INTRODUCTION TO PHYSIOLOGY Effects of pregnancy on thyroid Increased demand of thyroid hormones to maintain the requirements of fetus Total serum T3 T4 levels increase 50% during pregnancy thyroid hormones transfer to fetus during 1 st trimester, later iodine only Iodine excretion in urine increased in pregnancy due to increased GFR Good intrathyroid store cope with this demand, but in deficient reserved women, thyroid hormone level fall and stimulate TSH, make goitre
Maternal More than 1% occur, most common endocrine disorder in pregnancy TSH release 1-2 hrly cycle which increase synthesis & release of T3, T4 from thyroid Unbound hormones have biologically active, 75% bound to TBG, albumin In pregnancy, TBG production increase due to oestrogen in first 2 weeks HCG and TSH share common alpha subunit and similar beta subunits Increased thyroid activity found in molar pregnancy, multiple pregnancy and hyperemesis gravidarum
Fetal Require maternal T4 during first trimester for brain development Fetal thyroid is independent of mother, require only transplacental iodine Fetal level of thyroid hormone reach those of adult by 36 weeks Congenital hyperthyroidism can occur when TSH receptor stimulating antibodies cross placenta
Aetiology and management of thyroid diseases Iodine Women in area of iodine deficiency may have goiters and reduced reproductive success Iodine deficiency is the leading preventable cause of learning disability worldwide Fetal cochlea, cerebral neocortex and basal ganglia are particularly sensitive to iodine deficiency
Hyperthyroidism Commonest cause in pregnancy is Graves’ disease, almost 90% It is an autoimmune disorder caused by TSH receptor-stimulating antibodies Complicates about 1 in 500 pregnancies 50% affected women have positive family history of autoimmune thyroid disease Most cases already been diagnosed will already treated Other causes multinodular, toxic goiter, acute viral thyroiditis(de Quervains ) carcinoma, drug induced(amiodarone or lithium)
Diagnosis Similar symptoms like normal pregnancy such as palpitation, tachycardia, irritability, heat intolerance and fatigue Eye signs include diplopia, photophobia A diffuse swelling in thyroid area which move with deglutition may be due to physiology, Graves’ disease and thyroiditis TFT should be request, if facilities available, TRAb should be tested Raised free T3, T4 , TSH is suppressed
Effect of pregnancy on thyrotoxicosis Improve in 2 nd and 3 rd trimester Lower requirement of antithyroid drugs Exacerbations usually occur in 1 st trimester (HCG) and puerperium
Effects of thyrotoxicosis on pregnancy Inhibition of ovulation and infertility( severe or untreated cases) Increased rate of miscarriage, IUGR, Preterm birth, perinatal mortality if those become pregnant. Thyroid crisis may occur at the time of delivery if poorly controlled
Management Carbimazole , propylthiouracil most common used drugs Both drugs cross the placenta, so in high dose any cause fetal hypothyroid and goiter Aplastic cutis( carbimazole in 1 st trimester) 2-4% congenital anomalies Therefore, switching carbimazole to PTU before or in early pregnancy
Management ( contd ) Newly diagnosed thyrotoxicosis in pregnancy should be aggressively treated with PTU 450-600 mg daily for 4-6 week Almost 30% can stop all medication in the last weeks of pregnancy Graves’ disease can relapse postnatally as maternal antibody level rise postpartum blockers- early symptomatic management like tachycardia, sweating, tremor They also reduce peripheral conversion of T4 to T3 They are discontinued once the antithyroid drugs take effect(3 weeks) Propranolol 40 mg tds does not harm to fetus
Surgery is rare, if required perform in 2 nd trimester It usually made where dysphagia, stridor , suspected carcinoma or allergy to drugs 25-50% become hypothyroid after surgery Radioactive iodine is contraindicated in pregnancy and breastfeeding
HYPOTHYROIDISM Incidence – much more common in women than men 1% of pregnancy, most cases already been diagnosed and will be on replacement therapy As hyperthyroidism, features are common in normal pregnancy such as weight gain, hair loss, lethargy, tiredness constipation, dry skin, goiter and fluid retention Discriminated feature is delayed relaxation of tendon ( ankle) Associated with other autoimmune like pernicious anaemia , vitiligo and diabetes mellitus type 1
Pathogenesis most cases are due to autoimmune destruction of thyroid gland associated with microsomal autoantibodies Mostly two types- atrophic thyroiditis, Hashimoto’s thyroiditis May also be due to iatrogenic following radiotherapy, thyroidectomy, or drugs ( amiodarone, lithium, iodine, anti-thyroid) Commonest cause encountered during pregnancy are treated Graves’ disease
Diagnosis Low level of free T4, raised TSH Finding of thyroid autoantibodies Normal pregnant range for each trimester must be used
Effect of pregnancy on hypothyroidism 25% women require increased level of thyroxine in pregnancy Effect of hypothyroidism on pregnancy Inhibit ovulation and infertility if untreated or severe Present with oligomenorrhoea or menorrhagoia Increased rate of miscarriage, anaemia , fetal loss, pre-eclampsia, low birth weight Neurodevelopmental delay in her offspring Severe maternal iodine deficiency may cause permanent brain damage ( deaf mutism, spasmodic motor disorder and hypothyroidism)
Management Maintainance dose thyroxine 100-200ug/day TFT should be checked once in each trimester Starting thyroxine dose of 100ug/day for newly diagnosed hypothyroid in pregnancy if there is no history of heart disease
POSTPARTUM THYROIDITIS Incidence -1-17% More common in women with family history of hypothyroidism and those with thyroid peroxidase antibodies, in whom about 50% Most of them asymptomatic, present between 3-4 months postpartum Monophasic (may be hypo or hyper) 40%, biphasic 20% Represent an activation of previously subclinical thyroiditis
Diagnosis Test TFT 2-3 months postpartum to the patients whose already have thyroid peroxidase antibody Also common in type1 diabetes patients Almost 75-85% have positive antithyroid antibodies Radioactive iodine test can be performed to distinguish with flare up post partum Graves’ disease, because Graves’ need antithyroid drugs
Management Mostly recover spontaneously without requiring treatment Treatment is determine by symptoms rather than biochemical abnormal Betablocker for hyperthyroid, cause antithyroid reduce thyroxine synthesis Thyroxine need in hypothyroid and withdrawn after 6-8 months 3-4% remain hypothyroid (recurrence) 10-25% recurrence in future pregnancies Postpartum depression is more common in antibody positive women
references Handbook of Obstetric medicine.Catherine N Piercy 6 th ed Ian Donald Obstetrics & Gynaecology . An evidence-based Text for the MRCOG