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Biomedical subjects

R Ziegler

Publications and source records attributed to R Ziegler.

At least 361 records · Page 20Linked to original sources

[When should incidentalomas of the adrenal gland be surgically treated?].

Between January 1981 and December 1988 a total of 95 patients underwent surgery for adrenal tumors. In 24 cases (25.3%) a so-called "incidentaloma" was found. While seven of these tumors showed hormonal activity, in seventeen patients the tumor was hormonal inactive. The size of the tumors ranged between 2 and 11 cm. Histologically all tumors were found to be benign neoplasms. Because of the lack of lethality and minimal morbidity we indicate surgery on incidentaloma of the adrenal gland for the following reasons: tumors with hormone activity, tumor size larger than 3 cm, suspecting malignoma or metastasis and finally in proven enlargement of small tumors. Only in adrenal tumors smaller than 3 cm we suggest a follow-up by ultrasound or computed tomography.

Adenoma↗

[Primary hyperaldosteronism without arterial hypertension].

Treatment-resistant hypokalaemia (2.27 mmol/l) developed in a 43-year-old woman. Plasma renin activity was depressed (0.24 ng/ml.h), aldosterone and hydroxycorticosterone concentrations were elevated (123 ng/dl and 688 ng/dl, respectively). Mean blood pressure value (30 readings) was 133/88 mm Hg. An adrenal adenoma was diagnosed by ultrasound, computed tomography and subtraction angiography and then removed. Postoperatively the signs of hyperaldosteronism (Conn's syndrome) regressed and the average blood pressure was 112/76 mm Hg. Blood-gas analysis, which preoperatively had shown a minimal metabolic alkalosis, now revealed a mild metabolic acidosis. Preoperatively present bilateral renal calcifications in the region of the papillary tips were confirmed by computed tomography. An acid loading test revealed diminished renal acid secretion, making the diagnosis of distal renal-tubular acidosis. The latter, in combination with the primary hyperaldosteronism, may have been the cause of the low blood pressure, unusual in Conn's syndrome.

18-Hydroxycorticosterone↗

[3 beta-hydroxysteroid dehydrogenase deficiency and 21-hydroxylase deficiency in hirsutism].

Of 218 women with hirsutism 16 (7%) were found to have partial 21-hydroxylase deficiency, while 38 (17%) had partial 3 beta-hydroxysteroid dehydrogenase deficiency. Six women (3%) had a steroid constellation which resembled that of an augmented adrenarche. In the women with enzyme deficiency over-weight and abnormal menstruations were more frequent (50%) than in those without such deficiency (33%). The degree of hirsutism and age at diagnosis were similar in those with and those without partial enzyme deficiency. Furthermore, the diagnosis of partial enzyme deficiency could only be made with certainty by the ACTH stimulation test, because with sole measurement of basal levels (17-hydroxyprogesterone and 21-desoxycortisol in 21-hydroxylase deficiency, and 17-hydroxypregnenolone and dehydroepiandrosterone in 3 beta-hydroxysteroid dehydrogenase deficiency) the enzyme defects are in most instances not revealed.

3-Hydroxysteroid Dehydrogenases↗

Role of voltage-dependent calcium channels in secretion of calcitonin from human medullary thyroid carcinoma cells.

Extracellular calcium concentration is an important regulator of calcitonin secretion. We used primary cell cultures of human medullary thyroid carcinoma to study the role of voltage dependent calcium channels for stimulus secretion coupling. Increasing extracellular calcium concentration (1.6-5.0 mM) in the medium caused a dose dependent release of calcitonin. The calcium channel activator BAY K 8644, a dihydropyridine, stimulated calcitonin secretion in a dose dependent manner (10(-7)-10(-5) M). This effect was completely inhibited by equimolar concentrations of the calcium channel blocker nifedipine and abolished in the absence of extracellular calcium. Similarly, nifedipine suppressed the stimulatory action of extracellular calcium. The effects of calcium and BAY K 8644 with and without nifedipine suggest that calcium influx via voltage dependent calcium channels plays an important role in calcitonin secretion. The primary cell culture of human medullary thyroid carcinoma is a good model for the study of stimulus secretion coupling.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

[Cardiomyopathy in hypocalcemia].

A 48-year-old woman developed a hypocalcaemic cardiomyopathy, the hypocalcaemia being due to hypoparathyroidism after three previous thyroid operations for goitre with tracheal compression. She had signs of severe cardiac failure, but no tetany. She was put on calcium and vitamin D3 medication which raised calcium concentration. The cardiac status improved, as did the radiological and echocardiographic findings, without the patient having received any diuretics, digitalis or afterload lowering drugs.

Calcium↗

Primary glucocorticoid receptor defect with likely familial involvement.

A 29-year-old woman with moderately elevated blood pressure and signs of hyperandrogenism (hirsutism and acne) but without typical Cushing's syndrome symptoms has been followed for almost 6 years. Steroid and glucocorticoid receptor studies indicated a primary glucocorticoid receptor defect. Elevated androgen values were of special interest. Clinical manifestation of hyperandrogenism seemed not to be proportional to the biochemical findings. Therefore, the possibility of a partial androgen receptor defect should also be considered.

Acne Vulgaris↗

[Primary hyperparathyroidism--changes in the disease picture].

Two groups of patients with primary hyperparathyroidism, one early group surgically treated operated between 1970 and 1979 (n = 90), and the other late group from 1980 to 1984 were compared concerning signs, symptoms and laboratory parameters in order to find out the changing trends in the clinical spectrum of this disease during these years. The decade of manifestation decreased from the age of sixty to fifty. The most common mode of presentation in the early group were renal (30%), gastrointestinal (27%), and osseous (18%) symptoms of primary hyperparathyroidism, and 21% symptoms due to hypercalcemia. In the later series severity of the typical symptoms decreased, diagnosis was made in nearly half of the patients (47%) by the incidental finding of hypercalcemia on routine biochemical screening. Careful investigation revealed that the severity but not the occurrence of organic and functional manifestations differed between the two groups. Mean serum calcium level decreased from 3.4 mmol/l in the early group to 3.1 mmol/l in the recent series. Parathyroid hormone level was increased in 90% respectively 79% of the patients. The localization of the parathyroids was done in 58% by ultrasound in the late group. Diagnosis was clearly made in 60% of the recent group by the combination of elevated serum calcium and parathyroid hormone levels and two associated symptoms. Diagnosis was more difficult in 10% when serum calcium was elevated and only one symptom was present. There is a trend in symptoms of primary hyperparathyroidism from typical "disease of stones, bones and abdominal groans" to a mild and nearly asymptomatic presentation detected by routine calcium screening.

Adult↗

[Clinical features and diagnosis of mild 3-beta-hydroxysteroid dehydrogenase deficiency in men].

3 beta-hydroxysteroid dehydrogenase (HSD) deficiency was demonstrated in six males, aged between 18 and 24 years, who had gynaecomastia, hypogonadism or infertility. The predominant laboratory finding was a striking elevation of dehydroepiandrosterone sulphate (DHEAS) levels. The diagnosis of HSD deficiency was confirmed by finding a marked rise in dehydroepiandrosterone (DHEA) and 17-hydroxypregnenolone levels. In contrast to these findings in late-onset enzyme deficiency, in four males with the classical form of 21-hydroxylase deficiency the only sign was a reduction in adult height. The prevalence of late-onset HSD deficiency in men is not known and may be more relevant in patients with gynaecomastia or abnormal gonadal function than has hitherto been realized.

17-alpha-Hydroxypregnenolone↗

[Hyperthyroidism caused by a hormone-producing follicular thyroid cancer].

A well differentiated carcinoma of the thyroid is usually less productive with respect to thyroid hormones than normal thyroid tissue. Very rarely, it happens though that a metastatic follicular carcinoma of the thyroid produces hyperthyroidism as the following example illustrates. In our patient with follicular thyroid carcinoma the radioiodine scan demonstrated an increased uptake of 123I in the right thyroid lobe but also in a lung metastasis, even before thyroidectomy. In contrast, the iodine uptake of the left - normal - thyroid lobe was suppressed. Following thyroidectomy the levels of the thyroid hormones were normal and only dropped into the hypothyroid range after the beginning of the therapy with radioiodine. Hence we conclude that the metastases of a thyroid carcinoma can attain the hormone secretion of a normal thyroid gland and take up more radioiodine than normal thyroid tissue.

Adenocarcinoma↗

Detection of human serum amyloid A protein in very low density--and high density lipoproteins of patients after acute myocardial infarction.

Two acute-phase proteins have been identified in very low density (VLDL)- and high density lipoproteins (HDL) of patients after acute myocardial infarction. Both proteins have a relative molecular weight of 11,000 and isoelectric points pI 6.08 and 6.27, and do not contain cysteine or sugar residues. Polyclonal antibodies to these acute phase reactants did not cross-react with other serum apolipoproteins. Evidence is given that both proteins are polymorphic forms of the human serum amyloid A protein.

Blotting, Western↗

Treatment of tumor hypercalcemia with clodronate.

In an open, controlled study 34 patients with tumor hypercalcemia of different origin were treated with clodronate. The initial dosage was 300 mg intravenously daily. After achieving normocalcemia, treatment was continued orally using 400-3200 mg/day depending on serum calcium concentration. Most patients showed normocalcemia within 1 week of treatment - only few of them needed a longer time. Fifteen of 34 patients died within the observation time of up to 24 weeks, some being normocalcemic. However, a reincrease in plasma calcium during treatment was an indicator of deterioration. Measurements of plasma parathyroid hormone (PTH) using an intact molecule radioimmunometric assay showed depressed levels before clodronate treatment started, but PTH rose after achieving normal and especially low normal calcium levels. Starting 1,25-dihydroxycholecalciferol [1,25(OH)2D3] values were decreased or in the lower normal range in the majority of patients, but in 6/21 patients plasma 1,25(OH)2D3 was in the upper normal range or elevated despite hypercalcemia. After lowering plasma calcium the 1,25(OH)2D3 levels increased. However, there was no significant correlation between PTH and 1,25(OH)2D3. Therefore we assume that in some patients additional stimulation of renal 1 alpha-hydroxylase by tumor products is present.

Administration, Oral↗

Herpes simplex virus infection of the rat sensory neuron. Effects of interferon on cultured cells.

Embryonic rat dorsal root ganglion neurons were cultured in a two-chamber system allowing infection of neuritic extensions without exposure of neuronal cell bodies or vice versa. Herpes simplex virus type 1 was used to infect interferon-alpha and -beta treated or untreated neurons and the production of virus and interferon was assayed. Treatment of nerve cell bodies with interferon inhibited virus replication in a dose-dependent manner, whether virus was inoculated directly onto the nerve bodies or peripherally on the neuritic extensions. In contrast no antiviral effect was noted when neurities were treated with interferon suggesting possible lack of interferon receptors on neurites. On infection with herpes simplex virus the rat sensory neuron cultures did not produce interferon in amounts above the detection limit (0.5 units per ml) of the interferon assay used.

Animals↗

The hypercalcemic Walker carcinosarcoma 256 of the rat causes an increase in serum 1,25-dihydroxyvitamin D3.

We have studied vitamin D metabolism in rats with the transplantable hypercalcemic Walker carcinosarcoma 256, which is a well characterized animal model for humoral hypercalcemia of malignancy. 25-Hydroxyvitamin D3 (25(OH)D3) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) concentrations were determined in blood samples obtained from parathyroidectomized (PTX) female rats at different time intervals after intramuscular tumor cell inoculation. We observed a dramatic increase in serum 1,25(OH)2D3 (280 +/- 184 vs. 98 +/- 31 pmol/l) 6 days after tumor cell injection and 4 days after the initial rise of serum calcium, whereas 25(OH)D3 tended to decrease. In a separate control experiment we compared this to the effect of exogenous parathyroid hormone in PTX rats and found similar results. In contrast, rats exhibited no change in vitamin D metabolite blood concentration after inoculation of the normocalcemic Yoshida sarcoma, which obviously does not interfere with vitamin D metabolism. We conclude that the humoral bone-resorbing agent produced by the Walker tumor cells causes elevation of serum 1,25(OH)2D3 concentration by this fulfilling an additional criterion of PTH-like activity.

Animals↗