Clinics in Endocrinology and Metabolism最新文献

{"title":"Diagnosis and treatment of primary aldosteronism and isolated hypoaldosteronism","authors":"James C. Melby","doi":"10.1016/S0300-595X(85)80085-2","DOIUrl":"10.1016/S0300-595X(85)80085-2","url":null,"abstract":"","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 977-995"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80085-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14135941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ACTH and related peptides: Molecular biology, biochemistry and regulation of secretion","authors":"Hiroo Imura","doi":"10.1016/S0300-595X(85)80080-3","DOIUrl":"10.1016/S0300-595X(85)80080-3","url":null,"abstract":"<div><p>The precursor of ACTH and β-LPH is a glycoprotein with a molecular weight of more than 30000. Its gene consists of three exons with two intervening sequences and most of the protein coding sequence is in exon 3. The gene is expressed not only in the pituitary gland but also in extrapituitary tissues. The gene expression in the anterior pituitary gland is regulated by CRF and glucocorticoids, but it is regulated differently in other tissues. The processing of the ACTH/β-LPH precursor yields several peptides, but final products vary in tissues due to differential processing. The processing is abnormal in ACTH-producing tumours, especially in ectopic ACTH-producing tumours. Some abnormalities may also occur at the transcriptional or post-transcriptional level as well.</p><p>Peptides derived from the same precursor are secreted concomitantly from the pituitary gland. CRF is the major stimulating factor, but vasopressin and some other factors are also involved in stimulating ACTH release. On the other hand, glucocorticoids inhibit ACTH release by acting at the hypothalamic and pituitary levels. In the pituitary ACTH-producing adenomas of Cushing's disease, CRF, vasopressin as well as other non-physiological factors stimulate ACTH secretion. Such abnormal receptor mechanisms are also seen in ectopic ACTH-producing tumours.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 845-866"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80080-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14004714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adrenocorticosteroids: Chemistry, synthesis and disturbances in disease","authors":"V.H.T. James,&nbsp;J.D. Few","doi":"10.1016/S0300-595X(85)80081-5","DOIUrl":"10.1016/S0300-595X(85)80081-5","url":null,"abstract":"<div><p>The biosynthesis of adrenocortical steroids is now a reasonably well understood process, which proceeds by discrete, enzyme directed steps from cholesterol to the various hormonal steroids. However, much of our knowledge derives from studies of animal tissues and there is a need for further studies of human glands. In particular, the details of individual enzyme systems, and the extent and significance of compartmentalization of steroid intermediates requires further exploration. The adrenal metabolic errors also merit further study, to clarify some aspects of congenital adrenal hyperplasia and to explain the relationship between biochemical and clinical observations.</p><p>The advent of immunoassay methods for the measurement of steroid hormone levels in plasma has changed the approach to diagnostic steroid endocrinology, with less emphasis now on the measurement of urinary steroid metabolites, particularly in regard to androgens. The newer and sensitive methods available also allow the assay of steroid hormones in saliva, and the ready availability of this fluid, and the fact that sampling is a non-invasive technique makes salivary steroid assay an attractive alternative to other, traditional methods of investigation requiring blood or urine collection.</p><p>Inhibitors of steroid biosynthesis and of steroid action have been used with considerable success in diagnostic techniques and to a limited extent in the treatment of steroid disorders. As our understanding of the details of steroid biosynthesis, mechanism of steroid action, and control of steroid secretion improve, further progress in designing clinically useful inhibitors should be possible.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 867-892"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80081-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15026604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pituitary-adrenocortical axis.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"765-1042"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15197047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pituitary-adrenocortical axis and the immune system","authors":"J. Edwin Blalock,&nbsp;Eric M. Smith,&nbsp;Walter J. Meyer III","doi":"10.1016/S0300-595X(85)80087-6","DOIUrl":"10.1016/S0300-595X(85)80087-6","url":null,"abstract":"<div><p>Recent findings indicate that interactions between the pituitaryadrenocortical axis and the immune system involve more than simply the effects of glucocorticoid hormones. This altered view has resulted from the observations that: 1) cells of the immune system have receptors for and are directly acted upon by ACTH and endorphins, and 2) the immune system is an important non-pituitary source of these peptide hormones. In this chapter, while we review in a cursory way the older findings with glucocorticoid hormones, we concentrate on the newer developments which suggest that leukocyte- and pituitary-derived ACTH and endorphins perform regulatory functions within and between the immune system and the pituitary-adrenocortical axis.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 1021-1038"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80087-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14136032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The adrenal cortex and virilization","authors":"T. Joseph McKenna,&nbsp;Sean K. Cunningham,&nbsp;Therese Loughlin","doi":"10.1016/S0300-595X(85)80086-4","DOIUrl":"10.1016/S0300-595X(85)80086-4","url":null,"abstract":"<div><p>The physiological control of adrenal androgen secretion has not been definitively established. However, there is evidence to suggest that a dexamethasone-suppressible factor other than ACTH may have a specific role to play. The majority of patients with idiopathic hirsutism (hirsutism associated with regular menstruation) have findings suggestive of adrenal androgen excess, including enhanced androgen responsiveness following administration of metyrapone, and respond to treatment with dexamethasone, 0.5 mg given each night. Patients with idiopathic hirsutism have elevated androgens but normal oestrogen and gonadotrophin levels. In contrast, while patients with polycystic ovary syndrome (PCOS) also demonstrate evidence of adrenal androgen excess, these patients have elevated oestrone levels and gonadotrophin secretion is abnormal. Approximately 50% of patients with PCOS treated with dexamethasone resume regular menstruation. Oestrone excess appears to be primary to the abnormal gonadotrophin secretion and to the development of PCOS. In non-obese patients with PCOS elevated oestrone appears to occur as a consequence of the availability of the excessive amounts of its immediate precursor, androstenedione, an androgen mainly of adrenal origin. Androstenedione is converted to oestrone in fat. Obese amenorrhoeic subjects have normal androstenedione values but elevated oestrone levels with abnormal gonadotrophin secretion as seen in PCOS. These findings indicate that abnormal gonadotrophin secretion is associated with elevated oestrone levels whether these occur as a consequence of excessive adrenal androgen secretion, or the excessive conversion of normal amounts of available androstenedione. Patients with idiopathic hirsutism and elevated androstenedione levels but normal oestrone values appeared to be protected against the development of PCOS by relatively poor conversion of androstenedione to oestrone. It is likely, therefore, that if patients with idiopathic hirsutism gain additional adipose tissue, elevated oestrone levels will result and PCOS will develop. These observations explain the frequent association of PCOS and obesity. There is a close clinical association between elevated androgen levels and hirsutism and between elevated oestrone levels and menstrual disturbances. However, some patients with amenorrhoea but without hirsutism may demonstrate marked elevations of androgens and oestrone, the correction of which leads to the resumption of regular ovulation. This presentation, ‘amenorrhoea with cryptic hyperandrogenaemia’, is probably explained by diminished sensitivity of androgen receptors. While adrenal androgen excess may be associated with hirsutism and menstrual disturbances in patients with Cushing's syndrome, the features of glucocorticoid excess usually predominate. When frank virilization develops, the presence of an androgen-secreting adrenal or ovarian tumour should be suspected. Ultrasonography, CT scanning, adrenal rad","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 997-1020"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80086-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14135942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cushing's syndrome","authors":"T.A. Howlett,&nbsp;L.H. Rees,&nbsp;G.M. Besser","doi":"10.1016/S0300-595X(85)80083-9","DOIUrl":"10.1016/S0300-595X(85)80083-9","url":null,"abstract":"<div><p>Cushing's syndrome remains one of the most challenging problems in clinical endocrinology. Cushing's disease is caused in the majority of cases by basophil pituitary microadenomas which may be successfully treated by trans-sphenoidal hypophysectomy. Treatment with metyrapone or <em>o,p′</em>-DDD can always induce a clinical remission but not a cure, and neurotransmitter therapy may be effective in a minority of cases. Pituitary irradiation cures about half of cases in the long-term and may be used for surgical failures.</p><p>Tumours producing ectopic ACTH are frequently benign, small and occult and may produce a syndrome clinically indistinguishable from Cushing's disease. Biochemical investigations cannot absolutely distinguish pituitary from ectopic sources of ACTH and therefore body CT scanning and percatheter venous sampling are essential diagnostic investigations. Tumour localization may result in resection and complete cure, although even small tumours may have a malignant potential.</p><p>Adrenal tumours are readily diagnosed by plasma ACTH measurement and adrenal CT scanning. Adrenal adenomas are cured by adrenalectomy. Carcinomas may be treated by a combination of adrenalectomy, radiotherapy and <em>o,p′</em>-DDD, but long-term prognosis is poor.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 911-945"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80083-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14136036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Index","authors":"","doi":"10.1016/S0300-595X(85)80088-8","DOIUrl":"https://doi.org/10.1016/S0300-595X(85)80088-8","url":null,"abstract":"","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 4","pages":"Pages 1039-1042"},"PeriodicalIF":0.0,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80088-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138251883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3 Clinical, endocrinological and biochemical effects of zinc deficiency","authors":"Ananda S. Prasad","doi":"10.1016/S0300-595X(85)80007-4","DOIUrl":"10.1016/S0300-595X(85)80007-4","url":null,"abstract":"<div><p>The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal disease, certain diuretics, the use of chelating agents such as penicillamine for Wilson's disease, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during the growing age period. The clinical manifestations in severe cases of zinc deficiency included bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males and it is fatal if untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss and hyperammonaemia.</p><p>Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and in man. Inasmuch as zinc is needed for protein and DNA synthesis and cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis.</p><p>Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level and the hypothalamic-pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in a cell division, its deficiency may adversely affect testicular size and thus its function. In mice, the incidence of degenerate oocytes, and hypohaploidy and hyperhaploidy in metaphase II oocytes were increased due to zinc deficiency.</p><p>Zinc at physiological concentrations reduced prolactin secretion from the pituitary in vitro and it has been suggested that this trace element may have a role in the in vivo regulation of prolactin release. Thymopoeitin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent.</p><p>It is clear that zinc may have several roles in biochemical and hormonal functions of various endocrine organs. Future research in this area is very much needed.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 3","pages":"Pages 567-589"},"PeriodicalIF":0.0,"publicationDate":"1985-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80007-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15018757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"8 Aluminium toxicity in chronic renal insufficiency","authors":"John Savory,&nbsp;Roger L. Bertholf,&nbsp;Michael R. Wills","doi":"10.1016/S0300-595X(85)80012-8","DOIUrl":"10.1016/S0300-595X(85)80012-8","url":null,"abstract":"<div><p>Aluminium is a ubiquitous element in the environment and has been demonstrated to be toxic, especially in individuals with impaired renal function. Not much is known about the biochemistry of aluminium and the mechanisms of its toxic effects. Most of the interest in aluminium has been in the clinical setting of the haemodialysis unit. Here aluminium toxicity occurs due to contamination of dialysis solutions, and treatment of the patients with aluminium-containing phosphate binding gels. Aluminium has been shown to be the major contributor to the dialysis encephalopathy syndrome and an osteomalacic component of dialysis osteodystrophy. Other clinical disturbances associated with aluminium toxicity are a microcytic anaemia and metastatic extraskeletal calcification. Aluminium overload can be treated effectively by chelation therapy with desferrioxamine and haemodialysis.</p><p>Aluminium is readily transferred from the dialysate to the patient's bloodstream during haemodialysis. Once transferred, the aluminium is tightly bound to non-dialysable plasma constituents. Very low concentrations of dialysate aluminium in the range of 10–15 μg/l are recommended to guard against toxic effects. Very few studies have been directed towards the separation of the various plasma species which bind aluminium. Gel filtration chromatography has been used to identify five major fractions, one of which is of low molecular weight and the others appear to be protein-aluminium complexes. Recommendations on aluminium monitoring have been published and provide ‘safe’ and toxic concentrations. Also, the frequency of monitoring has been addressed.</p><p>Major problems exist with the analytical methods for measuring aluminium which result from inaccurate techniques and contamination difficulties. The most widely used analytical technique is electrothermal atomic absorption spectrometry which can provide reliable measurements in the hands of a careful analyst.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":"14 3","pages":"Pages 681-702"},"PeriodicalIF":0.0,"publicationDate":"1985-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(85)80012-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15018761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}