[Heart in endocrine diseases].
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Endocrine System Diseases↗
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[Psychopathology of endocrine diseases].
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Endocrine System Diseases↗
Antipituitary antibodies in adults with apparently idiopathic growth hormone deficiency and in adults with autoimmune endocrine diseases.
The role of antipituitary antibodies (APA) in autoimmune pituitary diseases still needs to be clarified. The aim of this study was 2-fold: first, to investigate the presence of APA in adults with idiopathic or acquired GH deficiency (GHD) and in adults with autoimmune endocrine diseases; and second, to evaluate whether in autoimmune endocrine patients APA titer is correlated to the pituitary function and particularly to GH secretion. We studied 12 adults with isolated and apparently idiopathic GHD who were treated with recombinant GH in childhood (group 1a), 14 patients with adult GHD secondary to surgery for pituitary and parasellar tumors (group 1b), and 180 patients with organ-specific autoimmune diseases (group 2). APA were evaluated by indirect immunofluorescence. In all APA-positive patients and in 20 APA-negative patients of group 2, GH secretion was investigated by testing its response to insulin-induced hypoglycemia (insulin tolerance test) and, when impaired, also to arginine. APA were found (at high titers) in 4 of 12 patients of group 1a (33.3%) but were absent in all patients in group 1b. APA were also found in 40 of 180 patients of group 2 (22.2%), 35 of them at low titers (group 2a) and 5 at high titers (group 2b). Twenty of the 140 autoimmune endocrine APA-negative patients studied (group 2c) and all APA-positive patients at low titers (group 2a) had normal pituitary function. Conversely, all APA-positive patients at high titers (groups 1a and 2b) had a severe isolated GHD. An inverse correlation between APA titers and GH peak serum response to insulin tolerance test in autoimmune endocrine patients was observed. Our results suggest that APA, when detected at high titers, may be considered a good diagnostic tool to highlight the possible occurrence of GHD in adults with autoimmune endocrine diseases. Moreover, they may indicate an autoimmune pituitary involvement in adults with apparently idiopathic GHD, suggesting that the prevalence of autoimmune GHD is much higher than that so far considered.
Adult↗
[Endocrine diseases in the age (author's transl)].
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Adrenal Gland Diseases↗
Animal models of autoimmune endocrine disease and their uses in developing new methods of intervention.
This review provides basic information concerning the major animal models in use for the study of autoimmune endocrine diseases (AEDs). Although several other models exist which parallel human AEDs such as autoimmune orchitis, most research in this area has centred on animal models of insulin-dependent diabetes mellitus (IDDM) and thyroiditis. These models, between them, appear to exhibit most of the disease manifestations of their human counterparts and thereby permit the study of possible methods of intervention in the disease process. While no one model represents a perfect correlation with the human disease it represents, common characteristics are recognizable between them. For instance, the central role of activated T cells in controlling the disease process. The chapter continues by examining the various ways in which models of autoimmunity, specifically IDDM and experimental allergic thyroiditis (EAT), have been used to investigate the possibility of preventing or arresting autoimmune destruction. Several different approaches are described that illustrate the variety of techniques that have proven both potentially, or in reality, effective and those that have proven less efficacious than first hoped.
Animals↗
Psychological factors affecting physical condition. Endocrine disease literature review.
Research exploring the relationship between psychological factors and the onset, exacerbation, and perpetuation of endocrine diseases has focused primarily on three diseases: diabetes mellitus (DM), Graves' disease, and Cushing's disease. There is insufficient evidence to support the position that psychological factors directly affect the onset of DM. Recent laboratory studies suggest that stress is associated with changes in glucose regulation in a subset of diabetic patients and that temperament and coping strategies influence glycemic control in diabetic children and adolescents. Relaxation training may improve blood glucose control in non-insulin-dependent DM patients. There is no good evidence that psychological characteristics affect the development and course of thyroid disorder or Cushing's disease. Recommendations are made for future research.
Depressive Disorder↗
Autoimmunity in endocrine diseases.
The realization that autoimmunity underlies many endocrine disorders of previously unknown etiology has greatly broadened our understanding of the pathogenesis of these diseases. It has provided new explanations for their heredity and their association with particular HLA haplotypes. It has also offered new tools for diagnosing these diseases as well as monitoring their course or predicting their outcome. Finally, establishing the autoimmune basis of these diseases offers new potential for their treatment. The next quarter century of research into immunologic aspects of endocrine diseases promises to be as fruitful as the last.
Animals↗
G protein mutations in endocrine diseases.
This review summarizes the pathogenetic role of naturally occurring mutations of G protein genes in endocrine diseases. Although in vitro mutagenesis and transfection assays indicate that several G proteins have mitogenic potential, to date only two G proteins have been identified which harbor naturally occurring mutations, Gsalpha, the activator of adenylyl cyclase and Gi2alpha, which is involved in several functions, including adenylyl cyclase inhibition and ion channel modulation. The gene encoding Gsalpha (GNAS1) may be altered by loss or gain of function mutations. Indeed, heterozygous inactivating germ line mutations in this gene cause pseudohypoparathyroidism type Ia, in which physical features of Albright hereditary osteodystrophy (AHO) are associated with resistance to several hormones, i.e. PTH, TSH and gonadotropins, that activate Gs-coupled receptors or pseudopseudohypoparathyroidism in which AHO is the only clinical manifestation. Evidence suggests that the variable and tissue-specific hormone resistance observed in PHP Ia may result from tissue-specific imprinting of the GNAS1 gene, although the Gsalpha knockout model only in part reproduces the human AHO phenotype. Activating somatic Gsalpha mutations leading to cell proliferation have been identified in endocrine tumors constituted by cells in which cAMP is a mitogenic signal, i.e. GH-secreting pituitary adenomas, hyperfunctioning thyroid adenomas and Leydig cell tumors. When the same mutations occur very early in embryogenesis they cause McCune-Albright syndrome. Although these mutations would in principle confer growth advantage, studies failed to detect differences in the clinical and hormonal phenotypes, suggesting the existence of mechanisms able to counteract the activation of the cAMP pathway. Activating mutations of Gi2alpha have been identified in a subset of ovarian, adrenal and pituitary tumors, but their prevalence and significance are still controversial. Finally, although Galpha subunits are the only components of the heterotrimeric GTP binding proteins which harbor known mutations, beta/gamma subunits should be considered possible targets of genetic alterations as suggested by the frequent presence of beta3 subunit variants in patients with essential hypertension.
Animals↗
Autoimmune endocrine disease induced by recombinant interferon-alpha therapy for chronic active type C hepatitis.
To elucidate the role played by interferon-alpha (IFN alpha) in the pathogenesis of autoimmune endocrine disease, we determined the autoantibody status, thyroid function test results, hemoglobin-A1c levels, and clinical symptoms of 58 patients who received IFN alpha for treatment of chronic active type C hepatitis. Each patient was treated for 6 months with a total dose of 391 +/- 140 x 10(6) U (mean +/- SD). Thyroid microsomal and/or thyroglobulin antibodies newly appeared or were increased in titer in 6 patients, 2 of whom developed hypothyroidism during IFN alpha therapy. Neither islet cell antibodies nor insulin-dependent diabetes mellitus developed during IFN alpha therapy, although hemoglobin-A1c levels were increased in 2 patients. One patient became positive for antimitochondrial antibodies, and another patient with preexisting antimitochondrial antibodies also manifested deterioration in liver function test results. Parietal cell antibodies and smooth muscle cell antibodies were the most frequent newly developed antibodies in 7 patients. Adrenal medullary cell antibodies and nuclear antibodies newly developed in 2 and 1 patients, respectively. At least 1 of 8 autoantibodies newly appeared in 19 patients (32.8%) and hypothyroidism developed in 2 patients (3.4%) during IFN alpha therapy. On the other hand, in 19 age- and sex-matched patients who did not receive IFN alpha, no autoantibody appeared, and no autoimmune disease developed during a follow-up period of 3 months. These findings suggest that IFN alpha acts as an immunomodulatory agent, inducing autoantibody production and the development of autoimmune disease in susceptible patients. Special attention should be paid to the development of hypothyroidism during IFN alpha therapy.
Adult↗
[Value of physical exercises in the most common endocrine diseases].
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Endocrine System Diseases↗
[Endocrine diseases at the National Hospital of Niamey (Niger). Apropos of 195 cases].
The authors report 195 cases of endocrine diseases diagnosed in a department of internal medicine at the National Hospital of Niamey (Niger) from January 1982 to December 1986. Diseases of the thyroid gland were largely predominant (70.8%), with simple (34.9%) and nodular (19%) goiters. Hypothyroidism and thyroiditis were not frequent (2 and 2.6%, respectively). The rarity of thyroid cancers (1%) was in relation to the direct hospitalization of these patients in the surgical department. They were not included in this study. In spite of the magnitude of tuberculosis endemicity in Niger, primary adrenocortical deficiency (Addison's disease) was absent. The frequency (15.4%) of postpartum hypopituitarism (Sheehan's syndrome) is explained by sahelian customs: a great majority of African women delivered at home without medical assistance.
Adolescent↗
[Endocrine diseases and diabetes].
Disorders of endocrine system are often associated with diabetes mellitus. Overproduction of hormones with hyperglycaemic effect, for example that of growth hormone or cortisol, can lead to impaired glucose tolerance or even to induce manifestation of diabetes mellitus. Autoimmune character of some endocrinopathies is a well-known cause of diabetes mellitus type 1 and also of the thyroid gland involvement. Diabetes mellitus, especially with a poor glycaemic control, influences various functions of endocrine organs. The most frequent disturbances are the slow down of the growth in children and adolescents and hypothalamo-pituitary-gonadal axis dysfunction in women. This review summarizes relationship between the most common endocrinopathies and diabetes mellitus.
Autoimmune Diseases↗
Mechanisms of disease: Mutations of G proteins and G-protein-coupled receptors in endocrine diseases.
G proteins and G-protein-coupled receptors (GPCRs) mediate the effects of a number of hormones. Genes that encode these molecules are subject to loss-of function or gain-of-function mutations that result in endocrine disorders. Loss-of-function mutations prevent signaling in response to the corresponding agonist and cause resistance to hormone actions, which mimics hormone deficiency. Gain-of-function mutations lead to constitutive, agonist-independent activation of signaling, which mimics hormone excess. Disease-causing mutations of GPCRs have been identified in patients with various disorders of the pituitary-thyroid, pituitary-gonadal and pituitary-adrenal axes, and in those with abnormalities in food intake, growth, water balance and mineral-ion turnover. The only mutational changes in G proteins unequivocally associated with endocrine disorders occur in GNAS (guanine nucleotide-binding protein G-stimulatory subunit alpha, or G(s)alpha). Heterozygous loss-of-function mutations of GNAS in the active, maternal allele cause resistance to hormones that act through G(s)alpha-coupled GPCRs, whereas somatic gain-of-function mutations cause proliferation of endocrine cells that recognize cyclic AMP as a mitogen. The study of mutations in G proteins and GPCRs has already had major implications for understanding the molecular basis of rare endocrine diseases, as well as susceptibility to multifactorial disorders that are associated with polymorphisms in these genes.
Adrenal Glands↗
Autoimmunity: basic mechanisms and implications in endocrine diseases. Part I.
Autoimmunity implies disturbances at several levels of the immune control. Self-tolerance and discrimination between self and non-self synergize to avoid the development of autoimmunity. Negative selection in the thymus, the transcription factor AIRE, CD4+CD25+ regulatory T cells, and dendritic cells cooperate to produce and maintain tolerance. Cytokines modulate deriving immune processes and influence the local micro-environment. Multiple mechanisms are involved in tolerance breakdown: genetic factors (major histocompatibility complex haplotypes, polymorphisms in the cytotoxic T lymphocyte antigen gene and epigenetic alterations), environmental factors (mainly infections), impaired apoptosis, and the emergence of autoreactive naive lymphocytes. These events may be involved in the pathogenesis of endocrine diseases at several levels.
Animals↗
Plasma and urinary luteinizing hormone levels in the diagnosis of endocrine disease.
The diagnostic value of measurements of plasma and urinary luteinizing hormone (LH) has been studied in 209 patients with endocrine disease. In 44 patients puberty was either delayed or had failed to occur. In those with chromosomal abnormalities the LH levels were often within the normal range, whereas those with a pituitary cause usually had low levels. In boys with delayed puberty plasma LH levels rose before physical changes occurred and had prognostic value. In patients with later gonadal failure, men with impotence or infertility, and women with secondary amenorrhoea LH assays proved of little value, although in one case a premature menopause was suspected and six patients with anorexia nervosa had low LH levels.Sixty patients with disorders of the hypothalamicpituitary area were studied. Levels of LH were measured and considered in relation to the other anterior pituitary hormones. Impairment of LH secretion was one of the first effects on hormone production of disease affecting this area, and this was, of course, most readily detected in postmenopausal women.The normal ranges of both plasma and urine LH are wide and there seems to be considerable day-to-day variation, especially of urinary output. Several samples should, therefore, be measured if therapeutic decisions are involved.
Adolescent↗
Psychological distress and quality of life in endocrine disease.
Despite an upsurge of research in psychoneuroendocrinology, there has been very little interest in the psychological aspects of clinical care in endocrine disease. The clinical and research implications of quality of life in endocrinology (life events preceding disease onset, psychological distress associated with acute illness and convalescence, abnormal illness behavior) are discussed.
Adaptation, Psychological↗
Transition from pediatric to adult care of children with chronic endocrine diseases: a survey on the current modalities in Italy.
We report on a survey carried out in 65 pediatric and adult endocrinological centers concerning: 1) the modalities of the transfer of children with chronic endocrine diseases from pediatricians to adult endocrinologists, 2) opinions and suggestions from physicians of the Centers, and 3) specific details regarding GH deficiency. The main results are: 1) The mean age of transfer is around 18 yr of age. 2) The reasons for the transfer are personal convincement of pediatricians in 47%, administrative reasons in 37% and patient's desire in 16% of cases 3) In the majority of cases a discharge summary is sent by the pediatrician to the endocrinologist often followed by a phone call, whereas 30% of endocrinologists do not send a report back to pediatricians. 4) Less than half of the Centers are satisfied with the modalities of the transfer and the remainder complain about the lack of communication, no common guidelines, and differences in the management of patients. However, all are willing to try to improve this important time for adolescents with chronic diseases. 5) As far as GH deficiency is concerned, the main differences between pediatric and adult endocrinological centers are the different tests used to re-evaluate the diagnosis and the higher doses of GH used by pediatricians to treat young adults. In conclusion, considering the interest and desire of physicians, a structural intervention of the scientific societies to help to overcome problems is highly desirable.
Adolescent↗
Sleep apnea syndrome in endocrine diseases.
It is increasingly recognized that sleep-disordered breathing (SDB) - from snoring to apnea-hypopnea syndrome (SAHS) - can affect patients with various endocrine diseases (ED). Different mechanisms are implied in SDB, promoting either central or, more frequently, obstructive apnea in different ED. In the past, acromegaly and hypothyroidism were first associated with both central and obstructive SAHS. Today, great attention is placed on the complex cause-effect relationship between diabetes mellitus and obstructive SAHS (and vice versa). Symptoms and signs of SAHS may complicate the clinical course of these diseases and should be promptly suspected to detect and possibly treat the accompanying SDB.
Cushing Syndrome↗