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Biomedical subjects

C Rudberg

Publications and source records attributed to C Rudberg.

32 records · Page 2Linked to original sources
PubMed1987

Patients with primary hyperparathyroidism operated on over a 24-year period: temporal trends of clinical and laboratory findings.

Temporal trends of clinical and laboratory data of 441 patients operated upon for primary hyperparathyroidism (HPT) during 1956-1979 were analysed retrospectively. There was a marked increase in the number of operations for HPT during that time period, from 32 during 1956-1964 to 326 in 1970-1979. In parallel there was a decrease in the proportion of patients with classical manifestations of HPT such as renal stones or bone disease, the latter being on the whole rarely seen in this population. The increased number of operations was instead largely attributable to the more frequent diagnosis of HPT in patients with vague psychiatric or neuromuscular symptoms or with no clinical manifestations; the majority of these persons were older women, the proportion of operations in women 45 years of age or older, increasing from 56% during 1956-64 to 71% during 1970-79. The increased number of operations for HPT during the last decades should be mainly the consequence of a greater awareness of the disease.

Adenoma↗
PubMed1987

Parathyroid hormone release in vitro in hyperparathyroidism associated with multiple endocrine neoplasia type 1.

Hyperparathyroidism (HPT) in the syndrome of multiple endocrine neoplasia type 1 (MEN-1) exhibits a different picture regarding its propensity for recurrence compared with sporadic primary HPT. In order to shed further light on the MEN-1 syndrome an investigation in vitro was made of parathyroid hormone (PTH) release of dispersed parathyroid cell from 11 patients with parathyroid hyperplasia associated with MEN-1, 10 patients with single parathyroid adenomas, and 10 preparations of normal bovine parathyroid glands. The two patient groups had the same average serum calcium value prior to surgery. Immunoreactive concentrations of PTH were measured after 2-h incubations at extracellular calcium concentrations of 0.5-3.0 mmol/l. Compared with the normal bovine parathyroid cells, the cells of the MEN-1 patients had a reduced calcium sensitivity of the PTH release and secreted smaller amounts of hormone at both low and high extracellular calcium concentrations. A similar abnormality of the PTH release was found for the cells of the hyperplastic and adenomatous parathyroid glands. Although individual parathyroid glands were investigated in only three MEN-1 patients, the results suggested the secretory regulation to be less defective in the small glands of each patient. It is concluded that in patient groups matched for serum calcium, the parathyroid tissue of MEN-1 patients has an abnormality of the PTH release similar to that of parathyroid adenomas.

Adenoma↗
PubMed1986

Histologic parathyroid abnormalities in an autopsy series.

The parathyroid glands from 422 subjects without clinical, biochemical, or advanced histologic signs of renal disease were dissected at autopsy. The glands were evaluated histologically in relation to the subjects' age, sex, histologic renal features, other diseases, and medical therapy. Normal parathyroid glands generally had diffuse cellular arrangements, with variable fat cell content. Increased nodularity was observed, especially in enlarged parathyroid glands. Hyperplasia was present in 7 per cent and adenomas in 2.4 per cent. Hyperplastic glands were often nodular and asymmetric, and numbers of oxyphil cells were frequently increased. Some large nodules were histologically indistinguishable from adenomas. Serum calcium levels were elevated in subjects with adenomas or with hyperplastic glands containing large nodules. The findings seem to indicate that nodularity of the parathyroid tissue is a sign of abnormality and that adenomas may arise from such nodular hyperplasia. Hyperplasia and adenomas were more common in elderly subjects and in those with slight or moderate nephrosclerosis. Other diseases or medical therapy were not found to be correlated with parathyroid weight or histologic features.

Adolescent↗
PubMed1986

Alteration in density, morphology and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism.

Dispersed parathyroid cells from normal human and bovine glands and from 10 patients with primary (7 adenomas, 3 hyperplasias) and 4 patients with uraemic hyperparathyroidism (HPT) have been investigated with respect to density, morphology and parathyroid hormone (PTH) release. Percoll density gradients enabled an efficient isolation of viable parathyroid cells which generally banded between 1.035-1.090 g/ml. The average density was significantly higher in cells from the normal than the abnormal glands. The pathological glands contained large chief cells, oxyphil and transitional oxyphil cells and, in one case, water-clear cells which were enriched in fractions with densities below 1.055 g/ml. Measurements of cell diameters revealed an increased proportion of enlarged cells in the preparation of abnormal glands. Nuclear diameters were similar in the normal human glands, adenomas and hyperplasias, but the variability was greater among the adenomas. In comparison to normal bovine parathyroid cells, PTH release of cells from the pathological human glands was reduced and abnormally insensitive to extracellular calcium. The oxyphil and water-clear cells secreted similar amounts of PTH as the chief cells of the abnormal glands. The disturbed PTH release in secondary HPT seemed to be confined mainly to cells within nodules of the hyperplastic glands. The results show that the disturbed hormone regulation in HPT is related to morphological changes of the cells and that buoyant density gradients can be used to accumulate the abnormal cells.

Adenoma↗
PubMed1986

Late results of operation for primary hyperparathyroidism in 441 patients.

The late results of operation for primary hyperparathyroidism (HPT) were analyzed in 441 patients operated on 4 to 27 years earlier (mean follow-up time, 7.7 years). A conservative surgical approach was mainly used, attempting if possible to visualize all four parathyroid glands and extirpate only the enlarged glands. Subtotal resection was performed in patients with hyperplasia. The histopathologic diagnosis was adenoma in 77% and hyperplasia in 18%. In 5% of the patients, the histopathologic classification was uncertain. Hypercalcemia persisted after operation in 8% of all patients. This generally occurred because of an incomplete neck exploration or too limited a resection in the patients with hyperplasia. Recurrent hypercalcemia occurred in 16% of the patients operated on for hyperplasia and was noted 1 to 19 years after surgery. Recurrences were also seen in 3% of the patients with adenomas but not earlier than 9 years after the operation. These findings suggest that primary HPT may even in patients with adenomatous disease, sometimes affect all parathyroid glands. Nevertheless, it was obvious that most of the patients with adenomas would not have benefited from a more radical procedure. On the other hand, it was evidently important to obtain a correct histopathologic diagnosis intraoperatively so that patients with hyperplasia could be identified and adequatley treated.

Adenoma↗
PubMed1984

Effects of epinephrine and norepinephrine on serum parathyroid hormone and calcium in normal subjects.

Infusions with stepwise increasing concentrations of epinephrine (from 2.5 to 10 micrograms/min) and norepinephrine (0.5-2.0 micrograms/min) were given to normal subjects. During infusion of epinephrine there was a clear rise of the serum parathyroid hormone (PTH) levels already at the lowest concentration. Concomitantly there was a fall in the serum concentrations of calcium. The PTH levels returned to baseline promptly after termination of infusion whereas hypocalcaemia persisted up to 30 minutes, indicating a primary response of PTH to epinephrine. When propranolol was given prior to and during the epinephrine infusion no significant changes occurred for either PTH or calcium. During infusion of norepinephrine no consistent significant changes were noted for either PTH or serum calcium. Thus, our data do not support any concept of a basal adrenergic tone which normally modulates the secretion of PTH. However, during conditions of stress the beta-adrenergic stimulation night be of importance.

Adult↗
PubMed1984

Effects of 1,25- and 24,25-dihydroxycholecalciferol on parathyroid hormone release from human parathyroid cells in vitro.

The effects of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure. The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2-16 h. There was a gradual suppression of PTH release (5-55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo. Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Ultrasound scanning for preoperative location of parathyroid tumours.

Ultrasonic examination of the parathyroid glands has been used in 50 consecutive patients with surgically verified hyperparathyroidism. It revealed 21 of 32 parathyroid adenomas located in the neck. In 16 patients with primary or secondary (uraemic) hyperplasia, 11 out of 48 hyperplastic glands in the neck were identified by ultrasound. A parathyroid adenoma was revealed in all (3) patients with hypercalcaemic crisis. Enlarged parathyroid glands were correctly located in all (5) patients with adenomas and previous explorations of the neck, whereas two out of three glands were visualized by ultrasound prior to secondary explorations in 3 patients with hyperplasia associated with the multiple endocrine neoplasia syndrome type 1. Undetected parathyroid glands were generally smaller than those visualized by ultrasonic examination. It was often difficult to unequivocally establish that identified lesions represented parathyroid glands. Irregular noduli and cysts of the thyroid as well as lymph nodes could be misinterpreted as parathyroid lesions. A nodular thyroid goitre was present in almost half of the patients with a negative ultrasonic examination of the parathyroid glands.

Adenoma↗
PubMed1982

Effects of beta-adrenergic blockade on serum parathyroid hormone in normal subjects and patients with primary hyperparathyroidism.

Recent experimental studies suggest that the autonomous nervous system can effect the secretion of parathyroid hormone (PTH) and that these effects could be of physiological importance. The short-term effects of propranolol were investigated in 13 patients with primary hyperparathyroidism (HPT) and 6 normal subjects. During a 2-hour infusion there were no changes in serum PTH or calcium concentrations in any of the individuals studied. During long-term treatment of HPT patients with beta-blocking agents for 2-6 months no reduction or raised PTH levels was detected and the hypercalcaemia was unaffected. These findings question the importance of the adrenergic system for the normal regulation of serum PTH levels and its role for hormone hypersecretion in primary HPT. Our experience does not support the use of propranolol as an alternative to surgery in patients with primary HPT.

Adrenergic beta-Antagonists↗
PubMed1982

Treatment with cimetidine in patients with primary hyperparathyroidism.

Treatment with cimetidine (1000 mg daily in four divided doses) was given for 3--30 weeks to 10 patients with primary hyperparathyroidism (HPT). All patients had hypercalcaemia and raised serum concentrations of parathyroid hormone (PTH). During treatment no consistent effects were noted on neither serum calcium or PTH and normalization did not occur in any case. Hypergastrinaemia was demonstrated in 6 patients and was also unaffected by therapy while in the 4 patients with normal pre-treatment gastrin values a slight increase was seen. This study does not support the view that cimetidine can be of use for the treatment of primary HPT.

Adult↗
PubMed1982

Regulation of parathyroid hormone release in primary and secondary hyperparathyroidism - studies in vivo and in vitro.

The effects of calcium on parathyroid hormone (PTH) release were studied in vivo and in vitro in primary hyperparathyroidism (HPT) and in vitro in secondary HPT. In vivo the serum PTH was clearly reduced by intravenous calcium infusion in all the examined patients with primary HPT caused by adenoma. In vitro the release of PTH from dispersed parathyroid cells was likewise suppressed by raising the calcium concentrations in the incubation media, though in all cases a basal release of PTH still persisted even at high calcium concentrations. The degree of suppressibility in vitro varied, but in both primary HPT with adenoma and in secondary HPT it was inversely related to the patients' serum calcium values. These results suggest that the secretion of PTH in patients with primary and secondary HPT is not autonomous either in vivo or in vitro. Furthermore, the non-suppressible basal release of PTH indicates that a major cause for the increased secretion of PTH is the increased number of parenchymal cells. However, the degree of suppressibility of the individual cells rather than the absolute number of cells, seems to be of great importance for the individual serum calcium values in HPT.

Adenoma↗
PubMedDate not supplied

Causes of failed primary exploration and technical aspects of re-operation in primary hyperparathyroidism.

Hypercalcemia was corrected in 62 (90%) of 69 patients after re-operation for primary hyperparathyroidism during a mean follow-up of 6.3 years. Failed primary exploration was mainly due to inadequate visualization of the pathological parathyroid glands, often in association with misleading or absent peroperative histology. Other causes included seeding of parathyroid adenoma tissue, truly recurrent adenomas, and recurrent hyperplasia, especially in patients with multiple endocrine neoplasia type 1. A considerable number of parathyroid glands missed at the primary operations were subsequently found in essentially normal positions. Ectopic superior glands were most frequently positioned para-esophageally or retro-esophageally, while abnormally placed inferior glands were generally situated within or close to the thymus. Glands in 3 patients were dissected from around the large vessels in the mediastinum. Concomitant thyroid procedures during the primary operation yielded few abnormal parathyroids and made the re-exploration considerably more difficult. We suggest a semilateral approach and caudal identification of the recurrent laryngeal nerve to reduce the hazards of difficult parathyroid re-operations. Mediastinal exploration may require total removal of the thymus and careful dissection of the middle mediastinum.

Adult↗