Monitoring TSH concentrations during treatment for congenital hypothyroidism

Article Abstract:

The thyroid gland is located in the neck in front of and on either side of the windpipe (trachea). This gland makes a hormone called thyroxine that is essential for the normal growth and development of the entire body. Hypothyroidism results when the thyroid gland does not make enough thyroxine; when the condition occurs in children, it is called cretinism. Hypothyroidism can cause growth retardation (dwarfism) and mental retardation. Therefore, it is very important to diagnose this condition as early in infancy or childhood as possible. One method of diagnosis involves measuring the amount of thyroxine in the blood. Very low levels of thyroxine in the blood indicate that the thyroid gland is not functioning properly. Another method for diagnosing hypothyroidism involves measuring the amount thyroid stimulating hormone (TSH) in the blood. TSH is made in the pituitary gland under control of a brain center (hypothalamus) and stimulates the action of the thyroid gland when the levels of thyroxine in the blood are low. Thus during hypothyroidism, when blood levels of thyroxine are very low, the amount of TSH released into the blood will tend to be high. Hypothyroidism is treated by thyroxine replacement therapy, which increase the amount of thyroxine in the blood and can prevent growth retardation in children if treatment is started early enough. Since treatment with thyroxine increases the amount of thyroxine in the blood, it will suppress the release of TSH. When adequate amounts of thyroxine are given to the patient the blood levels of TSH will return to normal. If not enough thyroxine is given the blood levels of TSH will remain high. Therefore, it is possible to determine if the patient is being treated with enough thyroxine by measuring the amount of TSH in the blood. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Measurement, Infants (Newborn), Newborn infants, Hypothyroidism, Thyroxine, Congenital hypothyroidism, Thyrotropin

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5-alpha-reductase deficiency without hypospadias

Article Abstract:

5-Alpha-reductase is the enzyme which converts testosterone into dihydrotestosterone, which is responsible for much of male sexual differentiation. Deficiency of this enzyme leads to underdevelopment of the male external genitalia. Many of these individuals have been initially raised as girls due to the female appearance of the genital organs at birth. All reported cases of males with 5-alpha-reductase deficiency have had some degree of genital ambiguity with hypospadias, an abnormal opening of the urethra on the underside of the penis. Two cases of 5-alpha-reductase deficiency are reported, affecting two brothers, one of whom did not have hypospadias. The parents were consanguineous (related by blood). The older brother had a small penis at birth, but did not receive medical attention until age 12, when his younger brother was referred. At birth, the younger boy had a small penis, hypospadias, and abnormal external genitalia; upon examination at age four, the boy had chordee (painful downward curvature of the penis on erection), a normal scrotum, but only one testicle. The younger boy was treated with testosterone to improve genital development. Laboratory investigations provided evidence for 5-alpha reductase deficiency in both boys. The older boy is considered unique, in that he is the first reported case of 5-alpha-reductase deficiency without hypospadias. These cases suggest that there is some heterogeneity in this type of disorder, with the older boy having produced sufficient dihydrotestosterone in utero to allow genital development, while the younger boy was apparently deficient in this enzyme during the second half of gestation. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Steroid hormones, Reproductive organs, Male, Male genitalia, Hypospadias

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Depot testosterone in boys with anorchia or gonadotrophin deficiency: effect on growth rate and adult height

Article Abstract:

Different disorders affecting boys such as anorchia (congenital lack of one or both testes), pubertal delay, or deficiency of gonadotropins (pituitary hormones which regulate sexual development and testosterone production) have commonly been treated with testosterone given in a slow-release depot form. Although testosterone treatment was thought to lead to reduction in final adult height, most studies suggest that the low doses used in these treatments, combined with relatively short duration of therapy, have little effect. To evaluate these conclusions, the cases of 11 teenage boys with bilateral anorchia and 12 with gonadotrophin deficiency who were given long-term treatments of testosterone were reviewed. The rate of growth increased during the first year of treatment and then declined during further therapy. In contrast, maximum growth velocity occurs at 18 to 24 months after the start of normal puberty, suggesting that the testosterone dose was too high. Patients' adult heights were similar to predicted values and greater than the parental average heights. The study indicates that testosterone replacement therapy is safe and effective in boys with deficient reproductive function, but that a lower dose might be preferable, depending upon the age at which treatment begins. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Drug therapy, Testosterone, Gonadotropin, Gonadotropins, Hypogonadism

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