Children hypothyroidism

In children, hypothyroidism can have a congenital (cretinism) or prepubertal (juvenile hypothyroidism) onset. 

These hormones cause few adverse reactions when administered as directed. Antibodies to somatropin may develop in a small number of patients, resulting in a failure to experience response to therapy, namely, failure of the drug to produce growth in the child. Some patients may experience hypothyroidism or insulin resistance Swelling, joint pain, and muscle pain may also occur. 

Methimazole is excreted in breast milk and can cause hypothyroidism and goiter in the newborn child. 

Weber G, Vigone MC, Rapa A, Bona G, Chiumello G. Neonatal transient hypothyroidism aetiological study. Italian Collaborative Study on Transient Hypothyroidism. Arch Dis Child Fetal Neonatal Ed 1998 79(l) F70-2. 

Chabrolle JP, Rossier A. Goitre and hypothyroidism in the newborn after cutaneous absorption of iodine. Arch Dis Child 1978 53(6) 495-8. 

Neonatal hypothyroidism has been reported after maternal use of antithyroid drugs (106,107). Transient neonatal hyperthyroidism in a female child born to a mother who had been treated with potassium iodide and carbimazole during pregnancy was followed by sexual precocity (108). 

Thyroid function tests are often altered by somatropin because of increased conversion of T4 to T3, but this is clinically insignificant at low doses (SEDA-21, 453). One child with Prader-Willi syndrome had a fall in serum thyroxine concentration during somatropin therapy and needed thyroxine replacement (33). Hypothyroidism developed in 11 of 46 growth hormone-deficient children treated with somatropin (34). Prior abnormalities in hypothalamic-pituitary function and alterations in thyroid hormone metabolism, probably both, contributed to the high incidence of hypothyroidism, which was similar to that in previous studies. 

There are many forms of hypothyroidism, differing in their cause and age of onset (see Table 31-1). Severe adult hypothyroidism (myxedema) may occur idio-pathically or may be caused by specific factors such as autoimmune lymphocytic destruction (Hashimoto disease). In the child, thyroid function may be congenitally impaired, and cretinism will result if this condition is untreated. Hypothyroidism may result at any age if the dietary intake of iodine is extremely low. Several other forms of hypothyroidism that have a genetic or familial basis also exist.54... 

Hypothyroidism can lead to a variety of end-organ effects and a wide range of disease severity, from entirely asymptomatic individuals to patients in coma with multisystem failure. In the adult, manifestations of hypothyroidism are varied and nonspecific. In the child, thyroid hormone deficiency may manifest as growth retardation. 

In congenital hypothyroidism, fuU maintenance therapy should be instituted early to improve the prognosis for mental and physical development. The average maintenance dose in infants and children depends on the age and weight of the child. Several studies demonstrate that aggressive therapy with levothyroxine is important for normal development and current recommendations are for initiation of therapy within 45 days of birth at a dose of 10 to 15 meg/kg per day. This dose is used to keep T4 concentrations at about... 

Grant DB. Congenital hypothyroidism Optimal management in the Ught of 15 years experience of screening. Arch Dis Child 1995 72 85-89. 

Hunter I, Greene SA, MacDonald TM, Morris AD (2000) Prevalence and aetiology of hypothyroidism in the young. Arch Dis Child, 83(3) 207-210. 

Gestational hypothyroidism has been associated with severe complications, such as hypertension, preterm birth, low birth weight, placental abruption and fetal death by Leung et al, (1993) and Allan et al. (2000). Many studies in children of hypothyroid pregnant women including Mans group (1976, 1991), and many later ones (Liu et al, 1994 Smit et al, 2000 Klein et al, 2001 Mitchell and Klein, 2004), have demonstrated the importance of maternal thyroid function on the neurodevelopmental evolution of the child. 

In a study by Pop et al. (1999) performed in the Netherlands, a country considered to be free of ID, the developmental index of the child was correlated to the first trimester free thyroxine (FT4) levels. One out of every two women with first trimester FT4 values below the tenth percentile had a child with a developmental index more than 1 SD below the mean. None of these women were clinically or subclinically hypothyroid. 

Iodine deficiency affects the socioeconomic development of an afflicted community in other ways than its important physiological manifestations, viz., goiter, hypothyroidism, cretinism, reproductive failure, and child mortality, among others. The socioeconomic retardation of the affected community occurs in two ways. People are mentally slower and less vigorous, so it is harder to educate and motivate them, and thus they are less productive in their work. Besides, iodine deficiency produces more handicapped individuals who depend on others for their care, which in turn diverts the community resources. Secondly, in most of the areas, agriculture is the most important economic activity, and domestic animals suffer from iodine deficiency in much the same way as people do. Therefore, domestic animals are smaller in size and produce less meat, eggs and wool. They also suffer from abortion and are often sterile. 

The prevalence of subclinical hypothyroidism (SCH), defined as serum thyrotropin (TSH) concentration above the upper limit of the reference range with normal free thyroxine (FT4), in women of child-bearing age may be as high as 5% (Canaris et al., 2000 Hollowell et al., 2002). Of these, approximately 2—5% per year will progress to overt hypothyroidism (OH), defined as low serum FT4 with elevated serum TSH concentration. When iodine nutrition status is adequate, the most frequent cause of hypothyrod is thyroid autoimmunity (Hashimoto s thyroiditis) and, in this respect, if we take into account women with thyroid autoimmunity and normal thyroid function who could become... 

Larsson, Mental development in congenital hypothyroidism after neonatal screening. Arch. Pis. Child. 62 1050-1055 (1987). 

M. Vanderschueren-Lodeweyckx, F. Debruyne, L. Dooms, E. Eggermont and R. Eeckels, Sensorineural hearing loss in sporadic congenital hypothyroidism, Arch. Pis. Child. 58 419-422 (1983). 

The first 3 cases (serial nos 604, 638, 515) in the table had hormonal profiles entirely consistent with severe hypothyroidism although these women did not exhibit the clinical features of hypothyroidism In all three cases the pregnancy outcome was a stillblrth/early neonatal death In the succeeding 3 cases (serial nos 568, 245, 430) the maternal total and free thyroxine values were low but triiodothyronine values were within the normal range In one of these the outcome was a stillbirth/early neonatal death and one child has a hearing/speech defect but no other abnormality and, by our definition, cannot be labelled as an endemic cretin ... 

Another case (serial no 398) is of particular interest in that the child exhibits the clinical features of cretinism The maternal thyroxine and TSH values were abnormal and consistent with hypothyroidism but the triiodothyronine values were within the normal... 

My comment is in response to Dr. Laurberg s comment. There is an important difference between a hypothyroid child bom in an iodine deficient area and congenital hypothyroidism. Congenital hypothyroid children probably develop normally after birth, when given adequate thyroxine treatment, because their brain was selectively protected by maternal T4 until birth. On the contrary, in severely iodine deficient areas, the fetal brain cannot benefit from the same protection because of the low thyroxine levels in maternal serum. 

Chanoine, J.P., Boulvan, M., Bourdoux, P. et al.. Increase recall rate at screening for congenital hypothyroidism in breast fed infants bom to iodine overloaded mothers. Arch. Dis. Child. 63 1027 (1988). 

MEDIAN UR.IOD. (Mg/dl) RECALL RATE (% OF NEWBORNS SCREENED) PERMANENT HYPOTHYROIDISM (% OF REC.CHILD)... 

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