Gebelik ve Hipotiroidi

Yazarlar

İlkcan Çerçi Koçar

Özet

Gebelikte maternal tiroid bezi fizyolojisinde, fetüsün normal beyin ve beden gelişimi için kritik olan yeterli tiroid hormonunu sağlamak amacıyla önemli değişiklikler meydana gelir. Maternal tiroid hormon eksikliği; aşikar hipotiroidizm, subklinik hipotiroidizm ve izole hipotiroksinemi olarak sınıflandırılmaktadır. Dünya genelinde en yaygın neden iyot eksikliyken, iyot yeterli bölgelerde otoimmün tiroidit (Hashimoto) öne çıkar. Gebelikte östrojen artışına bağlı olarak tiroksin bağlayıcı globulin (TBG) konsantrasyonu iki ila üç kat yükselir; bu durum toplam T4 ve T3 seviyelerini artırırken, renal klirensin artması iyot ihtiyacını doğurur. İlk trimesterde hCG hormonunun tirotropik aktivitesi nedeniyle TSH seviyelerinde geçici düşüşler görülebilir. Aşikar hipotiroidizm; preeklampsi, plasenta dekolmanı, düşük doğum ağırlığı ve fetal ölüm gibi ciddi obstetrik risklerin yanı sıra çocukta nörogelişimsel bozukluklara yol açabilir. Tanıda trimestere özgü TSH referans aralıklarının kullanılması önerilir. Tedavide altın standart levotiroksin (LT4) monoterapisidir; gebelik doğrulanır doğrulanmaz LT4 dozu %30-50 oranında artırılmalı ve tiroid fonksiyon testleri 4 haftada bir yakından izlenmelidir. Subklinik vakaların yönetimi tartışmalı olsa da risk faktörleri ve antikor durumuna göre tedavi planlanır.

During pregnancy, maternal thyroid physiology undergoes substantial adaptations to maintain adequate hormone levels crucial for normal fetal brain development, as the fetal thyroid gland is not mature until 18-20 weeks. Thyroid deficiency is categorized into overt hypothyroidism, subclinical hypothyroidism, and isolated hypothyroxinemia. Worldwide, iodine deficiency is the primary cause, whereas autoimmune thyroiditis dominates in iodine-sufficient areas. Elevated estrogen increases thyroxine-binding globulin (TBG) two- to three-fold, raising total T4 and T3 levels, while increased glomerular filtration enhances renal iodine clearance. Concurrently, high hCG levels in early pregnancy exert thyrotropic activity, transiently suppressing TSH. Overt maternal hypothyroidism significantly correlates with adverse outcomes, including gestational hypertension, preeclampsia, placental abruption, low birth weight, and impaired neurointellectual development. Diagnosis relies ideally on trimester-specific TSH reference ranges. Levothyroxine (LT4) monotherapy is recommended for overt cases; pre-existing LT4 doses should be increased by 30-50% immediately upon pregnancy confirmation, followed by monitoring every 4 weeks. Management of subclinical hypothyroidism remains controversial, yet treatment is tailored according to specific maternal risk factors and thyroid peroxidase (TPO) antibody status.

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5 Nisan 2023

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