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Biomedical subjects

W A Scherbaum

Publications and source records attributed to W A Scherbaum.

At least 253 records · Page 14Linked to original sources
PubMed1984

Anti-perinuclear and rheumatoid factor in different forms of autoimmune thyroid disease.

Anti-perinuclear factors (APF), IgM-, IgG- and IgA-rheumatoid factors have been detected in six, five, one and three out of 20 patients with primary myxoedema, respectively. We were unable to find APF in 22 patients with Hashimoto's thyroiditis nor in 20 patients with Graves' thyrotoxicosis. APF appears to be a marker for non-organ specific autoimmune diseases.

Adolescent↗
PubMed1983

[Autoimmune form of central diabetes insipidus with antibodies against vasopressin-producing hypothalamic cells].

Autoantibodies against vasopressin (AVP)-producing cells of the human pituitary gland as well as conventional antibodies were determined in 67 patients with central diabetes insipidus and in 141 controls without diabetes insipidus using an immunofluorescence technique. Eleven out of 30 patients (37%) with nonfamilial idiopathic diabetes insipidus, two out of 28 patients (7%) with symptomatic diabetes insipidus and none of the control persons had AVP-cell antibodies. Antibody titres were between 1 : 2 and 1 : 32, in 8 of the 13 cases the antibodies were complement-binding. In 9 patients with idiopathic diabetes insipidus and in none of the symptomatic cases one or more autoimmune diseases were demonstrable. Demonstration of autoantibodies against AVP-cells of the pituitary in the serum of patients with so-called idiopathic diabetes insipidus indicates an autoimmune basis of the disease. This interpretation of the new antibody results is supported by a frequent association of idiopathic diabetes insipidus with recognized auto-immune diseases.

Adolescent↗
PubMed1983

Myasthenia gravis: overlap with 'polyendocrine' autoimmunity.

81 patients with spontaneously acquired myasthenia gravis (MG) were investigated for the presence of autoimmune (AI) diseases and their sera were tested for a range of organ-specific autoantibodies. 77 of the patients were HLA-phenotyped. Antibody titres to acetylcholine receptors (AChR) were higher in non-thymomatous patients who possessed HLA-B8 (p less than 0.05) and/or -DR3 (p less than 0.05) as compared to patients lacking these HLA antigens. 3 out of 20 (15%) patients with ocular MG, 7/23 (30%) with generalized MG of early onset, 11/23 (48%) generalized MG of late onset and 5/14 (35%) patients with thymoma had either overt AI diseases or significant titres of organ-specific autoantibodies suggesting subclinical AI disease. In ocular MG, low titres and an infrequent finding of antibodies to AChR (32%) as well as the low prevalence of associated autoantibodies and AI diseases indicate that this subgroup of MG consists of patients with restricted AI reactivity. HLA-B8 and -DR3 were present in all the patients with associated AI disorders in the young onset group but in none of the patients with old age of onset. In the young group, 6 out of 7 patients with associated AI conditions were women whereas the sex ratio was about equal in the older cases in both, patients with and without associated AI diseases or autoantibodies. We conclude from these observations that ageing provides conditions that allow the breakdown of self tolerance. The simultaneous presence of HLA B8, DR3 and female sex provide important additional factors for early expression of MG.

Adult↗
PubMed1983

Autoantibodies to vasopressin cells in idiopathic diabetes insipidus: evidence for an autoimmune variant.

Autoantibodies to vasopressin-secreting cells of human hypothalamus were detected by means of indirect immunofluorescence (IFL) in 13 patients with diabetes insipidus (DI). 11 of 30 patients (36 . 7%) with "idiopathic" and 2 of 32 (6 . 3%) with symptomatic DI were positive, and 139 control patients were negative. The specificity of the reaction vasopressin cells was demonstrated with a 4-layer double-fluorochrome IFL test in which the second sandwich consisted of rabbit antivasopressin or anti-oxytocin counterstained with rhodaminated anti-rabbit immunoglobulin. 5 patients had also antibodies to oxytocin-producing cells. The antibodies reacted with cytoplasmic components distinct from the hormone; they were of IgG, IgA, or IgM class or a combination of these classes, and half of them fixed complement. Maximum titres were 1:32, and the antibodies could not be absorbed out by incubation with vasopressin, oxytocin, neurophysin I, or neurophysin II. Some sera stained as yet unidentified small cells in the hypothalamus. This report suggests that autoimmunity extends to the hypothalamus. Vasopressin-cell antibodies may prove to be useful markers for the diagnosis of an autoimmune variant of diabetes insipidus.

Adolescent↗
PubMed1983

[Possibilities and value of immunofluorescence in the diagnosis of endocrine diseases].

The indirect immunofluorescence (IFL) test is the method of choice for the detection of new organ-specific autoantibodies. It is also the standard method of detection of antibodies to pancreatic islet cells, adrenal cortex, and steroid-producing cells in gonads and placenta. A positive test is the essential diagnostic step to find out the etiology of some endocrine diseases, but the significance of this method varies in different organs. There is as yet no substitute for the IFL test in the determination of single cell antibodies within organs e.g. antibodies to endocrine cells of the pituitary and the gut. In some clinical situations it is advisable to look for the complement-fixing ability of cytoplasmic autoantibodies using the CF-IFL test and for scientific investigation the IFL test can be applied when looking for antigens on the surface of cells in suspension or culture.

Adrenal Cortex↗
PubMed1982

Development of adrenocortical failure in non-Addisonian patients with antibodies to adrenal cortex. A clinical follow-up study.

Out of 1036 sera tested for the presence of antibodies to adrenal cortex using the indirect immunofluorescence (IFL) method, fifteen out of 323 patients with Graves' thyrotoxicosis, 6/105 Hashimoto's thyroiditis, 3/29 myxoedema, 2/49 asymptomatic autoimmune thyroiditis, 1/12 subacute thyroiditis, and 4/130 with myasthenia gravis were positive. Thirty antibody-positive non-addisonian patients were tested for subclinical adrenocortical failure and followed up over a period of 1-3.5 years. Three women with Graves' disease had biochemical signs of early Addison's disease at the first Synacthen test. Two young women with controlled Graves' thyrotoxicosis developed a diminished adrenocortical reserve within 2 and 3 years, respectively; one of them developed anovulatory cycles which did not respond to clomiphene treatment. Both patients had high titres of complement-fixing adrenal antibodies before the adrenal failure could be recognized by functional tests. One elderly female patient in whom a euthyroid goitre with adrenal and thyroid antibodies was detected in 1977, developed Graves' thyrotoxicosis in 1980. These observations indicate that antibodies to adrenal cortex have a high clinical significance and may allow the early diagnosis of Addison's disease even in the absence of specific clinical symptoms.

Addison Disease↗
PubMed1982

Immunological and clinical characterization of patients with untreated euthyroid and hypothyroid autoimmune thyroiditis. Antibody spectrum, response to TRH and clinical study.

In a region of endemic goitres, 200 untreated patients in whom thyroid microsomal (MCHA) and/or thyroglobulin (TGHA) antibodies have been detected were analyzed and other organ specific autoantibodies were tested. Thyroid function was assessed by a TRH test in all of them. Patients with previous thyroid disease and patients with clinical or biochemical signs of thyrotoxicosis were excluded. In 58 (29%) of the patients diseases coexisted in which a high incidence of autoimmune reactions has been recognized. In the absence of the corresponding clinical disease, 13.7% of the patients had antibodies to parietal cells of the stomach, 3.1% had antibodies to adrenal cortex, 1% to steroid producing gonadal cells, 1% to pancreatic islet cells, and 0.5% of the patients had antibodies to striated muscle fibrils. The incidence of associated organ-specific autoantibodies was no higher in patients with hypothyroidism (34.6%) compared with patients who had a normal thyroid function (27.9%). The determination of a 'significant' thyroid antibody titre is discussed. In 24.5% of the 200 patients a form of hypothyroidism was recognized. Fifty of the patients with TGHA titres greater than or equal to 6400, and 56.2% of those with MCHA greater than or equal to 102 400 were hypothyroid. Patients with such titres of thyroid antibodies should be examined and followed up. Patients with associated islet cell or adrenal antibodies should be reinvestigated and followed up observing their glucose tolerance and adrenocortical function, respectively.

Adult↗
PubMedDate not supplied

Regulation of adrenocortical function by cytokines--relevance for immune-endocrine interaction.

The importance of the hypothalamic-pituitary-adrenalaxis (HPA) for the regulation of immunological functions has been greatly appreciated in the past (1-3). Activation of the HPA axis due to a given stimulus leads to a stress response which modulates the immune response. The interactions between the immune system and HPA-axis may be characterized by a circuit which includes I) activation of the HPA-axis and initiation of the stress response which, in term, has immune-modulating properties; II) a feedback mechanism derived from the immune system which regulates the HPA-axis. Current concepts on these regulatory circuits mainly favor the action of cytokines as mediators of the immune-endocrine regulation circuits which have been shown to interfere with the endocrine system on all levels of the HPA-axis. Over the past few years, it has become evident that the adrenal gland, itself, as the main effector organ of the HPA-axis, is a major site for both synthesis and action of numerous cytokines. This review summarizes current knowledge on production, action, as well as functional implications of cytokine action within the adrenal gland during development, health and disease.

Adrenal Cortex↗
PubMedDate not supplied

Sympathoadrenal regulation of adrenocortical steroidogenesis.

Sympathoadrenal regulation of adrenocortical steroidogenesis was studied on a physiological, cellular, molecular and morphological level. The effects of nerve activation and of epinephrine (EPI) on adrenal corticosteroid release were compared in isolated perfused pig adrenals with preserved nerve supply. Splanchnic nerve activation as well as perfusion with EPI provoked a significant release of cortisol, aldosterone and androstenedione. In cultured bovine adrenocortical cells steroid secretion and accumulation of P450scc, P450(17) alpha, P450c21 and P450(11) beta mRNAs were studied after stimulation with EPI with or without propranolol or phentolamine. Incubation with EPI stimulated steroidogenesis and increased the levels of all four P450-mRNAs. The beta-adrenergic antagonist propranolol totally blocked the effects of EPI while the alpha-antagonist phentolamine had no effect. Using immunohistochemistry, adrenals were studied morphologically. The contact zones of the two cell types were investigated on an electron microscopical level. Cortical and medullary cells were closely interwoven with cortical and chromaffin cells in direct apposition, providing the possibility for paracrine interactions. It is concluded that the release of corticosteroids can be stimulated through the sympatho-adrenal system. The stimulatory action of EPI upon adrenal steroid formation and accumulation of all four P450-mRNAs requires beta-adrenergic receptors. Taking into consideration the close colocalization of cortical and medullary tissue, this stimulation may be mediated by chromaffin cells in a paracrine manner.

Adrenal Cortex↗
PubMedDate not supplied

Leptin down-regulates the steroid producing system in the adrenal.

OB protein leptin inhibits the secretion of cortisol in primary cultures of bovine adrenocortical cells and down-regulates 17alpha-hydroxylase cytochrome P450 mRNA expression. To analyze if leptin regulates other major enzymes involved in adrenal steroidogenesis we tested its effect on mRNA expression for two further key enzymes, C21-hydroxylase (P450C21) and side-chain cleavage enzyme (P450SCC). Cultured bovine cortical cells were stimulated for 24 hours with 10 nM ACTH, with 10 nM ACTH plus 100 ng/ml leptin or left unstimulated as controls. Stimulation with ACTH led to a 1.75-fold increase of P450C21 mRNA and a 3.31-fold increase of P450SCC mRNA compared to unstimulated controls. Addition of leptin led to a reduction of ACTH-stimulated mRNA accumulation of 73% for P450C21 and of 45% for P450SCC. We therefore suggest that leptin reduces cortisol synthesis in the adrenal by down-regulating the steroid producing enzyme cascade in the cortical cell.

Adrenal Cortex Hormones↗