[The adolescent and secondary amenorrhea].
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Biomedical subjects
Publications and source records attributed to U Eiholzer.
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In three children with Down syndrome and acquired hypothyroidism echocardiography was performed before and after the start of L-thyroxine treatment. Initial studies revealed pericardial effusions which resolved during treatment suggesting that they were caused by hypothyroidism. The incidence of hypothyroidism in Down syndrome is high, but the diagnosis is often missed for lack of specific clinical criteria. The finding of pericardial effusion by echocardiography may be essential in discovering thyroid dysfunction. The cases illustrate that regular thyroid function tests are important in Down syndrome.
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In a retrospective growth evaluation, which included parental height, birth length and a longitudinal analysis of growth and bone maturation, it has been shown that short stature is a common finding in Duchenne muscular dystrophy already in an early or even preclinical stage. Normal length and weight at birth, slow subsequent growth with a curve crossing the centiles in the 1st years of life, and normal bone maturation are characteristic of this type of short stature.
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22 Boys with pubertal gynaecomastia (age 15.9 +/- 1.9 years) were treated with testolactone (450 mg daily by mouth) for 2 to 6 months without side-effects. The mean breast gland diameter regressed from 4.4 to 3.3, 3.2 cm, and 1.7 cm at 2, 4, and 6 months, while pubic hair and testicular volume progressed normally. Plasma androstenedione increased from 5.4 to 73.1 nmol/l. Testosterone, DHEA, and oestrone increased less, and oestradiol remained unchanged. Androgen/oestrogen ratios increased (most marked change: androstenedione/oestrone from 15 to 140). LH (basal and maximum after LHRH) did not change, but FSH increased somewhat (basal 133 to 173, maximum 225 to 269 micrograms/l). Prolactin remained unchanged. It is concluded that testolactone, an inhibitor of steroid aromatization, is an effective and safe medical treatment for pubertal gynaecomastia.
Plasma DHA, 17-OH-progesterone, androstenedione, testosterone, cortisol, oestrone and oestradiol were determined before and on high dose oestrogen treatment (1, 3, 6 and 16 months) given to excessively tall girls to reduce future adult height. Basal values were normal: DHA 16.4 +/- 0.8 nmol/l (n = 90), 17-OH-progesterone 4.9 +/- 0.3 (n = 20), androstenedione 5.6 +/- 0.3 (n = 25), testosterone 2.6 +/- 0.3 (n = 24) and cortisol 395 +/- 20 (n = 90). On treatment, DHA, 17-OH-progesterone and androstenedione decreased to a minimum of 9.3 +/- 1.0 nmol/l (3 months, n = 13), 2.4 +/- 0.3 (6 months, n = 7) and 2.6 +/- 0.2 (6 months, n = 9), respectively, while testosterone remained unchanged, and cortisol increased to a maximum of 825 +/- 99 nmol/l (16 months, n = 23). In 15 girls with XO gonadal dysgenesis, basal DHA was low (11.8 +/- 1.0 nmol/l), and did not significantly change on low dose oestrogen replacement (13.3 +/- 1.4). The cause of the fall in plasma concentrations of androstenedione, DHA and 17-OH-progesterone in treated tall girls is unknown, but it is speculated that it might be related to peripheral conversion in the augmented adipose tissue mass. The rise in plasma cortisol, on the other hand, is probably due to increased transcortin.