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Biomedical subjects

D Reinwein

Publications and source records attributed to D Reinwein.

At least 19 recordsLinked to original sources
PubMed1992

Cervical pheochromocytoma: a rare localization and a difficult diagnosis.

A 45-year-old hypertensive female with insulin-treated diabetes mellitus presented to our clinic with elevated urinary norepinephrine (NE) concentrations and a negative 131-metaiodobenzylguanidine (MIBG) scintigraphy, errouneously limited to the abdomen, for evaluation of a pheochromocytoma (Pheo). Despite antihypertensive medications blood pressure remained highly variable and frequently elevated. Further biochemical testing, including a glucagon provocation test and a clonidine-suppression test, revealed autonomous NE secretion. In order to avoid repeat MIBG-scintigraphy, other non invasive imaging techniques were performed, including real time sonography (7.5 MHz) of the neck which revealed a tumor. Fine needle aspiration of this tumor tissue demonstrated cells compatible with Pheo. Histology and immunohistochemistry of the excised tumor confirmed the diagnosis of Pheo. After surgical removal of the tumor, urinary and plasma NE levels normalized. Without any medication the blood pressure of the patient was now only slightly hypertensive. Only half of the daily insulin dose was needed to maintain the patient euglycemic.

Adrenal Gland Neoplasms↗
PubMed1992

Conservative and surgical management of incidentally discovered adrenal tumors (incidentalomas).

Of 50 patients with incidentalomas (INC), 18 were adrenalectomized and in 18 patients the INC was left in place. For 14 patients clinical data were insufficient for evaluation. Follow-up investigation of the 18 unoperated subjects 11-101 months (median 32.2) after the diagnosis had been made revealed unchanged size of the INC [initially 2.1 +/- 0.8 cm (mean +/- SD) at follow-up 2.0 +/- 1.0 cm]. Cushing's syndrome developed in one patient, which was not evident at the initial discovery of the INC 32 months before. "Pre-Cushing's Syndrome" was detected in 1 patient and confirmed in a second who had displayed a pathologically high dose dexamethasone suppression test 101 months before. In addition, 3 male patients with a hitherto unknown mild subclinical defect of 21-hydroxylase activity were identified. The remaining 12 patients had normal endocrine activity of their adrenals. Eighteen patients were adrenalectomized with an average tumor size of 3.96 +/- 1.88 cm. Histologically, 10 (52%) adenomas were observed, including 3 with signs of hypercortisolism. Adrenal hyperplasias were observed in 2 patients, metastasis in 1 patient. 31.5% of the INC which were removed were nonmalignant tumors of other than adrenal origin. We conclude that initially endocrinologically inactive adrenal tumors can eventually develop autonomous endocrine activity and therefore need to be reexamined at regular intervals. Conservative management with regular follow-up investigations is the preferable treatment for small incidentalomas when endocrine over-activity has been excluded and no indications of malignancy exist. Based on these observations and the literature a diagnostic and therapeutic strategy is presented.

Adrenal Cortex Function Tests↗
PubMed1991

[Familial panhypopituitarism].

Two Italian brothers showed identical subsequent loss of anterior pituitary function during the first decades of their life, developing panhypopituitarism. The investigations carried out indicate that in this family the etiology is hereditary in nature, being X-chromosomal recessive or autosomal recessive, with the defect located at the level of either the hypothalamus or the pituitary gland.

Adult↗
PubMed1990

A multihormonal response to corticotropin-releasing hormone in inferior petrosal sinus blood of patients with Cushing's disease.

Bilateral, selective, and simultaneous catheterization of the inferior petrosal sinus is not only a valuable tool in the differential diagnosis of Cushing's syndrome, but may also provide new insights into paracrine interactions at the pituitary level. We have investigated whether CRH (1 microgram/kg BW) has any effect on the release of PRL, GH, TSH, or the alpha-subunit of hCG during this procedure. Sixteen patients under evaluation for Cushing's syndrome (Cushing's disease, n = 12; ectopic ACTH syndrome, n = 2; glucocorticoid resistance, n = 1; hormonally inactive adenoma, n = 1) were catheterized. Two of the patients with Cushing's disease received 4.0 mg naloxone iv 15 min before stimulation with CRH. Patients with Cushing's disease demonstrated a central/peripheral gradient and an intersinus gradient not only for ACTH, but also for PRL, alpha-subunit, GH, and TSH, provided that the latter two hormones were not completely suppressed by the glucocorticoid excess. Moreover, all hormones increased in response to CRH on the side with the highest ACTH concentration; PRL rose from 31.2 +/- 6.4 to 61.6 +/- 12.4 micrograms/L (P less than 0.01), and alpha-subunit from 2.6 +/- 0.6 to 6.4 +/- 1.7 micrograms/L, (P less than 0.01). Naloxone was unable to abolish the PRL or alpha-subunit increase in response to CRH. A multihormonal response to CRH in inferior petrosal sinus blood was also observed in the patient with glucocorticoid resistance and in the patient with the hormonally inactive tumor, but not in the patients with ectopic ACTH secretion. The multihormonal response to CRH could be explained by cosecretion of other hormones together with ACTH from corticotroph adenoma, by an effect of CRH on pituitary blood flow, or by a paracrine action of pituitary corticotrophs on adjacent normal pituitary cells. Our results do not support the concept that such a paracrine action is mediated by beta-endorphin. However, a higher dose of naloxone may be required to antagonize the action of pituitary beta-endorphin.

Adrenocorticotropic Hormone↗
PubMed1990

New therapeutic approaches in thyroidal autoimmune diseases.

Antithyroid drugs (AD) still represent the most widely chosen therapy for hyperthyroidism of Graves' disease. Since their interaction with iodine is still poorly understood, this was addressed in multicenter clinical trials. The interaction of iodine and methimazole was studied in 260 patients from iodine deficient countries. Whereas patients with very low iodine supply needed low doses of methimazole, patients with even slightly increased iodine supply needed high doses of methimazole to remain euthyroid. In another study of 1256 patients side effects of AD were shown to be dose-dependent. Immunological markers of thyroid autoimmunity disappear in most patients during treatment with AD although with many exceptions. Remissions after treatment with AD may represent disease heterogeneity within a spontaneous disease course and the spectrum of relapsing hyperthyroidism over euthyroidism to hypothyroidism. Lastly therapeutic strategies in thyroid eye disease have not provided evidence which therapy is superior.

Antithyroid Agents↗
PubMed1990

[Experimental and epidemiological studies on the interrelationship of thiocyanate and thyroid function].

The testing of a SCN- dose (32 mg NaSCN/kg oral 21 d long) which is about 100 fold above the alimentary SCN(-)-uptake on guinea pig has shown neither histologic/morphometrical nor clinical clue to thyrostatic effect. In 6 regions of the GDR (1,349 persons) has not been secured epidemiologically any relationship between SCN- serum level as well as SCN- urine level and goiter. The partly in the tendency low increase of SCN- level by patients with bland goiter was always under the levels of smokers without goiter, exceeded indeed the threshold of significance in the area of Werdau. In the industrial agglomeration areas the I(-)-SCN(-)-quotient at the most unfavourable cases ran to 3.5 (Halle, smoker, struma), was consequently close to the critical level of the goiter risk.

Aged↗
PubMed1979

[Effect of a 2 mg thyroxine bolus on the hypophyseal-thyroid axis (author's transl)].

The effect of a single dose of 2 mg L-thyroxine on central and peripheral parameters of the hypophyseal-thyroid axis was studied on ten euthyroid and ten hypothyroid patients, and ten with euthyroid goitre. Without the occurrence of hyperthyroid symptoms, the T4 serum level was raised for five days in the euthyroid group, for 11 days in the hypothyroid ones. During this time the T3 serum level did not alter. Suppression of iodine uptake by the thyroid and TSH secretion of the hypophysis persisted longer, both for basal and TRH-stimulated liberation, than the substitution effect. Even when the T4 bolus has to be at a higher total T4 dose for the same therapeutic effect than with daily small single doses, it is a comparable alternative to present-day forms of treatment. It is of particular advantage where there are medical reasons for widely spaced drug intake or rapid normalisation of the T4 serum level is deemed desirable.

Female↗
PubMed1979

[Endocrine insufficiency in alcaptonuria? A case report and survey of the literature (author's transl)].

In a 49 years old patient with alcaptonuria we studied the question whether disturbances of the endocrine organs by deposition of products of homogenistic acid could be detected analogous to disturbances of connective tissue. The function of the hypothalamus and the pituitary gland were shown to be normal. The only defect of the endocrine organs was a hypergonadotropic hypogonadism with a serum testosterone of 5.4 and 9.4 mumol/l respectively (155 and 270 ng/dl rsp.) at elevated LH and FSH values. A sufficient stimulation of the testosterone in serum by chorionic gonadotropin (Primogonyl) could be demonstrated, thus supporting the diagnosis of a compensated insuffiency of the Leydig cells. This disorder might be a late endocrine defect due to the basic metabolic disturbance of the disease.

Alkaptonuria↗
PubMed1979

Binding of luteinizing hormone releasing hormone to human serum proteins--influence of a chronic treatment with a more potent analogue of LH-RH.

Binding of 125I-LH-RH and its analogue, 125I-6-D-Leu-10-Des-Gly-Ethylamide-LH-RH (6-D-LH-RH) in male serum was studied in 10 healthy males and in 11 patients with idiopathic gonadotropin deficiency (IGD) before and during treatment with 6-D-LH-RH. Using either equilibrium dialysis (A) or ethanol precipitation (B) 13.57 +/- 0.69% (A) or 19.32 +/- 1.73% (B) of LH-RH and 7.12 +/- 0.86% (A) or 14.56 +/- 1.06% (B) of the analogue were in the bound form, without difference between normal subjects and IGD. Capacity of this binding was high (greater than 9 less than 18 mu-Mol LH-RH/0.06 mMol of protein), affinity very low, and the binding almost completely disappeared following removal of albumins by affinity chromatography. Chronic treatment with 6-D-LH-RH did not alter these binding characteristics. These observations suggest non specific albumin binding of LH-RH in male serum and stress the role of this decapeptide as a rapid modulating regulator of gonadotropin secreting system.

Blood Proteins↗
PubMed1979

Immunoreactive somatomedin B in acromegaly and in Turner's syndrome.

Serum somatomedin B was measured by radioimmunoassay in forty-seven normal subjects, twenty-nine patients with acromegaly before and twenty-four after treatment, and eighteen patients with Turner's syndrome. Somatomedin B levels were significantly elevated in untreated acromegaly and in Turner's syndrome compared with the control group; they decreased following treatment of acromegaly. Because of the overlap between the groups, little information could be obtained from single somatomedin B estimations, which could, therefore, not replace dynamic tests of growth hormone secretion. No correlation between growth hormone and somatomedin B in acromegaly was detected; however, somatomedin B appeared to be related to the insulin response during the oral glucose tolerance test. In Turner's syndrome, no relationship between somatomedin B and insulin production, urinary oestrogen excretion, growth hormone secretion, gonadotrophin levels, age or height was found. The reason for the raised somatomedin B levels in Turner's syndrome remains at present unknown.

Acromegaly↗
PubMed1979

Gel filtration studies of serum growth hormone in acromegaly following bromocriptine administration.

Sera of 7 patients with active acromegaly were fractionated by Sephadex G-100 chromatography and the effects of bromocriptine on the concentrations of total growth hormone (hGH) and its different molecular forms studied. Three immunoreactive peaks were observed, corresponding to molecular weights of about 20,000 ('little hGH'), 40,000 ('big hGH'), and more than 100,000 ('big big hGH') Following bromocriptine administration, there was significantly more reduction of 'little hGH' than of 'big big hGH'. Careful interpretation of these changes is required in view of the possible influences of sample storage and handling on hGH heterogeneity. We suggest that either bromocriptine acts differentially on the release of 'little' and 'big big hGH', or that these components differ in their metabolic half-life. However, even the suppression of 'little hGH' is insufficient to explain the clinical response of the disease to bromocriptine.

Acromegaly↗
PubMed1979

[Pure gonadal dysgenesis. Case report with unusual anatomical and endocrine findings].

The syndrome of pure gonadal dysgenesis (PGD) cannot always easily be distinguished from other disorders of gonadal development. Relations are evident with Turner's syndrome, females with hypoplastic ovaries, male pseudohermaphroditism, mixed gonadal dysgenesis and the vanishing testes syndrome. The case is reported of a 40 year old female with primary amenorrhea, alopecia, eunuchoid features, XY karyotype with normal breast development and sexual hair after estrogen therapy. On laparotomy streak ovaries were found at ovarian site. Pathohistological examination revealed on the left side wolffian duct remnants such as ductuli deferentes and epididymis besides sparse Leydig-(hilus-)cells and on the right side only a rudimentary fallopian tube with subendothelial accumulation of hyperplastic Leydig-(hilus-)cells. Serum-testosterone elevation above the normal female range (630 ng/dl) persisted following gonadectomy (151 ng/dl). Ectopic Leydig-(hilus-)cells were regarded responsible for the continuing testosterone production. The present case lies on borderline between PGD and mixed gonadal dysgenesis because remnants of wolffian duct derivatives suggest unilateral fetal testicular activity; classification as PGD however was justified in purely female body features and lacking evidence of testicular tissue.

Adult↗