Antithyroid peroxidase 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... 

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. 

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. 

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). 

Endres D. Antithyroid peroxidase antibodies (antimi-crosomal antibodies) in thyroid disease. Endocrinology and metabolism on-service training and continuing education program. Washington, DC AACC Press 1991 10 3-5. 

Sundbeck G, Eden S, Jagenburg R, Lundberg PA, Lindstedt G. Prevalence of serum antithyroid peroxidase antibodies in 85-year-old women and men. Clin Chem 1995 41 707-12. 

Before providing data from India, it is relevant to summarize the information from other countries recently making the transition from an iodine-deficient to an iodine-sufficient state. Studies from Greece, Turkey and Iran report an increase in the prevalence of antithyroid peroxidase antibodies in the population after iodine supplementation (Zois et ai, 2003 Bastemir et aL, 2006 Heydarian et ai, 2007). Interestingly, other studies have provided data to the contrary. For example, the introduction of iodized salt to severely iodine-deficient children did not provoke thyroid autoimmunity in a study conducted in Morocco (Zimmermann et ai, 2003). 

Antithyroglobulin and antithyroid peroxidase antibodies were confirmed. 

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). 

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