Williams Textbook of Endocrinology
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For more than 65 years, Williams Textbook of Endocrinology has been the gold standard in the field, delivering authoritative guidance on every aspect of adult and pediatric endocrine system disorders. The 13th Edition has been thoroughly updated by Drs. Shlomo Melmed, Kenneth S. Polonsky, P. Reed Larsen, and Henry M. Kronenberg, to bring you state-of-the-art coverage of diabetes, metabolic syndrome, obesity, thyroid disease, testicular disorders, and much more, all designed to help you provide optimal care to every patient. Bridging the gap between basic science and clinical information, it is an essential, relevant resource for endocrinologists, endocrine surgeons, gynecologists, internists, and pediatricians – any clinician who needs the most reliable coverage available on the diverse features across the spectrum of endocrine disease.
- Obtain a better understanding of both scientific insight and clinical data
from the classic reference that delivers the current information you need in a highly illustrated, user-friendly format.
- Stay up to date with expanded discussions
- Update your knowledge and skills with all-new chapters
- Confidently manage any clinical endocrinopathy you may encounter
- Benefit from the expertise of dynamic new contributors
of autoimmune thyroid diseases, mechanisms, and the appropriate treatment of the ophthalmopathy of Graves’ disease; a new section on the interpretation of fine needle aspiration results in patients with thyroid nodules; and new coverage of when and when not to use radioiodine in the treatment of patients with thyroid cancer.
on Genetics of Endocrine Disease, Endocrinology of Population Health, and Laboratory Techniques for Recognition of Endocrine Disorders.
thanks to new information on recent FDA-approved drugs for pituitary disorders, a new focus on pediatrics, and new content on diabetes, obesity, and appetite control.
who offer fresh perspectives throughout.
eliminate interferences by human antimouse antibodies with a two-site immunoassay. Clin Biochem. 1996;29:145-148. 131. Wheeler MJ, D’Souza A, Matadeen J, et al. Ciba Corning ACS:180 testosterone assay evaluated. Clin Chem. 1996;42:1445-1459. Historical Perspective, 103 Neural Control of Endocrine Secretion, 104 Hypothalamic-Pituitary Unit, 106 Circumventricular Organs, 109 Pineal Gland, 113 Hypophyseotropic Hormones and Neuroendocrine Axes, 115 Neuroendocrine Disease, 157 CHAPTER
rhythm in corticosterone was restored by a constant infusion of CRH to CRH knockout mice,189 suggesting that CRH is necessary to permit pituitary or adrenal responsiveness to another diurnal rhythm generator. Corticotropin Release–Inhibiting Factor. Disconnection of the pituitary from the hypothalamus in several species leads to increased basal levels of ACTH, and certain responses to physical stress (in contrast to psychological stress) are retained in such animals. These observations led
psychosocial dwarfism) (see Chapter 17). Intrinsic disease of the anterior pituitary is reviewed in Chapter 8, and disturbances in neurohypophyseal function are discussed in Chapter 10. This chapter considers primarily diseases of the hypothalamic-pituitary unit. Pituitary Isolation Syndrome Destructive lesions of the pituitary stalk, such as may occur with head injury, surgical transection, tumor, or granuloma, produce a characteristic pattern of pituitary dysfunction.365-367 Central diabetes
70 30 FSH mIU/mL estrogen begins the process. Terminal end buds form and lead the process of mammary development by branching and extending into the substance of the mammary fat pad, leaving in their wake a network of ducts that virtually fill the mouse mammary fat pad.96,97 GH acts on the mammary stromal compartment to produce IGF1, which, in turn, stimulates formation of the terminal end buds and ducts in synergy with estrogen.95,98 Parathyroid hormone–related protein is essential for fetal
further studies are required to determine whether such differences are important in individual responses to various drugs (i.e., pharmacogenomics) or whether they create other subtle physiologic differences that could confer susceptibility to disease (i.e., complex disease genes). Evidence for an important role of adrenergic receptor polymorphisms in the development and treatment of heart failure supports the need for comparable studies of other GPCR family members.163 A large proportion of the