Thyroid disorder and pregancy

Iodine metabolism:--The   recommended daily intake during   pregnancy is at least 220  ug/day  .

The north east states of India (Sub Himalayan States & Union Territories) have iodine deficient in food & drinking water. So there is Iodide fortification   of table   salt    and bread products. This Govt policy    has diminished   iodide deficiency , though it  has remained a problem in some of the population. What about antenatal mothers?? Ans:-Adequate   iodide is requisite for normal   fetal neurological   development    beginning soon after conception.

Severe   deficiency    is associated with  endemic cretinism. Although   not quantified   it is presumed that moderate deficiency has intermediate and variable    effects    on intellectual and psychomotor function. Although    it is doubtful that mild deficiency causes intellectual impairment supplementation   prevents fetal goiter

Clinical  hypothyroidism its features and impact in pregancy.

  Clinical   or overt hypothyroidism   complicates  approximately  2 per  1000  pregnancies(in India)  . Clinical    hypothyroidism    is diagnosed when   an abnormally  high    serum thyrotropin level is   accompanied  by an abnormally low free thyroxine  level.  The most   common  etiology is glandular   destruction   by  autoantibodies or Hashimoto    thyroiditis  . Thyroid    peroxidase   antibodies   have been   identified  in 5 to 15   percent of pregnant  women up to half  of whom later    in life develop   an autoimmune    thyroiditis.

Overt   hypothyroidism is associated   with infertility. When    pregnancy   does occur there are   increased   rates of maternal and fetal complications to include preeclampsia placental   abruption   cardiac dysfunction    stillbirth and prematurity .

What will be the replacement dose ??  Ans:-Fortunately     perinatal  outcomes  are usually normal  with adequate treatment . Replacement therapy is with    thyroxine   50 to 100   ug daily .

How frequent monitoring?? Serum   TSH   and free thyroxine    levels   are measured at 4 to 6  week intervals    and thyroxine   adjusted    by 25 to 50 ug increments   until normal values  are reached. Pregancy is associated with an increase  in thyroxine    requirements  of about   a third however   care  should be individualized  as not all   women require an adjustment in therapy.

SUBCLINICAL  HYPOTHYROIDISM

 Subclinical hypothyroidism   is defined  by an abnormally  elevated  TSH level  with normal serum   free T in an asymptomatic woman. The prevalence   of subclinical  hypothyroidism  in pregnancy   is approximately  2.3   percent. Approximately 2 to  5 percent   of reproductive   age women with   subclinical disease   per year   progress   to overt    thyroid failure. Heredity is a potent risk factor    . Other    risk factors  for  thyroid     failure include  type -1  diabetes and thyroid   peroxidase antibodies . Effects    of subclinical    hypothyroidism   on pregnancy   outcome are not  clear. Pregnancies   with subclinical   hypothyroidism on pregnancy  outcome are not   clear. Pregnancies   with  subclinical hypothyroidism   may be   at increased risk for  preterm   birth    or placental  abruption. Effect of  maternal hypothyroidism   on the fetus   and infant . Hypothyroidism – either   overt  or subclinical -  has been   reported  to   cause   sub normal mental  development    Elevated  maternal   TSH  values have been associated    with  offspring     who have   diminished  school performance   reading recognition  and intelligence   quotient   scores as compared   with matched controls.

Some organization    have recommended prenatal    screening and treatment    for subclinical   disease. However the American College   of Obstetricians     and Gynecologists continues   to recommend   against routine screening  . Randomized placebo    controlled   trials  to determine risks  or benefits   of detecting    and treating  subclinical   thyroid  dysfunction    in pregnancy  are in progress.

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CONGENITAL  HYPOTHYROIDISM

newborn mass screening  will detect it at very early:  Congenital hypothyroidism   is found in about  1 in 2500   infants. Because the clinical   diagnosis of hypothyroidism  in neonates   is usually  missed newborn mass screening  was introduced in the United States   in 1974  and is now required    by law. Early   and aggressive thyroxine replacement   is critical . Follow up data  from infants  identified   by screening   programs   who were  treated  promptly  and adequately are  encouraging     Most   if not all sequelae  of congenital   hypothyroidism – including  intellectual   impairment -  are typically  preventable .

. Hyperthyroidism : Women    thyroid   stimulating   antibody  activity  declines during pregnancy   associated  with chemical    remission.  When   mild thyrotoxicosis may be difficult to diagnose   during pregnancy    overt can be easily diagnosed. The  diagnosis   is confirmed when   an abnormally  low thyroid    stimulating hormone level is accompanied by abnormally  high serum  triiodothyronine levels -   . The   major  cause of hyperthyroidism   in pregnancy     is Graves disease an organ specific   autoimmune process   usually associated with   thyroid  stimulating    antibodies. In many  women    thyroid   stimulating   antibody  activity  declines during pregnancy   associated  with chemical    remission.

Pregnancy    outcomes depend  upon   whether    metabolic   control is achieved   .women   who remain hyperthyroid  despite therapy    and in those whose   disease   is  untreated    there is a higher   incidence  of preeclampsia heart failure    and adverse   perinatal outcomes.

Thyroid   storm is encountered only  rarely in untreated   women  with Graves disease. Heart  failure is  more common  than T storm cases.