Antithyroid antibodies

Abbreviated New Drug Application antithyroglobulin antibody antithyroid peroxidase antibody area under the (time-concentration) curve beta-human chorionic gonadotropin central nervous system... 

Antimicrosomal antibodies Antithyroid peroxidase antibodies TSH receptor antibodies... 

Adrenal angiography Adrenal venography Adrenocorticotropic hormone stimulation test Aldosterone assay, blood Androstenedione Antidiuretic hormone Antithyroglobulin antibody Antithyroid microsomal antibody Blood glucose Calcitonin Calcium Catecholamines Chromosome karyotype Computed tomography of adrenals Cortisol blood urine C-peptide... 

Antinuclear antibody test Antiscleroderma antibody Anti-smooth muscle antibody Antispermatozoal antibody Anti-SS-A and anti-SS-B antibody Antistreptolysin O titer Antithrombin III Antithyroglobulin antibody Antithyroid microsomal antibody Apolipoproteins Aspartate aminotransferase Atrial natriuretic factor Basophils Bilirubin Bleeding time... 

Several patients have exhibited a clinical picture resembling FHH, but no CaR mutations could be identified. These individuals also exhibited various forms of autoimmunity (e.g., antithyroid antibodies) and harbored anti-CaR antibodies that reduced the high CaQ+ -evoked stimulation of MAPK and PLC in cells transfected with the wild type receptor. Thus both antireceptor antibodies and mutations in the CaR can render the receptor resistant to activation by Caq+, producing a clinical picture of mild, PTH-dependent hypocalciuric hypercalcemia [3]. 

Patients receiving amiodarone must receive monitoring for thyroid abnormalities. Baseline measurements of serum TSH, FT4, FT3, antithyroid peroxidase antibody (anti-TPOAb) and TSH receptor-stimulating antibodies (TSHR-SAb) should be performed. TSH, FT4, and FT3 should be checked 3 months after initiation of amiodarone and then every 3 to 6 months. 

A rise in the TSH level is the first evidence of primary hypothyroidism. Many patients have a free T4 level within the normal range (compensated hypothyroidism) and few, if any, symptoms of hypothyroidism. As the disease progresses, the free T4 concentration drops below the normal level. The T3 concentration is often maintained in the normal range despite a low T4. Antithyroid peroxidase antibodies and antithyroglobulin antibodies are likely to be elevated. The RAIU is not a useful test in the evaluation of hypothyroidism because it can be low, normal, or even elevated. 

Positive antithyroid antibody titers reported in patients with bipolar disorder. 

Cytokines Interferon- and interleukin-2 - Therapy with interferon- has been associated with the development of antithyroid microsomal antibodies in 20% of patients and some have transient hypothyroidism, hyperthyroidism, or both. Patients who have antithyroid antibodies before treatment are at higher risk of thyroid dysfunction during treatment. Interleukin-2 has been associated with transient painless thyroiditis in 20% of patients. 

Markowitz GS, Radhakrishnan J, Kambham N, et al Lithium nephrotoxicity a progressive combined glomerular and mbulointerstitial nephropathy. J Am Soc Nephrol 11 1439-1448,2000 Myers DH, Carter RA, Bums BH, et al A prospective study of the effects of lithium on thyroid function and on the prevalence of antithyroid antibodies. Psychol Med 15 55-61, 1985... 

The most common cause of hypothyroidism in the USA at this time is probably Hashimoto s thyroiditis, an immunologic disorder in genetically predisposed individuals. In this condition, there is evidence of humoral immunity in the presence of antithyroid antibodies and lymphocyte sensitization to thyroid antigens. Certain medications can also cause hypothyroidism (Table 38-5). 

Graves disease is considered to be an autoimmune disorder in which helper T lymphocytes stimulate lymphocytes to synthesize antibodies to thyroidal antigens. The antibody described previously (TSH-R Ab [stim]) is directed against the TSH receptor site in the thyroid cell membrane and has the capacity to stimulate growth and biosynthetic activity of the thyroid cell. Spontaneous remission occurs but some patients require years of antithyroid therapy. 

The complexity of the interaction between iodine intake and autoimmune thyroid disease has been highlighted by reports of evidence that iodide (compared with thyroxine) induces thyroid autoimmunity in patients with endemic (iodine deficient) goiter (43), while in those with pre-existing thyroid autoimmunity, evidenced by the presence of antithyroid (thyroid peroxidase) antibodies, administration of iodine in an area of mild iodine deficiency led to subclinical or overt hypothyroidism (44). 

Ototoxicity has rarely been attributed to antithyroid drugs (13). In one case progressive bilateral sensorineural hearing loss attributed to propylthiouracil was associated with myeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA) (14). 

Antithyroid drugs, especially propylthiouracil, can be associated with the development of antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis, often manifesting as renal disease. Atypical presentations, with pulmonary capillaritis (58) and lupus-like syndrome (59), have been described in individual cases. Furthermore, two cases of vasculitis have been associated with carbimazole, one presenting with eosinophilic granulomatous vasculitis localized to the stomach (60) and another with p-ANCA positive vasculitis causing simultaneous acute renal insufficiency and massive pulmonary hemorrhage (61). 

Stege R. Antithyroid drug therapy in hyperthyroidism. Recurrence, hypothyroidism and thyroid antibodies. Acta Chir Scand Suppl 1980 501 1-130. 

Slot MC, Links TP, Stegeman CA, Tervaert JW. Occurrence of antineutrophil cytoplasmic antibodies and associated vasculitis in patients with hyperthyroidism treated with antithyroid drugs a long-term followup study. Arthritis Rheum 2005 53(1) 108-13. 

Antineutrophil cytoplasmic antibody (ANCA)-positive cutaneous leucocytoclastic vasculitis associated with antithyroid therapy in Graves disease. Australas J Dermatol 1998 39(2) 96-9. 

A 45-year-old woman developed transient thyroiditis associated with antithyroid antibodies in taking leu-prorelin (31). 

In five patients who presented in Tasmania during 1 year, all of whom were taking amiodarone 200 mg/day, serum TSH was undetectable and the free thyroxine and triiodothyronine concentrations were raised (46). In one case there was a low titer of TSH receptor antibodies and in another a high titer of antithyroid peroxidase antibodies. In all cases the hyperthyroidism was severe and occurred after at least 2 years of treatment with amiodarone. In one of two patients in whom it was measured the serum concentration of interleukin-6 was raised, as has been previously shown (SEDA-19, 193). In two cases the hyperthyroidism was refractory to treatment with propylthiouracil, lithium, and dexamethasone in these cases thyroidectomy was required. Two patients responded to propylthiouracil, lithium, and dexamethasone, and one responded to carbimazole. 

The spectrum of interferon alfa-induced thyroid disorders ranges from asymptomatic appearance or increase in antithyroid autoantibody titers to moderate or severe clinical features of hypothyroidism, hyperthyroidism, and acute biphasic thyroiditis. Antithyroid hormone antibodies have also been found in one patient, and this could have been the cause of erroneously raised thyroid hormone concentrations (504). 

While no evidence of thyroid dysfunction or antithyroid antibodies was found in 20 patients receiving interferon beta during 24 weeks for hematological malignancies... 

Biological thyroid abnormalities without antithyroid antibodies have also been found (SEDA-20, 332). Overall, thyroid disorders with antithyroid antibodies were reported in only three patients on long-term interferon beta treatment for multiple sclerosis (555,556). 

An abstract reported that 23% of 61 children and adolescents taking lithium and divalproex sodium for up to 20 weeks had a TSH concentration over 10 mU/1 (reference range 0.2-6.0) however, no clinical information was provided (635). Another abstract reported that the prevalence of thyroperoxidase antibodies was higher in bipolar outpatients (28% of 226) than in psychiatric inpatients with any diagnosis (10% of 2782) or healthy controls (14% of 225), but this was not related to lithium exposure on the other hand, hypothyroidism was associated with lithium exposure, especially in the presence of antithyroid antibodies (636). 

Weijl NI, Van der Harst D, Brand A, Kooy Y, Van Luxemburg S, Schroder J, Lentjes E, Van Rood JJ, Cleton FJ, Osanto S. Hypothyroidism during immunotherapy with interleukin-2 is associated with antithyroid antibodies and response to treatment. J Clin Oncol 1993 ll(7) 1376-83. 

Clauvel JP. Antithyroid hormone antibodies induced by interferon-alpha. J Clin Endocrinol Metab 1992 75(6) 1484—6. 

In a controlled, cross-sectional comparison of 100 patients with mood disturbance who had taken lithium for at least 6 months and 100 psychiatrically normal controls, lithium did not increase the prevalence of thyroid autoimmunity a minimally larger number of control subjects had antithyroid peroxidase antibodies (11 controls versus 7 patients with mood disorders) and anti-thyroglo-bulin antibodies (15 versus 8) (259). 

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