Juvenile hypothyroidism

Van Dop C, Conte FA, Koch TK, Clark SJ, Wilson-Davis SL, Grumbach MM. Pseudotumor cerebri associated with initiation of levothyroxine therapy for juvenile hypothyroidism. N Engl J Med 1983 308(18) 1076-80. 

Insomnia, psychic stimulation, general nervousness, and tremor are among the hyperthyroid symptoms that result from relative overdosage. Pseudotumor cerebri has incidentally been observed shortly after levothyroxine was given for juvenile hypothyroidism. The headache and bilateral papilledema without focal neurological defects subsequently disappeared even when levothyroxine was continued (21). 

Talbot et al. (Tl) stated that patients with juvenile hypothyroidism have lower serum alkaline phosphatase values than age- and sex-matched controls, and that the values become normal after replacement therapy. Chertow et al. (C13), who studied 15 hypothyroid patients, found normal serum alkaline phosphatase activities in each case. 

Thyroid hormone is used in adult hypothyroidism, in adult myxedema, and in cretiifism and juvenile hypothyroidism. 

Patients with severe cases of EC, CH, or juvenile hypothyroidism can demonstrate irreversible motor, intellectual impairments and hearing problems. 

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

Juvenile hypothyroidism Impaired mental function Retarded physical development... 

Juvenile or adult patients with primary hypothyroidism (as indicated by low serum free T4 and high serum TSH concentrations) are usually treated with thyroxine with the aim of relieving symptoms and reducing the serum TSH concentration into the normal reference range. If the primary hypothyroidism is the result of iodine deficiency, then gradually increasing dietary iodine supplementation may also be instituted in addition to the thyroxine replacement therapy. Iodine supplementation alone may lead to the development of acute hyperthyroidism. 

As mentioned in Chapter 1, perhaps the purest form of drug therapy is the replacement of inadequate amounts of an endogenous substance such as a hormone. Any gland that normally secretes a hormone is a potential target for hypofunctioning. Classical examples include Addison s disease (adrenal cortex), dwarfism (anterior pituitary), juvenile-onset insulin-dependent diabetes (pancreas), and hypothyroidism (thyroid). 

Chu et al. [81,82] observed changes in the thyroid when rats were administered PCDEs. Rosiak et al. [104] have lately reported that some PCDEs can cause hypothyroidism in rats. PCDEs 71 and 102, which have closest resemblance to thyroxine (T4), were shown to cause hypothyroidism in pregnant rats and PCDEs 71,102, and 153 in juvenile rats exposed in utero. PCDEs 71 and 102 have been fetotoxic in mice [92]. Rosiak et al. [104] suggested that, e.g., the inhibition of the release of T4 from thyroid follicular cells by PCDEs or binding of PCDEs to thyroid hormone binding protein, transthyretin, could decrease T4 levels. Triiodothyronine (T3) levels were not altered by PCDEs 71,102, and 153. 

The major features of the IDD effects on brain function arise from fetal damage (neurological cretinism) or hypothyroidism at various stages of life - fetus, neonate, juvenile and adult (Table 62.3). 

Okamura et al. (1994) Observational study Japan Reversible recovery of thyroid function after iodine restriction in patients with juvenile goitrous hypothyroidism and high thyroidal radioactive iodine uptake despite chronic lymphocytic thyroiditis... 

Bernal (2005) reviewed the morphological aspects in the brain of the hypothyroid rat and found (1) altered cell migration, particularly in the cerebellum and cerebral cortex (2) increments in cell density, caused by a reduction in the neuropil (3) markedly reduced dendritic arborization in the Purkinje cells of the cerebellum, and decreased and altered distribution of the pyramidal dendritic spines in the cortex layer V and finally (4) delayed myelination and poor myelin deposit in the white matter and fewer myelinated axons. This study further showed that hypothyroidism produces changes in the colossally projecting neurons, which may be due to the maintenance of juvenile patterns of projections. In addition, a recent report (Lavado-Autric et al., 2003) indicates that focusing on maternal hypothyroidism can produce migration defects in the fetal cortex, when... 

Morreale de Escobar, Reversible morphological alterations of cortical neurons in juvenile and adult hypothyroidism in the rat. Brain Res. 185 91-102 (1980). 

Microtubule ausserobly from hypothyroid preparations (Fig.2) was also tested (19,20) at day 15 postnatal the polymerization activity was similar to that measured at earlier stages O-S days) with the euthyroid preparations. Analysis of the MAPs present at day 15 postnatad also showed a hi ier proportion of immature Tau than in the control of the same age (20). Hiis suggested that the transition betsi een juvenile and mature Tau is delayed in hypothyroidism, a conclusion i ch mi it be sufficient to e3q)lain the lower polymerization activity produced by thyroid hormone deficiency. 

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