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Biomedical subjects

K L Becker

Publications and source records attributed to K L Becker.

At least 91 records · Page 5Linked to original sources

Calcitonin as a marker for bronchogenic cancer: a prospective study.

A prospective study was done of serum calcitonin (HCT) levels in 61 patients with bronchogenic cancer. Initially, 52% of patients had hypercalcitonemia. Hypercalcitonemia was not confined to patients with any particular histologic type. Seventy-eight percent of those with high calcitonin remained normocalcemic. There was no correlation between high calcitonin levels and osseous metastases. Selective thyroid venous sampling delineated two types of hypercalcitonemia: thyroidal and ectopic. To date, the ectopic type has been associated with the small cell bronchogenic carcinoma. High initial calcitonin levels decreased significantly in 75% of patients on antitumor therapy. In 13 evaluable patients calcitonin levels mirrored clinical status changes 67% of the time. Calcitonin may be a useful marker to assess the results of therapy in patients with bronchogenic cancer.

Bone Neoplasms↗

Effect of thiazides on serum calcium.

A retrospective study of 22 hypertensive patients who were treated with thiazide diuretics for 2 to 12 yr revealed that 36% developed transient, self-limited asymptomatic elevations of serum calcium which occurred at varying periods of therapy and returned to normal within 2 to 4 wk despite continued administration of thiazides. These episodes of hypercalcemia correlated positively with increases in total protein, albumin, and globulin. The same phenomenon of intermittent hypercalcemia occurred in a prospective study of 11 patients but not in control subjects. The mean serum total calcium of the prospectively studied hydrochlorothiazide-treated patients was found to be higher than the nonthiazide control group. This difference was due to increased protein-bound calcium. The total proteins, serum albumin, and serum beta globulins of the treated group were higher, probably due to depletion of extracellular fluid. The presence of slightly elevated serum calcium in a patient treated with thiazides appears to be a common phenomenon and, unless it is marked, should not necessarily be construed as indicating covert hyperparathyroidism.

Adult↗

Urine calcitonin as a test for medullary thyroid cancer: a new screening procedure.

Although the radioimmunoassay of serum calcitonin (CT) has facilitated the diagnosis of medullary thyroid cancer (MTC) one may encounter patients whose basal serum levels of CT are normal or nearly normal. In such cases clinicians have utilized intravenous stimulation tests such as calcium or pentagastrin to obtain a diagnostic increase in serum CT. We have reported finding immunoreactive CT in the urine of man and have found it to be a useful technique for the diagnosis and study of patients at risk for MTC or other hypercalcitonemic diseases. Using basal urine CT alone we were able to separate 73% of patients at risk for MTC into clearly normal or abnormal groups. For the remaining 27% a stimulation test with subsequent determination of urine CT was required. The radioimmunoassay of urine CT is a simple, reliable, accurate test for the screening diagnosis of MTC. A protocol for the screening workup of a patient at risk for MTC is given.

Adolescent↗

Calcitonin in extrathyroidal tissues of man.

Prior studies have demonstrated detectable immunoreactive calcitonin in the serum and urine of totally thyroidectomized humans, suggesting that the hormone may be secreted by extrathyroidal tissues. Accordingly, a study of the immunoreactive calcitonin content of human tissues was undertaken, utilizing autopsy material from 23 patients. Significant amounts of calcitonin were found in many extrathyroidal tissues, ranging up to 40 ng/g wet weight. The hormone was detectable with two antibodies having different region specificities for calcitonin. Gel filtration and subsequent radioimmunoassay demonstrated that extrathyroidal tissue has calcitonin fractions of the same molecular size and charge characteristics as do the serum and thyroid. The finding of large amounts of extrathyroidal calcitonin may explain why thyroidectomy in man is not accompanied by marked changes in calcium metabolism.

Adolescent↗

Salmon calcitonin in hypercalcemia.

We have undertaken a study of 24 hypercalcemic patients with the use of salmon calcitonin as a therapeutic agent. Seventy-five percent of the patients exhibited a clinically significant decrease in serum calcium and approximately half became normocalcemic within 2 hr. Throughout salmon calcitonin administration, the mean serum calcium of the patients was lower than the pretreatment values. Although the drug did not always lower the calcium level to normal, it often brought the hypercalcemia to more tolerable levels. During the course of calcitonin therapy, the number of patients with normal or near-normal serum calcium ranged from 31.3% (at 96 hr) to 82.4% (at 30 hr). Many of the patients improved symptomatically. The only significant side effects were nausea and vomiting in 12.5% of the patients, which necessitated cessation of therapy in only one. The drug was well tolerated in patients with azotemia. Calcitonin-induced hypocalcemia was not encountered. Salmon calcitonin can be used safely alone or in conjunction with other hypocalcemic therapies.

Aged↗

Calcitonin heterogeneity in lung cancer and medullary thyroid cancer.

An investigation was made of the increased serum calcitonin in patients with medullary thyroid cancer and bronchogenic carcinoma in order to determine whether these conditions can be differentiated immunochemically. Exdogenous fractions of immunoreactive calcitonin were separated by gel filtration and radioimmunoassayed with calcitonin antibodies having different region specificities. The pattern of serum heterogeneity of patients with medullary thyroid cancer was characterized by the presence of at least seven different fractions of immunoreactive calcitonin, ranging from fraction I (greater than or equal to 30 000 molecular weight (MW) to fraction V (approximately 2500 MW). In contrast, most patients with bronchogenic cancer had a predominance of high MW fractions (i.e. fractions I and IIA). Following in vitro incubation of the serum, the typical MW pattern of bronchogenic cancer serum could be converted to the more diffuse pattern seen in the serum of medullary thyroid cancer. We were able to differentiate, pre-operatively, the hypercalcitonaemia serum of medullary thyroid cancer patients from that of bronchogenic cancer patients by determination of the ratio of calcitonin as radioimmunoassayed with midportion versus carboxyl terminal antibody.

Calcitonin↗

Immunochemical heterogeneity of calcitonin in man: effect on radioimmunoassay.

Determinations of blood levels of human calcitonin by radioimmunoassay have varied considerably in different laboratories. Much of the controversy over calcitonin levels can be attributed to the multiplicity of immunoreactive forms of the hormone (iCT), the differing region specificities of the antisera utilized for measurement by radioimmunoassay, protein effects, different rates of degradation of the various iCT fractions and the specific methodology of the radioimmunoassay.

Antibody Specificity↗

Calcitonin levels in chronic renal disease.

High levels of serum calcitonin were found in patients with chronic renal failure. Serum calcitonin correlated directly with the phosphate to total calcium ratio; calcitonin levels correlated inversely with serum calcium in those patients on dialysis and directly with serum calcium in nondialysis patients. All patients had elevated serum gastrin. The high levels of serum calcitonin usually decreased following successful kidney transplantation. The pathophysiology of this hypercalcitonemia and its relationship to renal osteodystrophy and the disordered calcium metabolism of uremia remains to be elucidated.

Adult↗

Increased serum calcitonin levels in bronchogenic cancer.

A study of 26 men with bronchogenic cancer demonstrated high serum calcitonin levels in 62 percent (16). Levels were particularly high in patients with small-cell cancer and adenocarcinoma. Two varieties of hypercalcitonemia have been encountered: (1) ectopic hypercalcitonemia, in which the hormone is secreted by the tumor, and (2) thyroidal hypercalcitonemia, in which the high values emanate from the thyroid gland. In several patients, serum calcitonin levels decreased following therapy for the cancer. Further studies are needed to evaluate the diagnostic value and clnical utility of serum calcitonin levels as a marker substance in bronchogenic cancer.

Adenocarcinoma↗

Hypercalcitonemia in bronchogenic cancer. Evidence for thyroid origin of the hormone.

Retrograde venous catheterization in a hypercalcitonemic patient with adenocarcinoma of the lung demonstrated that the thyroid gland was secreting a very large amount of hormone (14-fold higher than the peripheral level), while the venous drainage from the tumor deposits was similar in concentration to that of the periphery. Conceivably, the calcitonin is being elaborated in response to metastatic and humoral bone resorption or both. Radiotherapy resulted in a decrease in the calcitonin level. Further studies are needed to determine the diagnostic or prognostic implications of serum calcitonin in bronchogenic cancer.

Calcitonin↗

The effects of zinc on ectopic bone formation.

The effect of dietary zinc deficiency was studies in ectopic bone formation subsequent to Achilles tenotomy and also following the implantation of demineralized bone matrix in the muscle of rats. Three experiments were performed. The first was designed to investigate the relationship between zinc and calcium concentration during the formation of ectopic bone in rats fed a commercial laboratory ration, the second concerned the effects of dietary zinc deficiency on ectopic bone formation, and the third studies the subsequent effects of dietary zinc repletion on ectopic bone formation. The results indicated that, with the commercial ration, zinc increased concomitantly with calcium during ectopic bone formation in rats. Dietary zinc deficiency caused a retardation of ectopic bone formation and a significant reduction of in situ zinc and calcium concentration. Dietary zinc repletion to zinc-deficient animals restored the zinc concentration in ectopic bone to a level comparable to that of zinc-sufficient animals. Thus, these experiments present strong evidence that zinc plays an active role in bone metabolism.

Abdomen↗

In vitro studies of calcitonin release in man.

The influence of various agents on calcitonin release from human thyroid was studied in vitro. Under the condition of this investigation, calcium, magnesium and phosphate did not stimulate calcitonin release from short-term incubated slices of human thyroid. However, pentagastrin and USP glucagon were potent stimulators of calcitonin release. Theophylline and dibutyryl cyclic AMP were also potent stimuli. A highly purified preparation of pancreatic glucagon was without an effect. Those agents which stimulated calcitonin release were associated with augmented cyclic AMP accumulation. Although maximal discharge of calcitonin required the presence of calcium, out in vitro experiments raise the question as to whether a gastrointestinal hormone, rather than calcium, might not be the principal agent affecting calcitonin release.

Bucladesine↗

Paradoxical effect of salmon calcitonin on serum calcium: studies in intact and thyroparathyroidectomized men and dogs.

Total serum calcium of normal men, a hypoparathyroid man, two thyroparathyroidectomized men, and intact and thyroparathyroidectomized dogs were studied at multiple intervals following the acute administration of synthetic salmon calcitonin. Calcitonin produced marked fluctuations in serum calcium in one normal man and a biphasic hypocalcaemic response in another. In four of five intact dogs, calcitonin caused absolute or relative hypercalcaemia. In contrast, administration of calcitonin to thyroparathyroidectomized dogs caused a hypocalcaemia with less fluctuations and with no periods of hypercalcaemia. It is possible that some of the paradoxical responses of serum calcium induced by exogenous calcitonin are due to overcompensation by parathyroid hormone. However, other mechanisms may be involved. Our findings indicate that when the disturbing influence is sufficiently great, the control of serum calcium is not as well modulated as previously suspected. In addition, our findings of paradoxically hypercalcaemic responses to calcitonin indicates that the pathophysiologic interpretation of serum calcium at any single moment in time following the administration of this hormone to either intact or thyroparathyroidectomized men or dogs is a precarious endeavour.

Animals↗