Endocrinology and Metabolism: An Annotated Bibliography of Recent Literature
Authors: ENDOCRINOLOGY AND METABOLISM COMMITTEE, MEDICAL KNOWLEDGE SELF-ASSESSMENT PROGRAM VI, AMERICAN COLLEGE OF PHYSICIANS
Journal: Annals of Internal Medicine (1982)

The Literature of Medicine1 July 1982Endocrinology and Metabolism: An Annotated Bibliography of Recent LiteratureReferences to Journal Articles and Other PapersENDOCRINOLOGY AND METABOLISM COMMITTEE, MEDICAL KNOWLEDGE SELF-ASSESSMENT PROGRAM VI, AMERICAN COLLEGE OF PHYSICIANSENDOCRINOLOGY AND METABOLISM COMMITTEESearch for more papers by this author, MEDICAL KNOWLEDGE SELF-ASSESSMENT PROGRAM VISearch for more papers by this author, AMERICAN COLLEGE OF PHYSICIANSSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-1-151 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis bibliography includes references to 103 recently published journal papers and similar sources that represent important developments in the concept and practice of internal medicine. It has been compiled by the Endocrinology and Metabolism Committee* as part of the Medical Knowledge Self-Assessment Program VI Syllabus.In preparing this bibliography, the committee reviewed MEDLINE† bibliographic printouts of journal articles published since the beginning of 1978 and also drew on sources in libraries of hospitals and other clinical institutions in the United States and Canada; thus, only papers in English are listed, and most are from American journals....Neuroendocrine-Anterior Pituitary Ectopic Hormone Production Adrenal Cortex and Medulla The Reproductive System in Men The Reproductive System in Women Disorders of Bone and Mineral Metabolism Carbohydrate Metabolism and Diabetes Mellitus Disorders of Nutrition1. COBBSPAREREICHLIN WSS. Neurogenic diabetes insipidus: management with dDAVP (1-desamino-S-D arginine vasopressin). Ann Intern Med. 1978;88:183-8. Twenty-nine patients with neurogenic diabetes insipidus were treated with dDAVP by the intranasal route with minimal side effects. This drug is now the treatment of choice for this disorder. LinkGoogle Scholar2. COOKETURINWALKER CMW. The syndrome of inappropriate antidiuretic hormone secretion (SIADH): pathophysiologic mechanisms in solute and volume regulation. Medicine. 1979;58:240-51. A study of eight patients with SIADH examined the mech anisms of altered sodium metabolism and volume regulation in the syndrome. The increased sodium excretion was shown to play a major role in water excretion despite persistant antidiuretic hormone effects. CrossrefMedlineGoogle Scholar3. CROWLEYBEITINSVALE WIW. The biologic activity of a potent analogue of gonadotropin-releasing hormone in normal and hypogonadotropic men. N Engl J Med. 1980;302:1052-7. Describes the use of long-acting analog of luteinizing hormone-releasing hormone in hypogonadotropic patients. En hanced and sustained action in releasing luteinizing-hormone was seen even in patients unresponsive to natural luteinizing hormone-releasing hormone. CrossrefMedlineGoogle Scholar4. DUNGERLEONARDWOLFFPREECE DJOM. Effect of naloxone in a previously undescribed hypothalamic syndrome: a disorder of the endogenous opioid peptide system? Lancet. 1980;1:1277-81. A patient with disordered hypothalamic function involving neuroendocrine water regulation, food intake, sleep, and temperature disturbances was successfully treated with naloxone, implicating for the first time an endorphin-enkephalin pathogenetic mechanism for the disorder. CrossrefMedlineGoogle Scholar5. FAGLIABITENSKYPINCHERA GLA. Thyrotropin secretion in patients with central hypothyroidism: evidence for reduced biological activity of immunoreactive thyrotropin. J Clin Endocrinol Metab. 1979;48:989-98. In a subgroup of patients with hypothalamic hypothyroidism, the authors found evidence of immunologically active but biologically inactive thyroid-stimulating hormones, which indicates another cause of hypothalamic-pituitary hypothyroidism. CrossrefMedlineGoogle Scholar6. LAWSPIEPGRASRANDALLABBOUD EDRC. Neurosurgical management of acromegaly: results in 82 patients treated between 1972 and 1977. J Neurosurg. 1979; 50:454-61. A consecutive surgical series of 82 patients with acro megaly is described. The apparent cure rate varied with the type of adenoma found at operation. The greatest success rate occurred with microadenomas and the least with diffuse and invasive tumors. CrossrefMedlineGoogle Scholar7. MARCHKLETZKYDAVAJAN COV. Longitudin al evaluation of patients with untreated prolactin-secreting pituitary adenomas. Am J Obstet Gynecol. 1981;139:835-44. Of 43 patients with prolactinomas followed for up to 20 years and who did not have surgery, only two had an increase in tumor size requiring surgery. CrossrefMedlineGoogle Scholar8. RIDGWAYKLIBANSKILADENSON EAP. Pure alpha-secreting pituitary adenomas. N Engl J Med. 1981 ;304:154-9. Isolated secretion of the glycoprotein alpha subunit occur red in two men previously diagnosed as having "nonfunctioning" pituitary tumors. Its use as a tumor marker for such tumors is emphasized. CrossrefMedlineGoogle Scholar9. SCHLECHTEVANGILDERSHERMAN JJB. Predictors of the outcome of transsphenoidal surgery for prolactin-secreting pituitary adenomas. J Clin Endocrinol Metab. 1981 ;52:785-9. An analysis of the factors with predictive value for the outcome of prolactinoma surgery indicates the importance of estrogen; best results were seen in patients whose tumors were associated with exogenous estrogen therapy or endogenous estrogen overproduction. CrossrefMedlineGoogle Scholar10. THORNERMARTINROGOL MWA. Rapid regression of pituitary prolactinomas during bromocriptine treatment. J Clin Endocrinol Metab. 1980;51:438-45. Objective evidence is presented for the rapid onset of ac tion of bromocriptine in reducing the size of a suprasellar prolactinoma. Initial visual field improvement could be found in as few as 3 days. CrossrefMedlineGoogle Scholar11. TYRRELLBROOKSFITZGERALDCOFOIDFORSHAMWILSON JRPPPC. Cushing's disease: selective trans-sphenoidal resection of pituitary microadenomas. N Engl J Med. 1978;298:753-8. The results of treatment of 20 patients with Cushing's disease by microsurgical adenomectomy are presented. Even in the absence of evident changes in polytomography, a large fraction of patients were successfully treated. CrossrefMedlineGoogle Scholar12. IMURA H. Ectopic hormone syndromes. Clin Endocrinol Metab. 1981;9:235-60. A review of the major ectopic-hormone-secreting tumors with emphasis on clinical syndromes, biochemical aspects of hormones as tumor markers, and theories of ectopic hormone production. CrossrefGoogle Scholar13. SKRABANEKMCPARTLINPOWELL PJD. Tumor hypercal cemia and "ectopic hyperparathyroidism." Medicine. 1980;39:262-82. A review of 307 case reports of tumor hypercalcemia that analyzes the evidence for ectopic hormone production and discusses the multiple causes and mechanisms involved. CrossrefGoogle Scholar14. CRAPO L. Cushing's syndrome: a review of diagnostic tests. Metabolism. 1979;28:955-77. A comprehensive analysis of the results of various diag nostic tests used to evaluate Cushing's syndrome. Data from a large number of studies are compared and the most valid interpretations of the test results presented. Effective diagnostic protocols are suggested. CrossrefMedlineGoogle Scholar15. CRYER P. Physiology and pathophysiology of the human sympathoadrenal neuroendocrine system. N Engl J Med. 1980;303:436-44. Discussion of the physiology of catecholamines, includ ing their metabolic actions and the importance of adrenergic receptor regulation. The use of plasma catecholamine measurement in pheochromocytoma is discussed, and the point is made that elevations are also found in essential hypertension, diabetes and its various abnormalities, and myocardial infarction, thus indicating the lack of specificity of this test. CrossrefMedlineGoogle Scholar16. GILL J. Bartter's syndrome. Annu Rev Med. 1980;31:405-19. A review that discusses the pathophysiology, differential diagnosis, and management of this interesting syndrome. The difficult problem of distinguishing patients with Bartter's syndrome from patients that induce vomiting, abuse laxatives, or surreptitiously take diuretics is also addressed. CrossrefGoogle Scholar17. GOLD E. The Cushing syndromes: changing views of diagnosis and treatment. Ann Intern Med. 1979;90:829-44. A detailed review of the clinical findings in the various Cushing syndromes is given and methods of diagnosis are discussed. The therapeutic options available for treatment are evaluated. LinkGoogle Scholar18. HAHN T. Drug-induced disorders of vitamin D and mineral metabolism. Clin Endocrinol Metab. 1980;9:107-29. This article covers corticosteroid-induced osteopenia in addition to other drug-induced bone disorders. Clinical features, pathophysiology, and treatment are completely discussed. CrossrefMedlineGoogle Scholar19. HERFTEATESTEGTMEYERVAUGHANAYERSCOREY SDCECR. Identification and differentiation of surgically correctable hypertension due to primary aldosteronism. Am J Med. 1979;67:397-402. Findings in patients with primary aldosteronism due to an adenoma are compared with data obtained from patients with adrenal hyperplasia. Guidelines are provided to help ascertain whether hypertension in a given patient with aldosteronism is likely to respond to surgery. CrossrefMedlineGoogle Scholar20. HOLLENBERGWILLIAMS NG. Hypertension, the adren al and the kidney: lessons from pharmacologic interruption of the renin-angiotensin system. Adv Intern Med. 1980;25:327-61. Discussion of the pharmacologic agents that interrupt the renin-angiotensin system used to define the role of angiotensin II in controlling blood pressure and aldosterone secretion. Attention is given to Captopril, and inhibitor of converting enzyme, and saralasin, an angiotensin II analogue that interacts with the receptor. MedlineGoogle Scholar21. KAPLAN S. Diseases of the adrenal cortex. II. Congenital adrenal hyperplasia. Ped Clin North Am. 1979;26:77-89. Discussion of the spectrum of entities comprising congenital adrenal hyperplasia. CrossrefMedlineGoogle Scholar22. KOROBKINWHITEKRESSELMossMON TAGNE MEHAJ. Computed tomography in the diagnosis of adrenal disease. AJR. 1979;132:231-8. Computed tomography is increasingly important in tumor visualization and the differential diagnosis of endocrine disease. The findings in a large series of patients with all varieties of adrenal pathology including Cushing's syndrome, aldosteronism, and pheochromocytoma are presented. CrossrefMedlineGoogle Scholar23. KRIEGERLIOTTABROWNSTEINZIMMERMAN DAME. ACTH, β-lipoprotein and related peptides in brain, pituitary, and blood. Recent Prog Horm Res. 1980;36:277-344. Extensive discussion of the nature of adrenocorticotropic hormone lipoprotein lipase, and melanocyte-stimulatinghormone, including their origin from a common precursor molecule. Reports data on the levels of these hormones in the plasma of normal persons and patients with pituitary-adrenal disease. MedlineGoogle Scholar24. SCHAMBELANSEBASTIAN MA. Hyporeninemic hypoaldosteronism. Adv Intern Med. 1979;24:385-405. A review of hyporeninemic hypoaldosteronism with special emphasis on the differential diagnosis of hyperkalemia. The discussion includes pathogenesis and treatment. MedlineGoogle Scholar25. TYRRELLBROOKSFITZGERALDCOFOIDFORSHAMWILSON JRPPPC. Cushing's disease: selective trans-sphenoidal resection of pituitary microadenomas. N Engl J Med. 1978;298:753-8. The results of transphenoidal surgery in 20 patients with Cushing's disease. Early postoperative findings are encouraging and suggest that this therapeutic technique offers a low morbidity approach to the successful treatment of Cushing's disease. The data indicate a very high incidence of pituitary adenomas. CrossrefMedlineGoogle Scholar26. WEINBERGERGRIMHOLLIFIELD MCJ. Primary aldosteronism: diagnosis, localization, and treatment. Ann Intern Med. 1979;90:386-95. Clinical review of primary aldosteronism with emphasis on the clinical findings, diagnostic protocols, tumor localization, and the results of surgical intervention. The distinction between unilateral adenoma and bilateral hyperplasia also is emphasized. LinkGoogle Scholar27. ZUSMAN R. Prostaglandins and water excretion. Annu Rev Med. 1981;32:359-74. The formation of prostaglandins, the actions of various inhibitors of prostaglandin synthesis, and the interactions of prostaglandins with the many hormone systems that regulate water balance are reviewed. Thyroid CrossrefMedlineGoogle Scholar28. BLUMROTHSCHILD MM. Improved nonoperative diagnosis of the solitary "cold" thyroid nodule: surgery selection based on risk factors and three months of suppression. JAMA. 1980;243:242-5. Most thyroid cancers were found in patients selected for surgery on the basis of risk factors and findings on physical examination. Patients not initially selected for surgery were treated with thyroid hormone for three months; 25% of those whose nodules did not decrease in size also had thyroid carcinoma. It is presumed, but not proved, that patients whose nodules did decrease in size during thyroid therapy do not have thyroid carcinoma. CrossrefMedlineGoogle Scholar29. CAPLANPAGLIARAWICKUS RAG. Thyroxine toxicosis: common variant of hyperthyroidism. JAMA. 1980;244; 1934-8. Hyperthyroidism with elevated serum T4 but normal serum T3 concentrations was found in 13 of 83 patients; some had no other illness likely to decrease extrathyroidal T3 production. No patient had T3-hyperthyroidism. This high incidence of T4-hyperthyroidism may be unusual, but emphasizes the need for awareness of this disease. CrossrefMedlineGoogle Scholar30. CHOPRASOLOMONHEPNERMORGENSTEIN IDGA. Misleadingly low free thyroxine index and usefulness of reverse triiodothyronine measurement in nonthyroidal illness. Ann Intern Med. 1979;90:905-12. Low serum T4 concentrations and low serum free T4 index values are frequently found with severe nonthyroidal illness as well as hypothyroidism. Patients with nonthyroidal illness usually have normal serum free T4 concentrations. Because their low serum T4 concentrations reflect decreased T4 binding to serum proteins, rather than decreased T4 secretion, reverse T3 production is normal and reverse T3 degradation is decreased. Their serum reverse T3 concentrations are often elevated. This measurement may help in further excluding hypothyroidism when the serum thyroidstimulating hormone is normal. LinkGoogle Scholar31. COLACCHIOLOGERFOFEIND TPC. Fine needle cytologic diagnosis of thyroid nodules: review and report of 300 cases. Am J Surg. 1980;140:568-71. Fine-needle aspiration biopsy in 300 patients with hypofunctioning (cold) thyroid nodules was followed in most by coarse-needle biopsy or surgery. Three aspiration biopsies were falsely negative for thyroid carcinoma and four falsely positive. Fine-needle biopsy can greatly decrease the number of patients needing surgery. CrossrefMedlineGoogle Scholar32. DREXHAGEBOTTAZZODONIACHBITENSKYCHAYEN HGDLJ. Evidence for thyroid-growth-stimulating immunoglobulins in some goitrous thyroid diseases. Lancet. 1980;2:287-92. Autoantibodies that stimulate thyroid growth, as measured by increased DNA synthesis, were found in the serum of patients with goitrous autoimmune thyroiditis and other types of thyroid-hormone-resistant or recurrent goiter. There may be several classes of thyroid-stimulating autoantibodies, each with differing thyroid actions, in thyroid autoimmune disease. CrossrefGoogle Scholar33. GARDNERKAPLANSTANLEYUTIGER DMCR. Effect of tri-iodothyronine replacement on the metabolic and pituitary responses to starvation. N Engl J Med. 1979;300:579-84. Tri-iodothyronine given to normal subjects during fasting to prevent the fasting-induced fall in serum T3 concentrations inhibited the serum thyroid-stimulating hormone response to thyrotropin-releasing hormone and augmented the increase in urinary urea excretion during fasting. The decrease in T3 production that occurs during fasting and perhaps during other nonthyroidal illness as well may beneficially conserve muscle proteins. CrossrefMedlineGoogle Scholar34. GAVINROSENTHALCAVALIERI LMR. The diagnostic dilemma of isolated hyperthyroxinemia in acute illness. JAMA. 1979;242:251-3. Elevated serum total and free thyroxine concentrations may be found in various nonthyroidal illness without a history of hyperthyroidism. In most patients the abnormalities are transient. Differentiation from hyperthyroidism may be achieved by serial study, the finding of a low serum T3 concentration or a normal thyroid-stimulating hormone response to thyrotropin-releasing hormone. Transient hyperthyroxinemia with nonthyroidal illness is probably due to decreased T4 degradation. CrossrefMedlineGoogle Scholar35. KIDDOKITARowVOLPé ANVR. Immunologic aspects of Graves' and Hashimoto's diseases. Metabolism. 1980;29:80-99. Graves' and Hashimoto's diseases are closely related organ-specific autoimmune disorders. This review of the genetics and the abnormalities of humoral and cell-mediated immunity of these diseases concludes that the fundamental abnormality is a defect in immunosuppression. CrossrefMedlineGoogle Scholar36. LEVINE H. Compromise therapy in the patient with angina pectoris and hypothyroidism: a clinical assessment. Am J Med. 1980;69:411-8. In hypothyroidism with angina pectoris, the need for thyroid therapy must be balanced against aggravation of anginal symptoms. Treatment of hypothyroidism often must be incomplete, and even when combined with propranolol some manifestations of both must be accepted. Coronary revascularization should be considered early. CrossrefMedlineGoogle Scholar37. SCHIMPFFDIGGSWISWELLSALVATOREWIERNIK SCJPP. Radiation-related thyroid dysfunction: implications for the treatment of Hodgkin's disease. Ann Intern Med. 1980;82:91-8. Most patients treated with head and neck radiation for Hodgkin's disease or other tumors develop clinical or biochemical hypothyroidism that develops slowly. Because complications are relatively frequent, thyroid function should be carefully assessed in the follow-up period. LinkGoogle Scholar38. STERLING K. Thyroid hormone action at the cell level. N Engl J Med. 1979;300:117-23, 173-7. Review of the mechanisms of thyroid hormone action at intracellular sites. Despite the search for a single site of thyroid hormone that could explain its actions, both immediate and sustained, none has been found. Multiple mechanisms seem likely. CrossrefMedlineGoogle Scholar39. SUGRUEMCEVOYFEELYDRURY DMJM. Hyperthyroidism in the Land of Graves: results of treatment by surgery, radio-iodine and Carbimazole in 837 cases. Q J Med. 1980;49:51-61. Ninety-one percent of patients given antithyroid drug for less than 2 years had a relapse at 5 years; the relapse rate was 49% in those treated for more than 2 years. Patients treated with radio-iodine and thyroidectomy had much lower relapse rates, but many became hypothyroid. MedlineGoogle Scholar40. UTIGER R. Decreased extrathyroidal triiodothyronine production in nonthyroidal illness: benefit or harm? Am J Med. 1980;69:807-10. Extrathyroidal triiodothyronine production is decreased so commonly in nonthyroidal illness that it must be considered an adaptation to illness. This short review describes what is known about T4-5!-deiodinase activity, its regulation, and the consequences of decreased extrathyroidal T3 production in nonthyroidal illness. CrossrefMedlineGoogle Scholar41. WOODCYRUSSAMOLS DJE. LOW T4 and low FT4I in seriously ill patients: concise communications. J Nuc Med. 1980;21:432-4. Low serum T4 concentrations were found in 33% of patients admitted to an intensive care unit; nearly half had low serum free T4 index values as well, but their serum free T4 concentrations were usually normal. Excluding hypothyroidism requires careful clinical evaluation and measurement of serum free T4 and thyroid-stimulating hormone concentrations. MedlineGoogle Scholar42. WOOLF P. Transient painless thyroiditis with hyperthyroidism: a variant of lymphocytic thyroiditis? Endocr Rev. 1980;1:411-20. Painless thyroiditis with hyperthyroidism, relatively newly recognized, is transient, unlike hyperthyroidism due to Graves' disease. This review describes the diagnosis, course, and pathologic features and discusses the hypothesis that it is a type of lymphocytic thyroiditis (Hashimoto's disease). CrossrefMedlineGoogle Scholar43. ZAKARUAMCKENZIEBANOVAC MJK. Clinical significance of assay of thyroid-stimulating antibody in Graves' disease. Ann Intern Med. 1980;93:28-32. Thyroid-stimulating antibodies were measured in 187 patients by a method based on their ability to stimulate thyroid cyclic AMP production. Virtually all patients with newly diagnosed hyperthyroidism had thyroid-stimulating antibodies in their serum. Most patients whose serum was negative at the end of antithyroid drug therapy remained euthyroid, whereas positive tests indicated that hyperthyroidism was likely to recur. LinkGoogle Scholar44. BARDIN C. The neuroendocrinology of male reproduction. Hosp Pract. 1979;14:65-75. The interrelationships among the hypothalmus, pituitary, and testes are discussed. CrossrefMedlineGoogle Scholar45. GRIFFINWILSON JJ. The syndromes of androgen resistance. N Engl J Med. 1980;302:198-209. The physiology of androgen action is reviewed to provide a basis for understanding the pathophysiology of conditions in which androgens are secreted but not effective. CrossrefMedlineGoogle Scholar46. FRANCHIMONTVERSTRAELEN-PROYARDHAZEE-HAGELSTEIN PJM. Inhibin: from concept to reality. Vitam Horm. 1979;37:243-302. Evidence supporting the concept of a nonsteroidal testicular product that selectively inhibits follicle-stimulating hormone. CrossrefMedlineGoogle Scholar47. LIPSETT M. Physiology and pathology of the Leydig cell. N Engl J Med. 1980;303:682-8. Describes the control of testosterone secretion as well as the circumstances when testosterone secretion is diminished. CrossrefMedlineGoogle Scholar48. ODELLSWERDLOFF WR. Abnormalities of gonadal function in men. Clin Endocrinol. 1978;8:149-80. This is a comprehensive review of male hypogonadism. CrossrefMedlineGoogle Scholar49. SNYDERLAWRENCE PD. Treatment of male hypogonadism with testosterone enanthate. Clin J Endocrinol Metab. 1980;51:1335-9. Administering testosterone enanthate to men who have testicular damage shows which doses are effective in treating testosterone deficinecy. CrossrefGoogle Scholar50. WILSONAIMANMACDONALD JJP. The pathogenesis of gynecomastia. Adv Intern Med. 1980;25:1-32. A review of normal androgen and estrogen metabolism in men and the mechanisms by which abnormalities of androgen and estrogen metabolism produce gynecomastia. MedlineGoogle Scholar51. DURANDBRESSLER JR. Clinical pharmacology of the steroidal oral contraceptives. Adv Intern Med. 1979;24:97-126. The authors review the mechanism of action of oral contraceptives and their risks. MedlineGoogle Scholar52. FRISCHWYSHAKVINCENT RGL. Delayed menarche and amenorrhea in ballet dancers. N Engl J Med. 1980;303:17-9. Strenuous excercise and a minimal amount of body fat seem to inhibit normal cyclic ovarian function. CrossrefMedlineGoogle Scholar53. KIRSCHNERZUCKERJESPERSON MID. Idiopathic hirsutism—an ovarian abnormality. N Engl J Med. 1976:294:637-40. Data on ovarian and adrenal vein effluent testosterone and androstenedione concentrations suggested that the ovaries were the principal source of excessive androgen production in 42 of 44 women with idiopathic hirsutism, even when the androgens could be suppressed by dexamethasone administration. CrossrefGoogle Scholar54. KNOBILPLANTWILDTBELCHETZMARSHALL ETLPG. Control of the rhesus monkey menstrual cycle: permissive role of hypothalamic gondadotropin-releasing hormone. Science. 1980;207:1371-3. Monkeys whose gonadotropin-releasing hormone secretion had been abolished by hypothalamic lesions were treated with a single intravenous dose of gonadotropin-releasing hormone each hour. Normal, ovulatory menstrual cycles resulted, suggesting that although intermittent release of gondadotropin-releasing hormone from the hypothalamus is necessary for gonadotropin secretion, it is only permissive, and that the cyclical changes of the menstrual cycle are the result of interactions between the ovary and pituitary. CrossrefMedlineGoogle Scholar55. SHERMANKORENMAN BS. Hormonal characteristics of the human menstrual cycle throughout reproductive life. J Clin Invest. 1975;55:699-706. The relations of follicle-stimulating hormone, luteinizing hormone, and estradiol in the menstrual cycles of women from 18 to 50 years are defined. Hormonal changes occur even before menses become irregular. CrossrefMedlineGoogle Scholar56. WEINSTEIN M. Estrogen use in postmenopausal women — costs, risks, and benefits. N Engl J Med. 1980;303:308-16. The benefits of estrogen use in postmenopausal women are compared to the risks. CrossrefMedlineGoogle Scholar57. YEN S. The polycystic ovary syndrome. Clin Endocrinol. 1980;12:177-207. Discusses the hormonal abnormalities observed in this syndrome and therapy. CrossrefMedlineGoogle Scholar58. AUSTINHEATH LH. Calcitonin: physiology and pathophysiology. N Engl J Med. 1981;304:269-78. A complete and up-to-date review of the important aspects of the physiology and pathophysiology of calcitonin. CrossrefMedlineGoogle Scholar59. AVIOLI L. What to do with "postmenopausal osteoporosis"? Am J Med. 1978;65:881-4. A brief but lucid discussion of the advantages and disadvantages of various forms of therapy for this important disorder. CrossrefMedlineGoogle Scholar60. BiNSTOCKMUNDY MG. Effect of calcitonin and glucocorticoids in combination on the hypercalcemia of malignancy. Ann Intern Med. 1980;93:269-72. A retrospective study suggesting that the therapeutic benefits of calcitonin plus glucocorticoids are greater when compared to treatment with calcitonin alone. LinkGoogle Scholar61. BRESLAUPAK NC. Hypoparthyroidism. Metabolism. 1979;28:1261-76. A good summary of recent progress in the understanding and therapy of the various forms of hypoparathyroidism. CrossrefMedlineGoogle Scholar62. BROOKSBELLLOVE MNL. Vitamin-D-dependent rickets Type II: resistance of target organs to 1, 25-dihydroxyvitamin D. N Engl J Med. 1978;298:996-9. The first description of a syndrome suggesting peripheral resistance to the action of 1, 25-(OH)2 D. CrossrefMedlineGoogle Scholar63. FARFELBRICKMANKASLOWBROTHERSBOURNE ZAHVH. Defect in receptor-cyclase coupling protein in pseudohypoparathyroidism. N Engl J Med. 1980;303:237-42. The description of a probable molecular defect in pseudohypoparathyroidism type I. CrossrefMedlineGoogle Scholar64. FRAMEPARFITT BA. Osteomalacia: current concepts. Ann Intern Med. 1978;89:966-82. A scholarly and complete review of the basic aspects of bone metabolism as well as the differential diagnosis and treatment of osteomalacia. LinkGoogle Scholar65. GRAZESPILERTASHJIAN KLA. Natural history of familial medullary thyroid carcinoma: effect of a program for early diagnosis. N Engl J Med. 1978;299:980-5. A follow-up of a large group of patients showing the importance of provocative testing of calcitonin secretion in the early diagnosis of this tumor. CrossrefMedlineGoogle Scholar66. HABENERSEGRE JG. Parathyroid hormone radioimmunoassay. Ann Intern Med. 1979;91:782-5. An excellent discussion of the use and abuse of the radioimmunoassay for parathyroid hormone in the evaluation of hypercalcemic disorders. LinkGoogle Scholar67. HAUSSLERMCCAIN MT. Basic and clinical concepts related to vitamin D metabolism and action. N Engl J Med. 1977;297:974-83. An excellent review of the relevant aspects of viatmin D metabolism. CrossrefMedlineGoogle Scholar68. LEEZAWADAKLEEMAN DEC. The pathophysiology and clinical aspects of hypercalcémie disorders. West J Med. 1978;129:278-320. A comprehensive and readable discussion of the pathophysiology, differential diagnosis and treatment of hypercalcemia MedlineGoogle Scholar69. MARXSTOCKATTIE SJM. Familial hypocalciuric hypercalcemia: recognition among patients referred after unsuccessful parathyroid exploration. Ann Intern Med. 1980;92:351-6. Emphasis on the clinical features of familial hypocalciuric hypercalcemia and the need to consider this disorder when evaluating the patient with probable hyperparathyroidism. LinkGoogle Scholar70. PAPAPOULOSCLEMENSFRAHERLEWINSANDLERO'RIORDAN STLILJ. 1,25-dihydroxycholecalciferol in the pathogenesis of the hypercalcaemia of sarcoidosis. Lancet. 1979;1:627-30. An important paper suggesting that the increased sensitivity to vitamin D in sarcoidosis is due to enhanced formation of 1,25(OH)2D. CrossrefMedlineGoogle Scholar71. SIRISJACOBSCANFIELD ETR. Paget's disease of bone. Bull NY Acad Med. 1980;56:285-304. A concise review of the pathophysiology and available regimens for treating Paget's disease. MedlineGoogle Scholar72. STEWARTHORSTDEFTOSCADMANLANGBROADUS ARLERA. Biochemical evaluation of patients with cancer-associated hypercalcemia: evidence for humoral and nonhumoral groups. N Engl J Med. 1980;303:1377-83. A description of the essential features of humoral hypercalcemia of malignancy with nephrogenous cyclic adenosine monophosphate. CrossrefMedlineGoogle Scholar73. American Diabetes Association Workshop-Conference on Gestational Diabetes. Diabetes Care. 1980;3:399-501. The entrie issue is devoted to an international workshop on gestational diabetes. Data on screening results, morbidity, and therapeutic experiences from many countries are presented, and the magnitude of the problem is emphasized. Recommendations on diagnostic criteria and management. Google Scholar74. BARNETTEFFLESLIEPYKE ACRD. Diabetes in Identical twins: a study of 200 pairs. Diabetologia. 1981; 20:87-93. Analysis of identical twins has stimulated much current thinking about etiologic factors in