous production was accompanied by an increase in serum PTH levels.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

Verapamil improves defective duodenal calcium absorption in experimental chronic renal failure.

Experiments were carried out to establish whether abnormalities in cellular calcium metabolism in chronic renal failure contributed to the impaired production of 1,25-dihydroxy vitamin D3 [1,25(OH)2D3]. For this purpose the calcium influx blocker verapamil was administered chronically to 5/6 nephrectomized rats (SNX) and sham-operated rats (sham). SNX and sham-nontreated animals served as controls. Fractional duodenal calcium absorption was severely depressed in SNX rats, compared to sham group. Administration of verapamil to SNX rats caused an improvement in calcium absorption despite similar degrees of renal insufficiency as in the nontreated SNX animals. The effect of verapamil requires residual renal parenchyma, since it was not reproduced in bilaterally nephrectomized rats. 45Ca uptake by renal cortical slices obtained from SNX rats was significantly elevated, as compared to sham group, and was corrected in uremic rats treated with verapamil. Plasma concentrations of 25-hydroxy vitamin D3 (25-OH-D3) were similar in all experimental groups. The 1,25(OH)2D3 plasma level in SNX rats was similar to values obtained in the control group, with an almost 2-fold increase in verapamil-treated animals. Quin-2 measurements of cytoplasmic calcium concentration in cultured proximal tubular cells revealed that verapamil prevents calcium bursts provoked by anoxic insult, by parathyroid hormone and by alpha 1-adrenergic stimuli. We conclude that verapamil treatment of SNX rats improves the duodenal absorption of calcium via augmentation of 1,25(OH)2D3 production.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoquinolines↗
PubMed1985

Leiomyoblastoma associated with intractable hypercalcemia and elevated 1,25-dihydroxycholecalciferol levels. Treatment by hepatic enzyme induction.

A 42-year-old woman, with a previously resected jejunal leiomyoblastoma, was first seen with liver metastases 31/2 years after the tumor resection. Intractable malignant hypercalcemia appeared eight months later, together with renal insufficiency. No osteolytic lesions were detected. Levels of parathyroid hormone, cyclic adenosine monophosphate, and 1,25-dihydroxycholecalciferol (1,25[OH]2D) were not useful in distinguishing between the hypercalcemia of malignancy and concurrent hyperparathyroidism. Despite renal insufficiency, hypercalcemia, and subtotal parathyroidectomy, the 1,25(OH)2D levels remained elevated, consistent with the speculation that a tumor product stimulated 1-alpha-hydroxylation of 25-hydroxycholecalciferol. Phenytoin and phenobarbital (enzyme induction therapy), in combination with phosphorus and glucocorticoids, appeared to be useful in controlling the hypercalcemia.

Adult↗
PubMed1985

Parathormone, calcitonin, and vitamin D metabolites during normal fracture healing in geriatric patients.

In order to study the role of calcium-regulating hormones during callus formation in elderly patients, serum levels of parathormone (PTH), calcitonin (CT), 25-hydroxyvitamin D [25-OH-D], 1,25-dihydroxyvitamin D [1,25(OH)2D], 24,25-dihydroxyvitamin D [24,25(OH)2D], and calcium (Ca) were determined in 41 patients with fractures of long bones, primarily hip fractures. The parameters were measured on admission and after eight weeks. There were almost no changes in hormone serum levels during bone repair, except for a decrease in serum levels of 1,25(OH)2D from 25.3 +/- 2.3 pg/ml on admission to 21.0 +/- 2.0 pg/ml eight weeks later (p less than .001). Patients with fractures compared to normal elderly humans have lower serum levels of PTH (0.99 +/- 0.06 ng/ml versus 1.88 +/- 0.34 ng/ml; p less than .001), 25-OH-D (10.7 +/- 1.0 ng/ml versus 17.1 +/- 1.8 ng/ml; p less than .001), and Ca (9.1 +/- 0.1 mg% versus 9.7 +/- 0.1 mg%; p less than .001) and higher serum levels of 1,25(OH)2D (25.3 +/- 2.3 pg/ml versus 17.1 +/- 2.3 pg/ml; p less than .001). Female patients have lower serum levels of 24,25(OH)2D compared to males (1.65 +/- 0.15 ng/ml versus 2.06 +/- 0.29 ng/ml; p less than .05). A similar trend was noted in serum CT levels during callus formation (0.12 +/- 0.02 ng/ml versus 0.16 +/- 0.02 ng/ml; p less than .05). Patients with subcapital fractures of the femur have significantly lower serum levels of all vitamin D metabolites on admission, compared with patients suffering from extracapsular fractures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗