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J Bollerslev

Publications and source records attributed to J Bollerslev.

At least 37 records · Page 2Linked to original sources
PubMed2000

Leptin levels in relation to body composition and insulin concentration in patients with endogenous Cushing's syndrome compared to controls matched for body mass index.

Cushing's syndrome (CS) is associated with weight gain and visceral obesity. We examined the relationship between regional fat distribution and serum levels of leptin, cortisol and insulin. Twenty-three consecutive patients with recently diagnosed CS (18 with pituitary adenoma, 5 with adrenal tumor), where compared to obese controls, matched for age, sex and Body Mass Index (BMI). Serum insulin, leptin, cortisol, C-peptide and body composition determined by DEXA were measured. Serum leptin levels were significantly increased in patients with CS (36.9+/-3.8 vs 18.9+/-2.4 ng/ml, p<0.001; women: 40.1+/-4.6 vs 21.7+/-2.9 ng/ml, p<0.01; men: 27.9+/-5.7 vs 10.9+/-2.3 ng/ml; p<0.05), the same were fasting insulin levels (178+/-30 vs 81+/-10 pmol/l; p<0.01) and C-peptide (1.51+/-0.12 vs 0.77+/-0.07 nmol/l; p<0.001). In a subgroup of 12 patients, truncal fat mass was significantly elevated when compared to obese controls (19.2 kg vs 14.7 kg, p<0.01, and 42% vs 36% in percentage of truncal body tissue, p<0.05), whereas total fat mass was insignificantly increased. Serum leptin correlated positively to total body fat (%) as in patients with CS (r=0.94, p<0.001) as in controls (r=0.68, p<0.01). The correlation to truncal body fat (%) was also significant in both groups (CS: r=0.84, p<0.001; controls: r=0.63, p<0.01). Multiple regression showed that percent total body fat was the predictor of leptin concentrations among patients with CS (r2=0.88, p<0.001) whereas insulin did not contribute significantly to the variance in leptin concentrations. In controls, both leptin and insulin (r2=0.65, p<0.001) contributed significantly to the variations in leptin levels. Controlled for the differences in total body fat, patients with endogenous CS have significantly increased serum leptin levels, compared to BMI-matched obese controls. This suggests that hyperleptinemia in CS not primarily reflects changes in body composition, but is the result of different hormonal influences on adipose tissue.

Adipose Tissue↗
PubMed2000

Serum creatine kinase isoenzyme BB in mammalian osteopetrosis.

In mammalian osteopetrosis the different mutations exemplify reduced bone resorption leading to net accumulation of bone. Recently, high blood levels of creatine kinase-BB have been reported in some human forms, suggesting it as a marker of osteopetrosis. In the current study serum creatine kinase-BB was evaluated in relation to known osteoclastic pathophysiology in two human types of autosomal dominant osteopetrosis at baseline and after stimulation with triiodothyronine and in four different rodent mutations. Creatine kinase-BB was increased markedly in Type 2 autosomal dominant osteopetrosis and in the incisors absent rat, both characterized by large numbers of giant osteoclasts, and did not change significantly after stimulation. Although creatine kinase-BB was unchanged in Type 1 autosomal dominant osteopetrosis at baseline and after stimulation, the rodent counterparts characterized by small osteoclasts, microphthalmic and osteopetrotic mice and toothless rats, had significantly decreased levels. Similar differences were observed in both types of autosomal dominant osteopetrosis compared with controls concerning tartrate resistant acid phosphatase. Creatine kinase-BB in mammalian osteopetrosis is related to osteoclastic number and size, where it probably reflects the differentiation and maturation of inactive bone resorbing cells. The isoenzyme does not seem to be a valuable screening marker for osteopetrosis.

Adult↗
PubMed1999

[Borderline primary hyperparathyroidism].

The clinical presentation of primary hyperparathyroidism has changed considerably after the application of biochemical autoanalysers. The condition was previously found with characteristic symptoms in bone, kidneys and the gastrointestinal tract; less than 1% of patients were assumed to be asymptomatic. Today, most patients have mild and uncharacteristic symptoms. Primary hyperparathyroidism has been detected with increasing frequency in the western world, but there are large variations within demographically otherwise comparable areas. There are also regional differences regarding the incidence of surgical treatment of the disease. Demographic studies have shown increased morbidity and mortality primarily from cardiovascular and possibly malign diseases related to hypercalcemia. Follow-up studies based on surgical series have shown increased mortality related to preoperative serum calcium level. In view of the altered clinical picture of primary hyperparathyroidism, treatment of moderate and possibly "benign" primary hyperparathyroidism has been actualised. At an international consensus conference in 1990, this patient group was defined by an arbitrary serum calcium limit of 3.0 mmol/l, but this limit has been found to be unacceptably high. Regardless of where the upper limit is set, there are so far well accepted indications for surgery, but only one in two patients fulfil these criteria. A working group of endocrinologists and endocrine surgeons from nine university clinics in Scandinavia have recently initiated a prospective, randomised study evaluating surgical treatment and a systematic follow-up of patients with borderline primary hyperparathyroidism.

Bone Density↗
PubMed1999

[A Scandinavian multicenter study will investigate the question: surgery or not in mild primary hyperparathyroidism?].

Primary hyperparathyroidism is a common endocrine disease particularly prevalent among elderly women. A majority of these patients diagnosed today are mildly hypercalcaemic, and many seem to lack manifest symptoms or complications. In such cases, conservative follow-up rather than parathyroid surgery may be suggested. However, long-term follow-up may entail costly investigations and be difficult to accomplish. Moreover, conservative follow-up is associated with a risk of subsequent complications or even premature death due to cardiovascular disorders. A Scandinavian multicentre study has been initiated to assess survival, morbidity and quality of life in surgically vs. conservatively treated patients.

Aged↗
PubMed1999

Increased cortical bone content of insulin-like growth factors in acromegalic patients.

To investigate cortical bone composition and the role of the insulin-like growth factor (IGF) system in active acromegaly, iliac crest bone biopsies were obtained from 15 patients (3 women and 12 men), aged 21-64 yr (mean, 45.6 yr), and 25 age- and sex-matched controls (8 women and 17 men), aged 22-66 yr (mean, 44.6 yr). Levels of IGF-I, IGF-II, IGF-binding protein-3 (IGFBP-3), IGFBP-5, and total protein were determined in extracts obtained after ethylenediamine tetraacetate and guanidine hydrochloride extraction. Osteocalcin and calcium were determined in extracts after HCl hydrolysis. Cortical bone contents of IGF-I, IGF-II, and IGFBP-5 were significantly elevated in the acromegalic patients compared with control values [91% (P < 0.001), 44% (P < 0.04), and 115% (P < 0.004), respectively]. There was no significant difference in IGFBP-3, osteocalcin, protein, and calcium between patients and controls. This study suggests that the increased levels of growth factors in cortical bone from acromegalics is a reflection of local production, secondary to a chronic systemic excess of GH and IGF-I.

Acromegaly↗
PubMed1999

Decreased bone formative and enhanced resorptive markers in human immunodeficiency virus infection: indication of normalization of the bone-remodeling process during highly active antiretroviral therapy.

As cytokines and 1,25-dihydroxyvitamin D [1,25-(OH)2D] appear to have an important role in bone homeostasis, we examined the possibility that human immunodeficiency virus (HIV)-infected patients, characterized by enhanced levels of proinflammatory cytokines and 1,25-(OH)2D deficiency, have disturbed bone metabolism by analyzing serum markers of bone formation (osteocalcin) and bone resorption (C-telopeptide) in 73 HIV-infected patients. HIV-infected patients with advanced clinical and immunological disease and high viral load were characterized by increased C-telopeptide and particularly by markedly depressed osteocalcin levels. HIV-infected patients had enhanced activation of the TNF system. Serum concentrations of p55 and p75-TNF receptors were negatively correlated with osteocalcin, and p75-TNF receptor was positively correlated with C-telopeptide. HIV-infected patients with advanced disease also had decreased serum concentrations of 1,25-(OH)2D, but this parameter was not correlated with osteocalcin or C-telopeptide. During 24 months with highly active antiretroviral therapy there was a marked rise in serum osteolcalcin levels together with a profound fall in viral load and TNF components and a marked rise in CD4+ T cell counts. Also, there was a shift from no correlation to a significant correlation between osteocalcin and C-telopeptide levels during such therapy. The present study suggests disturbed bone formation and resorption during HIV infection. Our findings indicating synchronization of bone remodeling during highly active antiretroviral therapy may represent a previously unrecognized beneficial effect of such therapy and expand our knowledge of the interactions between cytokines and bone in the bone-remodeling process.

Adult↗
PubMed1999

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome.

It is well established that chronic excess of glucocorticoids has negative effects on bone and collagen turnover, and that secondary osteoporosis is a known clinical complication of endogenous Cushing's syndrome (CS). The aim of the present study was to evaluate bone dimension and bone mineral content in relation to biochemical markers of bone and collagen turnover, in a consecutive series of 23 patients with endogenous CS (18 with pituitary adenoma and 5 with adrenal tumor; 17 women, 6 men; mean age 39.7+/-2.8 (S.E. M.) and 44.3+/-3.1 years respectively), compared with 23 age-, sex- and body mass index-matched healthy controls. Bone mineral densities were uniformly reduced in the different regions analyzed: lumbar spine (16.1%, P<0.001), femoral neck (15.2%, P<0.001), total body (11.5%, P<0.001), and the subregions of arms (8.4%, P<0.05), legs (10.1%, P<0.05) and trunk (15.8%, P<0.001). Similar results were observed for bone mineral content, although these were less prominent. The calculated area was significantly decreased in trunk (13.8%, P<0.01) and total body (11.6%, P<0.05). Serum levels of osteocalcin were significantly decreased (28%, P<0.03) in patients with CS. No significant differences were observed for the formative markers carboxyterminal propeptide of type I procollagen and aminoterminal propeptide of type I procollagen. Markers of bone resorption, serum Crosslaps and carboxyterminal cross-linked telopeptide of type I collagen were increased in patients compared with controls, although only significantly for Crosslaps (P<0.02). No correlations between formative and resorptive markers were found in the patients, but in controls, the formative markers were positively correlated with resorptive markers. In conclusion, bone dimension and bone mineral content of the entire skeleton are found to be decreased in endogenous CS. As judged by biochemical markers of bone remodeling, this is caused by decreased bone formation and an increased bone resorption.

Adult↗
PubMed1998

Effects of short-term treatment with prednisolone and calcitriol on bone and mineral metabolism in normal men.

To study the effects of treatment with glucocorticoid and calcitriol on biochemical markers of calcium and bone metabolism, 48 normal male volunteers (aged 21-54 years) were randomized to treatment for 7 days with either (A) prednisolone, 10 mg twice daily, (B) prednisolone, 10 mg twice daily, and calcitriol, 1 microg twice daily, (C) calcitriol 1 mg twice daily, or (D) placebo. The study period was 28 days. Renal calcium excretion increased (mean maximal increase +44.7%, p < 0.01) as well as serum parathyroid hormone (PTH) (max. +18.5%, p < 0.01) during prednisolone treatment. Concomitant treatment with calcitriol or calcitriol alone equally enhanced renal calcium excretion (max. +185.2%, p < 0.001) and decreased serum PTH (max. -43.1%, p < 0.001). Prednisolone administration was followed by prompt declines in markers of bone formation [serum osteocalcin (max. -34.7%, p < 0.001) and serum procollagen type I C-terminal propeptide (PICP) (max. -25.9%, p < 0.05)], whereas serum bone alkaline phosphatase (bone AP) remained unchanged. Calcitriol in combination with prednisolone attenuated the decrease in PICP (max. -8.9%, not significant), but it had no effect on osteocalcin (max. -40.1%, p < 0.001), and decreased bone AP (max. -22.2%, p < 0.05). Calcitriol alone increased osteocalcin (max. +37.8%, p < 0.03) and PICP (max. +26.0%, p < 0.05). Among markers of bone degradation, prednisolone suppressed serum C-terminal telopeptide of type I collagen (ICTP) (max. -28.4%, p < 0.001), but not the fasting renal excretion of hydroxyproline (OHP) and collagen type I N-terminal telopeptide (NTx). Calcitriol partially antagonized the decrease in ICTP (max. -17.2%, p < 0.001). Calcitriol alone had no effect on resorptive markers. Extraosseous matrix synthesis was suppressed by prednisolone evaluated by serum procollagen type III N-terminal propeptide (max. -30.8%, p < 0.001) and was not affected by concomitant treatment with calcitriol or calcitriol alone. In conclusion, short-term administration of prednisolone to healthy men leads to fast and protracted suppression of biochemical markers of bone formation and extraosseous connective tissue metabolism. The effect on bone was partially antagonized by simultaneous calcitriol treatment, and points toward a potential role of calcitriol in the prevention of steroid induced osteoporosis.

Adult↗
PubMed1998

Biochemical markers of bone metabolism in benign human osteopetrosis: a study of two types at baseline and during stimulation with triiodothyronine.

Biochemical markers of bone remodelling were used to evaluate bone turnover in two types of autosomal dominant osteopetrosis (ADO) at baseline and during stimulation with triiodothyronine (T3). Eight patients with Type I (aged 23-61 years, mean 40.4 years) and nine patients with Type II ADO (aged 20-49 years, mean 32.8 years) were compared with 10 normal controls (aged 22-54 years, mean 35.4 years). The participants were treated with 100 microg T3 daily for 7 days and followed for a total of 16 weeks. Serum concentrations of T3 increased and corresponding suppression of TSH was observed in all participants. Both formative and resorptive bone markers were normal at baseline. After stimulation with T3, a significant increase was seen in all groups for the formative markers used. Secondary increments were observed at the end of the observation period for all groups, indicating activation of bone remodelling. A variety of resorptive markers was assessed, but no differences between patients and controls were seen. After stimulation, highly significant responses were found in all parameters in all groups, in accordance with stimulation of existing resorptive cells. However, no secondary increments were seen at the end of the observation period. A more pronounced response was found in crosslinks-related assays. The study demonstrates that it is possible to stimulate bone resorptive and formative cells with thyroid hormones in both types of ADO. Moreover, it indicates that the remodelling process is activated by a short course of T3 treatment.

Adult↗
PubMed1997

[Scintigraphic localization of ectopic parathyroid tissue].

Ectopic parathyroid adenomas and hyperplastic glands are difficult to locate during surgical exploration. Failure to find and remove them is the most usual cause of surgical failure in the treatment of hyperparathyroidism. Earlier methods of preoperative localization of pathological parathyroid tissue had low sensitivity and were not generally recommended. Recent advances in parathyroid scintigraphy have improved this technique; the sensitivity is now as high as 95% for parathyroid adenomas. In the present study, ectopic parathyroid adenomas and hyperplasia were correctly localized by scintigraphy and were verified surgically in seven patients. Six of the patients had previously undergone ten unsuccessful operations altogether. Preoperative parathyroid scintigraphy might have saved these failed surgical explorations. In a pregnant woman, a mediastinal parathyroid adenoma was correctly localized by preoperative parathyroid scintigraphy. This patient was successfully operated by a sternotomy, and she was the only one of five patients with a mediastinal parathyroid adenoma who escaped unnecessary neck exploration. Preoperative parathyroid scintigraphy may reduce the number of surgical failures in hyperparathyroidism and shorten the operation time by less extensive exploration and thus fewer complications.

Adenoma↗
PubMed1997

Localization of a gene for autosomal dominant osteopetrosis (Albers-Schönberg disease) to chromosome 1p21.

Albers-Schönberg disease, the classical form of osteopetrosis, is an autosomal dominant condition with generalized increased skeletal density due to reduced bone resorption. Characteristic radiological findings are generalized osteosclerosis, with, most typically, end-plate sandwichlike thickening of the vertebrae (Rugger-Jersey spine) and the bone-within-bone (endobones) phenomenon. We studied an extended kindred with Albers-Schönberg disease and found linkage with several markers from chromosome 1p21. The Albers-Schönberg gene is located in a candidate region of approximately 8.5 cM flanked by markers D1S486 and D1S2792. A maximum LOD score (Z(max)) of 4.09 was obtained in multipoint analysis at loci D1S239/D1S248. Possible linkage of osteopetrosis to this chromosomal region was analyzed because the CSF-1 gene, which is mutated in the op/op mouse model for osteopetrosis, is located in 1p21. However, SSCP and mutation analysis in patients did not reveal any abnormality, which excludes the CSF-1 gene as the disease-causing gene. This was confirmed by refined physical mapping of the CSF-1 gene outside the candidate region for the Albers-Schönberg gene. The identification of the molecular defect underlying Albers-Schönberg disease will therefore be dependent on the isolation of other genes from an 8.5-cM candidate region on chromosome 1p21.

Chromosomes, Human, Pair 1↗
PubMed1996

Cortical bone remodeling in autosomal dominant osteopetrosis: a study of two different phenotypes.

Previous analyses of cancellous bone remodeling in autosomal dominant osteopetrosis (ADO) have suggested a diminished osteoclastic resorption at the endocortical surface. Consequently, cortical width increases with age in both ADO type I and II. By means of histomorphometric methods, the remodeling cycle of the Haversian surface in the iliac crest has recently been reconstructed in normal individuals. The aim of the present investigation was to study cortical bone remodeling in ADO type I and II. Transcortical iliac crest bone biopsies obtained from 21 ADO patients were studied. Of these, 14 had ADO type I and seven had ADO type II. Twenty of the patients had received intravital double labeling with tetracycline before the biopsies were obtained. The static histomorphometric parameters for cortical bone mass and structure were compared with a control group of 21 sex- and age-matched individuals. Regarding the dynamic histomorphometric parameters for reconstruction of the cortical bone remodeling cycle, the ADO type I material was compared with control material from 14 sex- and age-matched individuals, whereas the ADO type II material was compared with control material from six sex-matched but younger individuals. Significant increases were seen in absolute as well as fractional cortical widths in both ADO types. Furthermore, an age-related increase was observed in both absolute and fractional cortical widths in ADO type I, whereas ADO type II was nonsignificant with regard to age. The fractional cancellous width was reduced in both type I and type II. However, only in ADO type I did the fractional cancellous width significantly correlate inversely with age. In the control group, neither cortical dimensions nor cancellous width correlated significantly with age. No significant differences were observed between patients and the control group in osteon dimensions; fractional resorptive, formative, or quiescent sites; resorptive or formative remodeling rates; remodeling periods; or activation frequency. An age-related increase in cortical porosity was seen in the group of normal individuals, but not in the two patient groups. The fractional remodeling space was increased in the ADO type II group. In conclusion, cortical dimensions are increased in both ADO type I and II and positively correlated to age in type I. However, cortical remodeling at the Haversian surface is essentially normal in both ADO type I and II. This could be explained by a defective endocortical bone resorption, as no periosteal accretion was observed, and because cancellous bone remodeling previously has been described to be normal.

Adult↗
PubMed1996

Dose-response effect of short-term calcitriol treatment on bone and mineral metabolism in normal males.

To evaluate the effects of short-term treatment with calcitriol on biochemical markers of calcium and bone metabolism, 36 normal male volunteers (aged 21-54 years) were randomized to oral treatment for 7 days with either (A) calcitriol, 1 microgram twice daily, (B) calcitriol, 0.5 microgram twice daily, or (C) placebo twice daily. Serum calcium increased slightly in a dose-dependent manner (maximal increase 2.5%, p < 0.05) followed by a heavy increase in both 24 h (max. 156.1%, p < 0.001) and fasting urinary calcium excretion (max. 123.1%, p < 0.001), and a striking reduction in serum PTH (max. -43.1%, p < 0.001). Biochemical markers of osteoblast activity and bone formation increased immediately in a dose-dependent manner [serum osteocalcin (max. 37.8%, p < 0.03) and serum procollagen type I C-terminal propeptide (PICP) (max. 26.0%, p < 0.05)], whereas there was no effect on serum bone alkaline phosphatase. Calcitriol treatment had no effect on biochemical markers of bone resorption [serum C-terminal telopeptide of type I collagen (ICTP) and fasting urinary excretion of hydroxyproline/creatinine (OHP)]. Extraosseous collagen matrix synthesis was not affected evaluated by serum procollagen type III N-terminal propeptide (PIIINP). In the follow-up period (15 weeks) no unequivocal changes were observed. The fast and protracted increase in biochemical markers of osteoblast activity and bone formation, without affecting bone resorption and extraosseous connective tissue metabolism points toward a selective effect of calcitriol on bone matrix formation.

Administration, Oral↗
PubMed1996

Dose-dependent effects of recombinant human growth hormone on biochemical markers of bone and collagen metabolism in adult growth hormone deficiency.

Administration of growth hormone (GH) to patients with growth hormone deficiency (GHD) has beneficial effects, but so far has been employed only empirically. We have, therefore, investigated the dose-dependent effect of GH on target tissue by studying biochemical markers of bone and collagen turnover in GHD. Then patients with GHD (nine males and one female aged 21-43 years, mean age 28 years) participated in the study. Growth hormone deficiency was defined as a peak serum GH response of less than 15 mU/l in two provocation tests. After a 4-week run-in period, the study population received increasing doses of GH at 4-week intervals (1, 2 and 4 U/m2). Blood samples were collected in the fasting state at 7.00 h on the last day of each period and assayed for serum levels of osteocalcin (S-BGP), bone alkaline phosphatase (B-ALP), C-terminal propeptide of type I collagen (S-PICP), carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (S-ICTP) and N-terminal propeptide of type III collagen (S-PIIINP). Following replacement therapy, serum insulin-like growth factor I and insulin-like growth factor binding protein 3 increased sequentially with time (p < 0.001 and p < 0.001, MANOVA) and the values were elevated significantly over baseline levels after treatment with 1 U/m2. Serum BGP values were below normal at the start of the study and increased gradually following GH treatment to levels in the low-normal range. Baseline values for serum bone alkaline phosphatase (B-ALP), PICP and PIIINP were within the normal range. The collagen parameters increased with GH replacement (p < 0.001, MANOVA) to levels above normal, whereas B-ALP stayed within normal limits. Serum ICTP values were elevated above the normal range at baseline, indicating increased bone resorption in GHD. A linear increase in values was observed with GH treatment (p < 0.001, MANOVA). Serum ICTP did not correlate significantly with the bone formative parameters but was correlated positively to PIIINP. The sensitivity of S-ICTP as a bone resorptive marker is thus questioned. In conclusion, a dose-dependent increase in markers of growth hormone metabolism and in biochemical markers of both bone and non-bone collagen synthesis was seen following incremental doses of GH in GHD.

Adult↗
PubMed1995

Effect of 4 weeks of octreotide treatment on prolactin, thyroid stimulating hormone and thyroid hormones in acromegalic patients. A double blind placebo-controlled cross-over study.

We aimed to test the hypothesis, that octreotide has a suppressive effect on unstimulated and TRH-stimulated PRL levels in both normo- and hyperprolactinaemic acromegalic patients, and besides to evaluate the effect of octreotide on unstimulated TSH and thyroid hormones. The present study is a doubleblind placebo-controlled cross-over trial; the 12 acromegalic patients were treated with octreotide or placebo (300 micrograms/d) for 4 weeks separated by a 12 weeks washout period. Before and after each 4 weeks period a TRH-test (200 micrograms iv) was performed and serum GH and PRL levels were determined. Serum TSH and thyroid hormones were determined after 0, 2, 3, and 4 weeks. In the whole group unstimulated PRL levels were 18 micrograms/l +/- 5 before and 7 micrograms/l +/- 1 during octreotide treatment (p < 0.01). The PRL lowering effect of octreotide was significantly more pronounced in hyperprolactinemic patients compared to normoprolactinaemic patients (p < 0.05). Patients with the highest pretreatment PRL levels had the most pronounced percentage suppression of unstimulated PRL levels during octreotide treatment. Eight out of 12 patients had a TRH-stimulated PRL response > or = 100%, both during placebo and octreotide treatment, but in the group as a whole maximal TRH-stimulated PRL levels were suppressed during octreotide treatment, PRL levels were 50 micrograms/l +/- 20 before and 18 micrograms/l +/- 3 during octreotide treatment (p < 0.05). Unstimulated GH levels were 48 mU/l +/- 15 before and 13 mU/l +/- 2 during octreotide treatment (p < 0.01). Serum total T3 was significantly reduced during octreotide treatment (p < 0.05); serum TSH, total T4 or free T4 index were not significantly changed during treatment. We conclude that patients with acromegaly and hyperprolactinemia will normalize PRL levels during 4 weeks of octreotide treatment and octreotide will reduce total T3 levels in acromegalic patients.

Acromegaly↗
PubMed1995

Autosomal dominant osteopetrosis: bone mineral measurements of the entire skeleton of adults in two different subtypes.

Bone mineral content (BMC) and density (BMD) were measured by dual-energy X-ray absorptiometry in two subtypes of autosomal dominant osteopetrosis (ADO). Both types have been radiologically characterized by diffuse symmetrical osteosclerosis, but with characteristic differences. Increased thickness of the cranial vault is a typical finding in type I ADO, whereas endobones in the pelvis and end-plate thickening in the spine are obligate findings in type II. Eleven patients with type I from three kindreds, and seven patients with type II, one family participated in the study, and were compared with 18 age- and sex-matched normal controls. Whole-body BMC and BMD were measured, and regions of special interest were selected: head, axial, and appendicular skeleton. Moreover, lumbar spine and femoral neck scans were performed. Whole-body BMC and BMD, mostly reflecting cortical bone, were markedly increased in both types compared with normals. A pronounced osteosclerosis was present in the axial as well as the appendicular skeleton. Median BMD was markedly increased in the axial skeleton by 51% (44-56) and 42% (33-56), (median differences with 95% CI), respectively, for types I and II compared to normal controls, and in the appendicular skeleton by 48% (37-59) and 38% (16-45). No overlap between observed ranges of patients and controls was observed. A positive correlation between age and whole-body BMD was demonstrated in ADO, but not in the control group, indicating progressive osteosclerosis with age. Median BMD of the lumbar spine, which mostly reflects trabecular bone, showed increased densities in both types, 71% (51-84) and 59% (37-93), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1995

Biological variation of serum and urinary magnesium in apparently healthy males.

The biological variations of serum (S-) magnesium and urinary (U-) magnesium concentrations and excretions have been investigated. Serum samples, 24-h and fasting urinary samples were collected from each of 60 supposedly healthy male volunteers. In addition, 12 volunteers collected additional samples 7 and 112 days after the initial sample. The reference interval for S-magnesium was 0.765-0.997 mmol l-1. The biological variation for S-magnesium was 3.2% within subjects and 7.4% between subjects. This indicated an index of indivduality of 0.5, which means that significant changes in S-magnesium can occur within the limits of the reference interval, and that serial determinations of S-magnesium might prove useful as an indicator of changes in whole body magnesium status. It is, on the other hand, unlikely that a single determination of S-magnesium can be used in assessing whole-body magnesium status in the individual. The reference interval for the 24-h U-magnesium excretion, corrected for surface area, was 1.306-4.762 mumol min-1 1.73 m-2. The 24-h U-magnesium excretion exhibited a biological within-subject variation of 36% and a between-subject variation of 26%. The 24-h U-magnesium excretion did not correlate with S-magnesium, and only slightly (r = 0.58) with the fasting U-magnesium/creatinine concentration. This, and the very large coefficients of variation, make it unlikely that the renal magnesium excretion can be used as a measure of whole body magnesium status, or that changes in the renal magnesium excretion can be used as a measure of changes in whole body magnesium status.

Adult↗