Autoimmune Endocrine Diseases

8/16/00 (Mansour)

Group: Wednesday Residents

RE: 29 year old female presenting with 'tiredness', 40-lb weight gain,

parasthesias, and history of amenorrhea.

Question:  How are the autoimmune endocrine diseases recognized and treated?

   Dr. Rott had selected #2.

<1>

Unique Identifier: 99029583

Authors: Davies TF. Roti E. Braverman LE. DeGroot LJ.

Institution: Mount Sinai School of Medicine, New York, New York, USA. TDavies@smtplink.mssm.edu

<2>

[Link Directly to Fulltext Article in OVID]

Unique Identifier: 98057362

Authors: Baker JR Jr.

Abstract: Autoimmune endocrine diseases are serious disorders that utilize immense health care resources and cause tremendous disability. They include type 1 diabetes mellitus, thyroiditis, Graves disease, Addison disease, and polyglandular syndromes. Analysis of the basis of autoimmune diseases has been aided by the application of new knowledge in immunologic physiology. Recent investigations using these techniques have revealed complicated disorders that have varied pathogenesis and complex genetic predispositions. While the mainstay of treatment for these diverse diseases remains the replacement of hormones produced by the damaged endocrine organ, investigations into the pathogenesis of these disorders provide hope for the development of specific therapeutic measures to block their pathologic basis. [References: 66]

<3>

[Link Directly to Fulltext Article in OVID]

Unique Identifier: 96266361

Authors: Dayan CM. Daniels GH.

Institution: University Department of Medicine, Bristol Royal Infirmary, United Kingdom.

<4>

Unique Identifier: 91015276

Authors: Wilkin TJ.

Institution: Endocrine Section, Southampton General Hospital, United Kingdom.

Abstract: The discovery in 1956 of the long-acting thyroid stimulator of Graves' disease, now known as thyroid-stimulating antibodies, was seminal. A new mechanism for disease was revealed that appears applicable to virtually all endocrine systems, involving the growth as well as the function of endocrine cells. An endocrine gland may fail through at least three autoimmune mechanisms: destruction, atrophy, and inhibition of function. Destruction is probably irreversible but is not usually distinguishable clinically from receptor blockade causing atrophy or from metabolic unresponsiveness. The contribution made by receptor autoimmunity to endocrine diseases other than thyroid disease is at present unclear, but with immunologic manipulation it is potentially reversible, improving the replicative capacity of the gland, its metabolic responsiveness, or both. [References: 52]

<5>

Unique Identifier: 88231978

Authors: Anonymous.

<6>

Unique Identifier: 88184407

Authors: Meyerson J. Lechuga-Gomez EE. Bigazzi PE. Walfish PG.

Institution: University of Toronto Post-Graduate Endocrine Training Program, Ont.

Abstract: The polyglandular autoimmune syndrome (PGAS) is characterized by the association of two or more endocrine disorders that are mediated by autoimmune mechanisms and usually lead to a hypofunctional state. In this review we classify the various types of PGAS and discuss their clinical features and the pathophysiologic autoimmune mechanisms that are thought to play an important role. Circulating organ- and cell-specific autoantibodies are frequently detected in patients with the syndrome and may be a marker of future organ failure. PGAS should be considered in patients with one or more of the disorders constituting the syndrome; this should facilitate early diagnosis and perhaps even prevention of other components of the disease. Early recognition and replacement therapy can be life-saving, particularly when there is adrenal or thyroid insufficiency. [References: 80]

<7>

Unique Identifier: 87288727

Authors: Fisher DA. Pandian MR. Carlton E.

Abstract: Autoimmune thyroid disease classically has included Hashimoto's thyroiditis and Graves' disease. Hashimoto's thyroiditis probably also includes focal thyroiditis, fibrous thyroiditis, primary myxedema, and Hashitoxicosis as variants. Graves' disease is associated with ophthalmopathy and dermopathy, and recent evidence suggests that these manifestations are autoimmune phenomena as well. Other associated autoimmune disorders include idiopathic thrombocytopenic purpura and antigen-antibody complex nephritis. Nonthyroid endocrine autoimmune deficiency disorders also have been classified as part of the spectrum of thyroid autoimmune disease. With the recent recognition of the spectrum of autoimmune mechanisms and antibody types and methods to distinguish antibody functions or types, our understanding of postpartum and neonatal thyroid disorders has been advanced considerably. The spectrum of neonatal thyroid disorders in the infants of women with autoimmune disease relates to the levels and types of antithyroid antibodies acquired from the mother. Finally, there is suggestive evidence that nonspecific goiter, including simple adolescent goiter and multinodular goiter as well as some cases of sporadic cretinism, may be part of an even more expanded spectrum of autoimmune thyroid disease. [References: 48]

<8>

Unique Identifier: 85304240

Authors: Leshin M.

Abstract: Dysfunction of multiple endocrine glands may develop as the result of hypopituitarism, various infiltrative disorders, or an organ-specific autoimmune mechanism. When dysfunction of two or more endocrine glands occurs in association with circulating organ-specific antibodies directed against the involved glands, the term polyglandular autoimmune syndrome is applied. Characteristics of polyglandular autoimmunity include specific patterns of disease association and frequently a family history of similar involvement. The principal endocrine components of these syndromes are adrenal insufficiency, autoimmune thyroid disease, insulin-dependent diabetes mellitus, and premature gonadal failure. In addition, primary hypoparathyroidism is a key feature of one form of polyglandular autoimmunity that occurs in children. Several nonendocrine organ-specific autoimmune disorders are also associated with polyglandular autoimmunity, of which pernicious anemia is the most frequent. The underlying abnormality responsible for polyglandular autoimmunity is most likely a defect in T suppressor cell function, but there is evidence that aberrant expression of HLA DR antigens also plays an important role in the pathogenesis of these disorders. [References: 92]

<9>

Unique Identifier: 83062685

Authors: Strakosch CR. Wenzel BE. Row VV. Volpe R.

<10>

Unique Identifier: 78122321

Authors: Anonymous.

Abstract: Thyroid-related autoimmune diseases (Graves' thyroid disease, Graves' ophthalmopathy, and Hashimoto's thyroiditis) may occur alone or in any association. The diagnosis of Hashimoto's thyroiditis requires multiple criteria; pathologic changes in the thyroid are not due to antibodies but may result from cytotoxic lymphocytes or a deficiency of suppressive T cells. In Graves' and Hashimoto's diseases the increased prevalence of HLA-B8 may not be significant, but that of HLA-AW30 in Hashimoto's disease is. In 48 first-degree relatives of patients with Graves' disease, thyroid abnormalities were frequent but not correlated with HLA type. Elevated serum thyroglobulin levels in all patients with hyperthyroidism fell to normal after surgical resection or radioiodine therapy. Patients whose illness recurred after antithyroid drug treatment was stopped had higher pretreatment thyroglobulin levels and no fall during treatment; those whose illness remitted had lower initial levels and a significant fall during treatment. Sodium ipodate lowered serum triiodothyronine and thyroxine levels in hyperthyroid patients and may be useful in the treatment of hyperthyroidism. [References: 80]

<11>

Unique Identifier: 74124337

Authors: Beall GN. Solomon DH.

<12>

Unique Identifier: 72162563

Authors: Forcier RJ. McIntyre OR. Frey WG. Andrada JA. Streiff RR.