Biomedical subjects

J Silberbusch

Publications and source records attributed to J Silberbusch.

52 records · Page 3Linked to original sources

PubMed1982

Enhanced calcitonin release in chronic renal failure depending on the absence of severe secondary hyperparathyroidism.

In 27 patients with end-stage chronic renal failure an elevated calcitonin (CT) and parathyroid hormone was found. On stimulation with Ca i.v. there were 9 cases in whom delta CT proved to be higher than the maximal response of 50 pg ml-1 in controls. Supranormal CT responses were found predominantly in patients with normal alkaline phosphatase, who as a group increased their CT from 94.5 +/- 61 to 142.0 +/- 94 pg ml-1 (p less than 0.02). In contrast to this, patients with elevated alkaline phosphatase who also had a higher level of parathyroid hormone maintained unchanged CT on Ca stimulation. It is concluded that in chronic renal failure with severe secondary hyperparathyroidism, delta CT on stimulation is normal, while an enhanced delta CT often exists when hyperparathyroidism is of insufficient degree to cause a raised alkaline phosphatase.

Adult↗

PubMed1981

Value of serum calcitonin estimation in clinical oncology.

In 132 consecutive patients with carcinoma of various organs, a higher serum immunoreactive calcitonin (ICT) concentration (median level 50 pg/ml) was found than in 68 normal subjects (median level 20 pg/ml). The incidence of hypercalcitoninaemia was 40%. All 9 patients with primary liver-cell carcinoma were hypercalcitoninaemic. On the other hand, none of the 7 patients with a carcinoma of the breast had raised ICT levels. In bronchogenic cancer a relationship between ICT and cell type was found, with a predominance of high ICT in patients with oatcell and other undifferentiated types, whereas in squamous-cell carcinomas and adenocarcinomas of the lung hypercalcitoninaemia was relatively rare. When we divided all our patients according to differentiation of the tumour cell, it was found that the lower the degree of differentiation, the higher the ICT concentration, whereas opposite results were observed for CEA. When ICT and CEA were estimated concurrently, we found at least one marker increased in 70% of our patients. Our results demonstrate that patients with metastases in the liver have more frequently and increased ICT. In addition, we conclude that lifespan can be expected to be lower in patients with high ICT levels. In a longitudinal study of 46 patients, there was a positive correlation between change in serum ICT and tumour mass.

Aged↗

PubMed1981

Dissociation between changes in immunoreactive parathormone and its biological indices induced by cimetidine in primary hyperparathyroidism.

In three out of four patients with primary hyperparathyroidism, 2 000 mg of cimetidine daily caused a reduction of immunoreactive parathormone (iPTH) when measured at 8.30 and 11.30 on days 16 and 17 on treatment. Serum Ca, PO4 and maximal tubular reabsorption of PO4 remained unchanged. Excretion of cAMP/100 ml GFR remained elevated to at least the same extent as before treatment. Two patients, in whom cimetidine treatment was continued for an additional 4 weeks, did not show further hormonal or biochemical changes compared with the evaluation on days 16 and 17. We conclude that reduction of iPTH is not accompanied by any change in biological activity of this hormone. The reason for this discrepancy remains unclear.

Cimetidine↗

PubMed1981

Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction.

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.

Acute Disease↗

PubMed1980

Proliferation of T gamma cells with killer-cell activity in two patients with neutropenia and recurrent infections.

Two patients with severe granulocytopenia and recurrent infections of the skin and oropharynx had excess T lymphocytes with receptors for the Fc portion of IgG (T gamma cells) in blood and bone marrow. The abnormal T gamma cells killed antibody-sensitized target cells in vitro (killer-cell activity) but did not suppress immunoglobulin production by B lymphocytes (suppressor-cell activity). T gamma lymphocytes from normal persons showed both killer-cell activity and suppressor-cell activity. In the serum of one patient, granulocyte antibodies, possibly of an autoimmune nature, were detected. The clinical picture in conjunction with the hematologic and immunologic findings characterized the disease of both patients as a distinct entity among the chronic lymphoproliferative diseases of T-cell origin.

Aged↗

PubMed1980

A simple method for the quantification of biliary reflux.

99mTc-diethyl-IDA is completely excreted into the bile. When cholecystokinin is given after priming of the biliary tract with this tracer, gallbladder contraction leads to expulsion of bile into the duodenum. At the same time cholecystokinin causes contraction of the pylorus, which should normally prevent substantial reflux of tracer into the stomach. We have applied these physiological characteristics in a method to quantify biliary gastric reflux. Fourteen controls had a median reflux of 4.3% of the intravenous dose (93% of controls had values less than 9%). In 18 patients with Billroth II gastrectomies the median reflux was 46% (p less than 0.001). Patients with chronic gastritis (no. = 18) had also increased reflux (median 18.1%, p less than 0.001). The same was found in gastric ulcer (no. = 18, median 11.8%, p less than 0.003). In duodenal ulcer (no. = 7) increased reflux existed in only two patients with pyloric deformation. Patients with hiatal hernia did not show increased reflux (no. = 10, median 2.2%). Bilirubin measurements tended to underestimate reflux in pathological cases, whereas bile acid measurements and reflux percentages of tracer showed a close relationship (r = 0.87, p less than 0.001).

Bile Reflux↗

PubMed1980