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Biomedical subjects

M Kleerekoper

Publications and source records attributed to M Kleerekoper.

At least 109 records · Page 6Linked to original sources
PubMed1981

Acute severe hypercalcemia in a la Münchausen.

A 51 year old nurse had a long complicated medical history with repeated medical and surgical interventions. Her condition fits the clinical description of the Münchausen syndrome. She presented to the hospital with hyperabsorptive hypercalcemia of over 20 mg/100 ml. Many diagnostic studies and intriguing detective investigations were undertaken before the cause of the extreme hypercalcemia was determined. The patient had been secretly ingesting between 20 and 30 Os-Cal 500 tablets daily which she repeatedly denied and which eventually were found in a false compartment of her purse. This is thought to be the highest recorded serum calcium level observed following the clandestine ingestion of excessive amounts of oral calcium.

Acute Disease↗
PubMed1980

Hyperparathyroidism following head and neck irradiation.

A history of head and neck irradiation in childhood or adolescence was found in 22 of 130 patients with primary hyperparathyroidism compared with only 12 of 400 control patients, a significant difference (P less than .025). Among 200 patients with a known history of childhood irradiation, biochemical or surgical evidence of hyperparathyroidism was found in ten, a prevalence of 5%. This is at least 30 times the prevalence of hyperparathyroidism in the general population (P less than .025). The data indicate that head and neck irradiation should be regarded as an important risk factor in the subsequent development of hyperparathyroidism.

Adenoma↗
PubMed1978

Idiopathic multicentric osteolysis. Report of an affected father and son.

Genetic, rheumatologic, immunologic, metabolic, and renal studies of a father and son with idiopathic multicentric osteolysis are reported. The disorder appeared through mutation. The father developed symptoms as an infant, his son at age 4 years and 9 months. Both have micrognathia and hypotelorism and were exceptionally tall during the symptomatic phase of their disease. Biopsies of the son's wrist showed normal synovium, encroachment on cartilage by fibrocellular tissue, and both osteoclastic resorption and repair of affected bone. Hydroxyproline in his urine was increased. No immunologic, renal, or other metabolic abnormalities were identified.

Adult↗
PubMed1977

Hypercalcemic hyperparathyroidism in hypophosphatemic rickets.

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.

Adolescent↗
PubMed1975

Hyperparathyroidism after renal transplantation.

Renal transplantation reduced circulating parathyroid hormone in recipients of renal allografts. Nevertheless, biochemical and histological evidence of mild hyperparathyroidism persisted up to eight years after renal transplantation despite good graft function.

Bone and Bones↗
PubMed1975

Effects of sodium depletion on plasma renin activity and on the urinary excretion of cyclic AMP and aldosterone in hypoparathyroid patients.

The effect of sodium depletion on plasma renin activity (PRA), urinary cyclic AMP and urinary aldosterone excretion was studied in hypoparathyroid patients whose basal urinary cylic AMP excretion (urinary cAMP) was less than 50% of that observed in normal subjects. During 7 days of sodium depletion, PRA, urinary aldosterone and urinary cAMP each rose significantly. Administration of the beta-blocker propranolol, 160 mg/day, during 5 further days of sodium depletion produced a fall in PRA and urinary cAMP, but no change in urinary aldosterone excretion. The dissociation in these effects suggests that the increase in aldosterone secretion during sodium depletion may be mediated by pathways other than the renin-angiotensin and adenyl cyclase systems. There was a high degree of correlation between PRA and urinary cAMP (P less than 0.001) during the period of sodium depletion, but not significant relationship between these parameters was found during control and propranolol phases, or in control studies in normal subjects. These findings suggest that beta-adrenergic receptors have a role in mediating the effects of sodium depletion upon renin secretion and adenyl cyclase activity.

Adult↗