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Biomedical subjects

A McElduff

Publications and source records attributed to A McElduff.

At least 37 records · Page 2Linked to original sources
PubMed1998

People with mental retardation have an increased prevalence of osteoporosis: a population study.

Prevalence of and risk factors for osteoporosis in a community population of 94 young adults with mental retardation was examined. Results show lower bone mineral density in this group than in an age-matched reference population. Factors associated with low bone mineral density included small body size, hypogonadism, and Down syndrome in both genders and a high phosphate level in females. Low vitamin D levels were common in both genders, despite high levels of exposure to sunshine. A history of fracture was also common. Low bone mineral density and fracture were associated in females but not males. Because morbidity following fracture is likely to be more serious in this population, further investigation of osteoporosis and prevention strategies for both osteoporosis and fractures are important.

Adult↗
PubMed1995

Medical disorders of adults with mental retardation: a population study.

This study was conducted to determine the frequency of medical disorders in people with mental retardation. The prevalence of mental retardation among adults, ages 20 to 50 years, living in Northern Sydney, was determined, and 202 persons were randomly selected for medical examination. Compared to the local population, the study group had significantly increased cardiovascular risk factors, rate of medical consultation, rate of hospitalization, and mortality. The research sample had an average 5.4 medical disorders per person, half of which had not been detected previously. We concluded that the provision of health care to adults with mental retardation needs to be improved.

Adult↗
PubMed1994

A direct comparison of the measurement of a random plasma glucose and a post-50 g glucose load glucose, in the detection of gestational diabetes.

We have compared the use of a random plasma glucose measured within 2 hours of a meal and a plasma glucose measured 1 hour after a 50 g glucose load to detect pregnant patients likely to have an abnormal 100 g glucose tolerance test at 28 weeks' gestation. The 50 g glucose load detected 24 of 28 women with gestational diabetes whereas the random plasma glucose detected only 13 of these patients. The 50 g glucose load gave fewer false positives, that is, patients who had an abnormal screening test but went on to have a normal glucose tolerance test (8.8% versus 13.4%). These data support the use of the 50 g glucose load to screen pregnant women for gestational diabetes as recommended by Australian authorities (1).

Blood Glucose↗
PubMed1994

Premature ovarian failure and ovarian dysgenesis associated with balanced and unbalanced X-6 translocations, respectively: implications for the investigation of ovarian failure.

This study reports the effect of an inherited (X;6) translocation which has not previously been described. The proband was intellectually delayed and had ovarian dysgenesis. Karyotyping revealed an unbalanced karyotype: 46,X,der(X)t(X;6)(q22; p11.2)*. Her mother was shown to be a carrier of an apparently balanced translocation between the X chromosome and chromosome 6: 46,X,t(X;6)(q22;p11.2). This finding in the mother raises to 7 the number of cases reported which involve a break within the X chromosome 'critical region', at band Xq22, without causing ovarian dysgenesis, although it was associated with premature ovarian failure. These cases aim to highlight to clinical specialists the range of gonadal and other phenotypic anomalies (apart from those associated with Turner syndrome) which can occur due to partial deletions of the X chromosome. These findings have implications for the investigation of both ovarian dysgenesis and premature ovarian failure.

Adult↗
PubMed1992

Antiidiotypic PTH antibodies as a cause of elevated immunoreactive parathyroid hormone in idiopathic hypoparathyroidism, a second case: another manifestation of autoimmune endocrine disease?

A 69-year-old man became hypocalcemic under medical observation. The hypocalcemia occurred in the presence of circulating immunoreactive parathyroid hormone (PTH). Common causes of secondary hyperparathyroidism were excluded, as was PTH resistance using PTH infusions. The immunoreactive PTH was examined in detail. PTH immunoreactivity (1) was not retained on a C18 SPE-column, suggesting unusual molecular or physicochemical properties, unlike bona fide PTH; (2) was precipitated with 15% PEG, indicating a molecular size far in excess of native PTH; (3) had an apparent molecular size similar to immunoglobulins on size exclusion chromatography; (4) was retained on affinity chromatography with both Protein A and anti-hIgG antibodies. These data lead us to conclude that the immunoreactive PTH was due to antiidiotypic PTH autoantibodies. No significant quantities of true PTH were found in the patient's serum suggesting that his hypoparathyroidism was a result of PTH deficiency. Autoimmunity might explain the occurrence of both processes if an arrested antiidiotypic antibody cascade is assumed.

Aged↗
PubMed1992

Primary hypothyroidism with pituitary enlargement and a visual field abnormality.

A 23 year old man presented with classical hypothyroidism of 9 years duration. This was associated with pituitary enlargement, documented on magnetic resonance imaging (MRI), and abnormal half-field visual evoked responses (VERs). Following the initiation of thyroxine therapy the pituitary enlargement and the VER abnormalities resolved. The final diagnosis was of primary hypothyroidism with secondary pituitary hyperplasia.

Adult↗
PubMed1992

Does Graves' disease or thyrotoxicosis affect the prognosis of thyroid cancer.

Twenty-one patients who underwent surgical treatment for thyrotoxicosis and who were found at operation to have thyroid cancer are presented. Sixteen had Graves' disease and 5 had toxic nodular goiter. The group with Graves' is compared with 110 euthyroid patients with thyroid cancer who underwent their initial surgery in the same time period and who were of the same age (+/- 1 yr) and sex as the patients with Graves' disease. None of the thyrotoxic patients died during follow-up of 2-24 yr or developed subsequent metastases. The 1 patient with a local lymph node metastasis has not shown evidence of recurrence. Hypoparathyroidism appeared as a complication in only 1 patient. The size of tumors in the patients with Graves' disease was significantly smaller than in the euthyroid group. The course of the disease in both the patients with Graves' disease and the thyrotoxic group as a whole was relatively benign. This series does not support the recent suggestions that thyroid cancer in patients with Graves' disease is more aggressive than in either patients with toxic nodular goiter or euthyroid subjects. Patients with Graves' disease and thyroid cancer should be treated identically to other patients with thyroid cancer. Therapy should consist of total thyroidectomy followed by a postoperative 131I scan. Residual tissue or metastases found on the scan should be ablated with 6 GBq 131I. The patient should receive a suppressive dose of T4.

Adult↗
PubMed1991

Longitudinal changes in forearm bone mineral content in primary hyperparathyroidism.

Forearm bone mineral content was measured in 28 patients with primary hyperparathyroidism before and 1 year after successful parathyroidectomy. The forearm bone mineral content rose from a mean value of 1.068 to 1.092 g/cm (P less than 0.05, paired t-test). Those patients with the lower initial values had the largest rise. In an additional study, the forearm bone mineral content was measured in 10 women over the age of 40 years (mean age 58.6 +/- 7.9SD years) with hyperparathyroidism before and for 2 years after successful parathyroidectomy and compared with the forearm bone mineral content measured over 2 years in 12 women (mean age 56.3 +/- 5.5SD years) with continuing hyperparathyroidism and with the forearm bone mineral content of 12 eucalcemic control women (mean age 58.8 +/- 8.2SD years), also measured over 2 years. The parathyroidectomized group gained bone, whereas the ongoing hyperparathyroid group and the eucalcemic control group lost bone. The difference between the parathyroidectomized group and the ongoing hyperparathyroid group was significant after 2 years (P less than 0.05). The percentage loss of forearm bone mineral in the eucalcemic control subjects was not significantly different from the percentage loss of forearm bone mineral in the ongoing hyperparathyroid group, although the initial mean bone mineral content in the eucalcemic group was significantly higher than in the ongoing hyperparathyroid group, suggesting that a possible determinant of bone mineral loss in women in this age group is the initial bone mineral content.

Adult↗
PubMed1990

Insulin sensitizes a cultured rat osteogenic sarcoma cell line to hormones which activate adenylate cyclase.

Pretreatment of the osteogenic sarcoma cell line UMR-106-01 with insulin results in sensitization to both parathyroid hormone (PTH) and isoproterenol. In insulin-pretreated cells, the two hormones cause a significantly greater cyclic AMP (cAMP) accumulation than in noninsulin-treated cells. In the presence of cholera toxin, which enhances cAMP production by these cells in both the basal and PTH-stimulated state, the effect of insulin is maintained. In the presence of pertussis toxin, which has no effect on basal cAMP accumulation but enhances both PTH and isoproterenol stimulation, insulin sensitization for both hormones is abolished. These data suggest that insulin sensitizes these cells to subsequent hormone stimulation by lessening the action of an inhibitory guanine nucleotide regulatory protein, possibly Gi.

Adenylate Cyclase Toxin↗
PubMed1990

Medroxyprogesterone induced Cushing's syndrome.

A 74-year old female taking medroxyprogesterone acetate (MPA) presented with Cushing's syndrome together with low serum cortisol and plasma ACTH and an impaired response to synthetic ACTH (Synacthen, CIBA). When the medroxyprogesterone therapy was ceased the cushingoid features resolved and serum cortisol, ACTH and ACTH responsiveness all returned to normal. The MPA was acting as an exogenous glucocorticoid causing Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMed1990

Parathyroid hormone sensitivity in primary hyperparathyroidism and idiopathic hypercalciuria: effects on postadenylate cyclase parameters.

We performed 6-h human PTH-(1-34) infusions in 8 control subjects, 10 subjects with primary hyperparathyroidism, and 7 men with idiopathic hypercalciuria. We measured serum calcium, serum 1,25-dihydroxyvitamin D, urinary calcium, and fractional phosphate excretion. The PTH-induced rise in serum 1,25-dihydroxyvitamin-D was significantly smaller in the hyperparathyroid patients than in either the controls or the hypercalciuric patients. The rise in serum calcium was similar in all 3 groups. The hyperparathyroid subjects had higher basal fractional phosphate excretion than the other two groups. PTH failed to increase fractional phosphate excretion in the hyperparathyroid individuals, whereas there was a statistically significant increase in the other two groups. PTH was without significant effect on urinary calcium excretion in any of the three groups. There were no discernible differences between the responses of the hypercalciuric patients and those of the normal subjects. These findings suggest that while responses to PTH are normal in hypercalciuria, some hyperparathyroid patients are resistant to exogenous PTH. This resistance is limited to specific arms of the PTH response pathway and may not involve PTH receptors.

Adenylyl Cyclases↗
PubMed1990

Spontaneously occurring antibodies to parathyroid hormone.

A 76-yr-old female with acute pancreatitis and a normal/borderline elevated serum calcium level was found to have an elevated immunoreactive circulating PTH concentration using a C-terminal assay. This high PTH concentration misled the attending physicians and resulted, in retrospect, in an unnecessary neck exploration. When the patient's serum was examined it was found to contain a binding component that bound both C-terminal and PTH-(1-84). This binding component was not retained on a Sep-Pak column and was precipitated by antiserum directed against human immunoglobulin M. The presence of circulating anti-PTH immunoglobulin M explains the apparently high PTH concentrations measured by RIA. The antibodies occurred spontaneously. To the best of our knowledge, this phenomenon has not previously been described.

Acute Disease↗
PubMed1989

Familial hypoparathyroidism due to an abnormal parathyroid hormone molecule.

The case of a 53-year-old man with familial hypoparathyroidism in the presence of circulating immunoreactive PTH is discussed. The patient responded to exogenous PTH by an increase in urinary cAMP excretion and by several post cyclase parameters including an increase in serum calcium and 1,25-dihydroxyvitamin D, an increase in urinary phosphate excretion and a decrease in urinary calcium. Immunoreactive PTH was detected in this patient's serum by three separate anti-PTH antisera. This immunoreactive PTH behaved aberrantly with these antisera. Nonparallelism to the standard curve was seen in two radioimmunoassays and the material was detected by an antiserum which preferentially binds bovine PTH. No circulating PTH binding activity was detectable. Family studies confirmed the genetic nature of the abnormality. HPLC studies revealed the presence of an abnormally hydrophobic fraction containing immunoreactive PTH. We believe these findings constitute strong evidence for the presence of an abnormal PTH molecule with reduced biological activity resulting in hypoparathyroidism.

Adult↗
PubMed1989

Insulin promotes growth of the cultured rat osteosarcoma cell line UMR-106-01: an osteoblast-like cell.

The rat osteogenic sarcoma subclone UMR-106-01 is a cell type with osteoblast-like properties. This cell line has been shown to process specific receptors for insulin and insulin-like growth factor I (IGF-I), but not IGF-II. Insulin at physiological concentrations (1-5 ng/ml) in serum-free medium can maintain cell growth, as assessed by protein accumulation, thymidine uptake, and an increase in cell number. IGF-I is less potent than insulin, but, based on relative binding affinities for the insulin receptor, possibly acts via its own receptor. Insulin also enhances PTH-stimulated cAMP accumulation in these cells both by increasing cell number and an effect independent of cell number. Insulin may have a role in bone homeostasis.

Animals↗