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Biomedical subjects

H K Ibbertson

Publications and source records attributed to H K Ibbertson.

At least 19 recordsLinked to original sources
PubMed1991

The acromegalic rosary.

Palpable enlargement of the costochondral junctions on the anterolateral chest wall was detected in 26 of 27 patients with acromegaly. In a further study three doctors wearing eyemasks examined a further 13 acromegalic patients and 12 control subjects; costochondral enlargement was detected with a sensitivity of 77% and specificity of 86%. It was not found in normal subjects in the absence of previous chest injury. The presence and extent of costochondral enlargement was unrelated to the duration of active or cured acromegaly, the initial or present growth hormone concentrations, or other clinical features of growth hormone excess. Costochondral enlargement is a common clinical sign in acromegaly and can serve as a biological marker of previous or current growth hormone excess.

Acromegaly↗
PubMed1990

Previous pet ownership and Paget's disease.

The relationship between pet ownership and Paget's disease (PD) of bone was investigated in 112 patients with PD who were matched with a similar number of community-based controls. There was a significantly increased frequency of dog ownership by patients with PD aged less than 60 years. Multivariate logistic regression analysis revealed that there was a significant age-related increase in risk of PD associated with past or present ownership of either dogs or cats, with younger patients having the greatest risk. These results suggest that slow virus infection of osteoclasts by paramyxoviruses acquired from pets may contribute to the development of Paget's disease in the younger patient.

Age Factors↗
PubMed1989

Effects of aminobisphosphonate infusion on biochemical indices of bone metabolism in rheumatoid arthritis.

In a phase 1 study, seven patients with classical rheumatoid arthritis were treated with intravenous 3-amino-1-hydroxypropylidene-1-1-bisphosphonate (APD). Following this treatment, bone resorption as measured by fasting urine calcium/creatinine and hydroxyproline/creatinine ratios, was reduced. This was sustained for 6 months in only three patients. Elevations of these ratios often coincided with flares of active arthritis in the remaining four patients. Bone turnover as measured by serum osteocalcin levels was reduced in all patients but serum alkaline phosphatase levels remained unchanged. There was no consistent improvement in clinical indices of disease activity.

Adult↗
PubMed1989

Insulin-like growth factor 1 and bone turnover in glucocorticoid-treated and control subjects.

The role of the growth hormone-somatomedin axis in the genesis of steroid osteoporosis has been studied by measuring circulating insulin-like growth factor 1 (IGF-1) levels in asthmatic subjects either receiving or not receiving therapy with oral glucocorticoids. There was no difference in IGF-1 levels between the two groups (60.6 micrograms/l (95% confidence interval 47.3-77.8) in the control subjects vs 69.1 micrograms/l (49.3-96.9) in the steroid-treated group). IGF-1 declined with age in the control subjects but not in those taking steroids. When IGF-1 levels were correlated with biochemical indices of bone turnover, a significant relationship was found with urine hydroxyproline in the control subjects (r = 0.55, P less than 0.02) but not in those taking steroids. It is concluded that glucocorticoid therapy does not alter mean circulating levels of IGF-1 but that the growth hormone-somatomedin axis may influence bone turnover in normal subjects. Interference by glucocorticoids with the normal regulation of IGF-1 and its influence on bone turnover is suggested.

Adult↗
PubMed1988

Prevention of steroid-induced osteoporosis with (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (APD).

In a prospective, randomised, placebo-controlled trial comparing the effect of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (APD) (150 mg/day) plus calcium (1 g/day) with that of calcium alone on the bone mass of patients receiving long-term glucocorticoid therapy, the mean metacarpal cortical area in patients receiving APD increased by 1.2% between 0 and 6 months (p less than 0.06) and then remained stable between 6 and 12 months. In contrast, this index progressively declined in the placebo group (p less than 0.05 at 12 months). The two groups differed significantly in the changes at both 6 and 12 months (p less than 0.01). Mean vertebral mineral density, as measured by quantitative computed tomography, increased by 19.6% over 12 months in the APD group (p less than 0.02) but showed a non-significant decline of 8.8% in controls. The differences between the changes were again significant (p less than 0.005). Biochemical indices and bone histomorphometry indicated a reduction in bone resorption and bone formation but there was no evidence of osteomalacia. APD may thus prevent bone loss in glucocorticoid-treated patients over a year.

Calcium↗
PubMed1988

Aminobisphosphonate inhibition of interleukin-1-induced bone resorption in mouse calvariae.

Interleukin-1 (IL-1) is probably an important lymphokine mediator of inflammation and bone resorption. IL-1 derived from mononuclear cells, a melanoma cell line (MM96 cells), and recombinant human IL-1 (rHuIL-1 beta) increased in vitro bone resorption, as measured by the release of 45Ca from cultured mouse calvariae. The 50% maximum active resorption was observed with 0.125 ng/ml or approximately 10(-11) M rHuIL-1 beta. The resorptive action of IL-1 was not entirely dependent on prostaglandin mediation, since its effect was evident when prostaglandin synthesis was inhibited in the cultures by indomethacin. IL-1-induced resorption has been shown to be inhibited by 10(-5) M 3-amino-1-hydroxypropylidene-1-1-bisphosphonate (APD). This inhibition was partially reversed by increasing doses of IL-1. In vitro toxicity studies showed that at concentrations of 10(-4) M, APD inhibited the growth of cultured MM96, murine myelomonocytic P388D1, and rat osteosarcoma UMR 106 cells, but not other mast and lymphoid cell lines. These in vitro observations may have relevance to the use of APD in bone and joint diseases in which inflammation and bone resorption are prominent.

Animals↗
PubMed1988

Treatment of metastatic prostate carcinoma with the depot LRH analog Zoladex.

A long-acting LRH agonist (ICI 118630, Zoladex) was given by monthly subcutaneous injection to 25 patients with previously untreated symptomatic advanced prostatic carcinoma. The medication was well tolerated with the only side effect being hot flushes in 15 patients. Subjective improvement occurred in 22 patients, and disease remission or stabilization judged by objective criteria was seen in 21 and 18 patients from the total group at 3 and 6 months of treatment, respectively. Twelve of 18 patients followed for 1 year were still in objective remission/stabilization. Prostate volume measured by ultrasound decreased by a mean value of 75% and urine flow increased significantly. There were significant falls in serum testosterone and gonadotrophin levels and significant although lesser reductions in serum androstenedione and dehydroepiandrosterone. These changes were accompanied by significant reductions in serum acid and alkaline phosphatase and a rise in serum osteocalcin. Four patients (16%) experienced an initial tumor flare. Although only a small number of patients were studied, Zoladex appeared to be a well-tolerated agent for treatment of prostatic carcinoma, with an initial clinical response similar to that seen with standard endocrine therapy.

Adult↗
PubMed1988

Zoladex treatment of symptomatic prostatic carcinoma.

The depot LH-RH agonist Zoladex was used to treat 38 patients with previously untreated symptomatic stage D2 prostate carcinoma. Side effects were minimal and patient acceptability excellent, although temporary tumor flare occurred in 11% of patients. Eighty-four percent experienced subjective improvement and 87% had objective evidence of initial disease stabilization or remission lasting 3 months. Serum levels of gonadotrophin and free testosterone as well as androgens of adrenal origin fell significantly with treatment. Long-term survival to date appears at least as good as that described for conventional endocrine therapy.

Buserelin↗
PubMed1987

Evidence for decreased tubular reabsorption of calcium in glucocorticoid-treated asthmatics.

Fasting urine calcium excretion was measured in 15 asthmatic patients receiving long-term glucocorticoid therapy (steroid group) and in age- and sex-matched asthmatics not receiving these drugs. In the steroid group, the mean urinary calcium/creatinine ratio and the mean calcium excretion per liter of glomerular filtrate (CaE) were both approximately twice the control values (p less than 0.005). When CaE was plotted as a function of serum calcium it more often exceeded the mean normal value in the steroid-treated patients than in the controls (p less than 0.05), suggesting a reduction in tubular calcium reabsorption. Calculation of the tubular maximum for calcium reabsorption confirmed a significant reduction in the glucocorticoid-treated patients (p less than 0.005). It is concluded that glucocorticoid drugs probably inhibit the tubular reabsorption of calcium and that this is likely to contribute to the development of osteoporosis in patients receiving this treatment.

Asthma↗
PubMed1987

Radiological assessment of Paget's disease of bone after treatment with the bisphosphonates EHDP and APD.

The effects of therapy on the osteolytic bone lesions of Paget's disease have been assessed from serial bone radiographs. Changes in the rate of progression of lytic "wedge" lesions were measured and alterations in the texture of lytic "blade" lesions were graded on an empirical scale. Useful matching was possible using standard radiographs, although special care was needed to avoid artefacts from suboptimal positioning, magnification and variation in exposure. Serial radiographs were obtained of 57 lytic blade lesions in 54 patients receiving treatment with the bisphosphonate 1-hydroxyethylidene-1, 1-bisphosphonate (EHDP) and of 20 lesions in 20 patients treated with oral or intravenous 3-amino-1-hydroxypropylidene-1, 1-bisphosphonate (APD). Treatment with EHDP was associated with a significant deterioration in bone texture in 50% of lytic blade lesions, and with healing in only 20%. Deterioration was accompanied by an increase in local bone pain in 17% of these patients. In contrast, significant healing was observed in 17 of 20 lytic lesions (eight wedge, nine blade) within 6 months of beginning a course of intravenous or oral APD. In four of eight patients the progression of a lytic tibial wedge was arrested and in the remaining four the direction of wedge movement was reversed. In two patients the wedge had almost completely "filled in", making measurement difficult. Bone healing was usually accompanied by pain relief, reduction in skin temperature and rapid suppression of the urine hydroxyproline (uHP) into the normal range. However, in four patients who received intravenous APD, repair of lytic bone lesions was observed despite persisting elevation of uHP. These improvements with APD were sustained at 12 months, although in one patient whose biochemical indices were restored to normal the resorption front showed further progression, despite initial temporary reversal. The trends apparent in these short-term studies were also seen in four patients in whom wedge velocities were measured over periods of 6-10 years. These results confirm that after treatment of Paget's disease, bone healing or deterioration can be accurately assessed from serial standard radiographs. Reproducible matching is best achieved by ensuring that all radiographs are taken by the same radiographer. Minor alterations in radiological bone texture provide an important index of drug effect which is not always apparent from measurement of biochemical and other indices.

Aged↗
PubMed1986

Bone mineral content in Polynesian and white New Zealand women.

The forearm bone mineral content of Polynesian and European women in New Zealand was measured to assess whether the inter-racial differences found in other populations also occurred in these two groups. The bone mineral content of the nondominant distal radius and ulna was measured by single photon absorptiometry in 123 European and 80 Polynesian women. The mean values were about 20% higher in Polynesians than in Europeans. The reason for this difference in bone mineral content is unknown but the findings do show that high bone density is not confined to African races and that inter-racial differences in bone mineral content may be more common than has been thought hitherto.

Adolescent↗
PubMed1986

The effects of hydrocortisone, parathyroid hormone and the bisphosphonate, APD, on bone resorption in neonatal mouse calvaria.

The effects of hydrocortisone and parathyroid hormone (PTH) upon bone resorption rates in neonatal mouse calvaria have been studied. Bone resorption (measured as 45Ca release) was significantly increased by hydrocortisone (10(-7) M and 10(-6) M) and there was a dose-dependent rise with PTH (0.3-0.9 micrograms/liter). When both PTH 0.3 micrograms/liter and hydrocortisone 10(-8) M were present in the incubating medium, bone resorption did not differ from control, but increasing the hydrocortisone concentration to 10(-7) M augmented 45Ca release by 25% (P less than 0.02) and doubling of the PTH level was associated with a 10% increase (nonsignificant). When both PTH and hydrocortisone were present in the higher concentrations (0.6 micrograms/liter and 10(-7) M, respectively) 45Ca release increased by 39% (P less than 0.005) above that resulting from the lower levels of both hormones (0.3 micrograms/l and 10(-8) M, respectively). (3-Amino-1-hydroxypropylidene)-1,1-bisphosphonate (APD) in concentrations of 3 X 10(-5) M and 10(-4) M, produced inhibition of basal and hydrocortisone/PTH-stimulated bone resorption without evidence of toxicity. These results indicate that hydrocortisone stimulates bone resorption in neonatal mouse calvaria in vitro, in contrast to the results found in fetal rat bone culture systems. PTH has a similar effect, which is additive to that of hydrocortisone and the combined stimulation can be overcome by APD. The possible relevance of these results to the development and prevention of glucocorticoid-induced osteoporosis is discussed.

Animals↗
PubMed1986

The assessment of intestinal calcium absorption using stable strontium.

The availability of currently used methods of measuring intestinal calcium absorption is limited by their expense and complexity. Since this measurement may be important in selecting appropriate therapies for patients with osteoporosis, a simpler procedure is required. This paper describes a test which measures the intestinal absorption of stable strontium. A comparison of this test with the single-isotope radio-calcium absorption test in the same group of patients showed a close correlation between the fractional absorption rates of the two elements (r = 0.93, P less than 0.001). Subjects were correctly categorized as having normal or low absorption in 12 out of 13 cases (92%) and the value in the misclassified subject was at the borderline between normal and low calcium absorption. The convenience, low cost, and freedom from radioactivity of stable strontium make it suitable for routine clinical use and, if necessary, repeated testing. If these early results are confirmed, this test will make the assessment of calcium absorption much more widely available.

Aged↗
PubMed1986

Calcium supplements in the prevention of steroid-induced osteoporosis.

The long-term use of glucocorticoid drugs frequently results in the development of osteoporosis. To assess the value of calcium supplementation in preventing this loss of bone, the metabolic effects of administering 1 g of elemental calcium/day have been studied in 13 steroid-treated patients. After 2 mo, the fasting urine hydroxyproline-creatinine ratio decreased from 27.1 +/- 2.5 (SEM) to 21.8 +/- 2.4 (p less than 0.001) and there was an increase in fasting urine-calcium excretion (p less than 0.05). Serum alkaline phosphatase and osteocalcin showed no change. We concluded that calcium supplementation suppresses bone resorption without detectable suppression of indices of bone formation and is, therefore, likely to result in increased bone mass. The safety and low cost of calcium make it a very suitable prophylactic agent in glucocorticoid-treated patients.

Adolescent↗
PubMed1986

The acute biochemical effects of four proprietary calcium preparations.

Changes in serum and urine biochemical indices have been studied in ten normal subjects in the four hours following the ingestion of four proprietary calcium supplements. Each was taken in a dose containing 1 gram of elemental calcium. The four preparations were ranked according to the amount of calcium absorbed in the order Spar-Cal and Calcium Sandoz greater than Os-Cal greater than Ossopan. There were no significant differences between the four preparations in the changes in parathyroid hormone (PTH) and urine hydroxyproline levels. For this reason, the four results from each subject were averaged. Following the calcium load there was a reduction in mean PTH from 0.16 +/- 0.01 to 0.10 +/- 0.02 micrograms/l (p less than 0.001) and a decline in urine hydroxyproline/creatinine ratio from 20 +/- 1 to 17 +/- 1 (p less than 0.02), suggesting that bone resorption responds immediately to dietary calcium intake. There was a rise in urine sodium excretion which correlated with the indices of calcium absorption (r = 0.63, p less than 0.01) but not with the sodium content of the calcium preparations. This effect could be important, particularly in elderly patients on borderline sodium intakes.

Administration, Oral↗
PubMed1986

Low serum osteocalcin levels in glucocorticoid-treated asthmatics.

Serum osteocalcin (OC) levels were measured in 19 asthmatic patients receiving long term glucocorticoid therapy and in age- and sex-matched asthmatic patients not receiving this treatment. In the glucocorticoid-treated patients, the mean OC level was approximately 50% less than that in the control group (P less than 0.001), and there was a direct correlation between serum OC and 1,25-dihydroxyvitamin D [1,25-(OH)2D; r = 0.71; P less than 0.001]. Multiple regression analysis in a total of 39 glucocorticoid-treated patients indicated that OC correlated directly to 1,25-(OH)2D and inversely to glucocorticoid dose. There was no correlation between OC and 1,25-(OH)2D in the control group and no significant difference in mean serum 1,25-(OH)2D between the steroid-treated asthmatic patients and the asthmatic control patients. The effect of a 4-day course of oral 1,25-(OH)2D on serum OC was studied in six patients with glucocorticoid excess and six normal subjects. There was a similar percent increase in OC levels in both groups, though the basal concentrations and absolute increases were substantially less in the steroid-treated group. It is likely that the depression of serum OC in glucocorticoid-treated patients results from the reduction in the rate of bone formation induced by these hormones.

Administration, Oral↗