Post-partum hyperthyroidism.
The importance of recognizing the frequent occurrence of the destructive (i.e. PPT) and stimulatory (i.e. PGD) causes of PH have been discussed. The estimated prevalence of PH in several geographical regions of Japan, North America and Europe ranges from 2.0-5%. Although the autoimmune basis for GD has been well-established, the clinical and laboratory features of PPT as well as the alterations of humoral and cellular thyroidal immune parameters, the typical needle biopsy evidence of lymphocytic infiltration, and the association with HLA and Gm allotypes associated with the PPT syndrome, favour the view that it is also likely a variant form of subclinical ATD which becomes transiently more active post-partum. Post-partum transient hyperthyroidism with or without transient or permanent hypothyroidism and relapse of GD thyrotoxicosis have been observed in patients with or without a previous history of GD. Hence, an RAIU test is the preferred diagnostic test in differentiating between these two entities, especially in the absence of associated stigmata of GD. When the RAIU test is suppressed, other causes such as thyrotoxicosis factitia and iodine exposure should be excluded. Without an RAIU test, only a rapid and spontaneous resolution of post-partum hyperthyroidism, accompanied by laboratory confirmation of a subsequent hypothyroid phase, can indirectly facilitate the differentiation between PGD and PPT. In the first trimester of pregnancy, an increased FT4I has been proposed as a risk factor for PGD and an increased AMA titre for PPT. Depending upon clinical manifestations, severity, patient and physician preferences, PGD can be treated by one of several choices of conventional therapy. The transient thyrotoxic phase of PPT when relatively asymptomatic may require no therapy, but when symptomatic, only conservative therapy with beta-adrenergic blockers, sedatives and/or tranquilizers is indicated. Close follow-up and long-term surveillance of mothers with PH due to PPT is essential for early detection and management of a possible subsequent hypothyroid phase, which may be symptomatic, but is seldom permanent. Treatment of recurrent episodes of PPT is controversial. Thyrotoxic symptoms are usually mild and transient and can best be managed by symptomatic therapy as indicated. In a few exceptional patients with recurrent episodes, prophylactic treatment with corticosteroid may be warranted but thyroidectomy and ablative radioactive iodine therapy is seldom justified.(ABSTRACT TRUNCATED AT 400 WORDS)
Walfish
P G
PG
Chan
J Y
JY
D013956:Antithyroid Agents / Q000627:therapeutic use; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000175:diagnosis / Q000276:immunology; D003430:Cross-Sectional Studies; D003937:Diagnosis, Differential; D005260:Female; D006044:Goiter, Nodular / Q000175:diagnosis; D006111:Graves Disease / Q000175:diagnosis; D006680:HLA Antigens / Q000235:genetics; D006801:Humans; D006980:Hyperthyroidism / Q000175:diagnosis* / Q000276:immunology; D007111:Immunity, Cellular; D007126:Immunoglobulin Allotypes / Q000032:analysis; D011247:Pregnancy; D011644:Puerperal Disorders / Q000175:diagnosis* / Q000276:immunology; D013960:Thyroid Function Tests
D013956:Antithyroid Agents; D001323:Autoantibodies; D006680:HLA Antigens; D007126:Immunoglobulin Allotypes