Biomedical subjects
C J Partsch
Publications and source records attributed to C J Partsch.
[Results of 204 expert opinions on the problem of hardness of hearing caused by noise].
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[Otologic annotations to VDI rule 2058].
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[Chromosome aberrations in the Waardenburg-Klein-Syndrome].
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[The diagnostic value of the cisternography in acoustic neuroma].
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[Congenital ear abnormalities as a cause of deafness].
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[Detonation-traumatic load during military service].
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[On the development of the ductus and saccus endolymphaticus and their behavior in pathologic conditions].
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[Trials and measurement results of a plastic ear mould as individual protection from noise].
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[Development disturbances of the ductus and saccus endolymphaticus as causes of inner ear abnormalities].
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[Thalidomide-embryopathies and their effect on dentition].
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Pathogenesis and epidemiology of precocious puberty. Effects of exogenous oestrogens.
Precocious puberty is generally defined as the appearance of secondary sex characteristics before age 8 years in girls (or menarche before age 9 years) and before 9 years in boys. The overall incidence of sexual precocity is estimated to be 1:5,000 to 1:10,000 children. The female-to-male ratio is approximately 10:1. In addition to the psychosocial disturbances associated with precocious puberty, the premature pubertal growth spurt (with less time for prepubertal growth) and the accelerated bone maturation result in reduced adult height. Precocious puberty may be gonadotrophin-dependent [i.e. of central origin with premature activation of the gonadotrophin-releasing hormone (GnRH) pulse generator] or gonadotrophin-independent (i.e. peripheral where the GnRH pulse generator is suppressed). This can be determined by GnRH testing. The pathophysiology is the basis for different diagnostic and therapeutic strategies, i.e. in the first case a stimulated LH/FSH ratio >1 and suppressive treatment with GnRH agonists (e.g. in hypothalamic hamartoma), and in the second decreased gonadotrophins and removal or suppression of the endogenous or exogenous sex steroid source (e.g. congenital adrenal hyperplasia). While several cases of gonadotrophin-independent precocious puberty due to oestrogen exposure via the transdermal, oral, or inhalative route have been reported, no case is known with the development of subsequent secondary central precocious puberty. Food contamination with oestrogens is theoretically possible, but would most probably be sporadic and, thus, would not lead to precocious puberty. As steroid hormones in meat production are banned in the European Union, no data on the impact of environmental oestrogenic substances on human maturation are currently available. In conclusion, the risk for children to develop precocious puberty through exposure to oestrogens (or androgens) in the environment or in food is very low. Nevertheless, studies of the effects of defined environmental oestrogenic substances on the human reproductive system and on pubertal development are warranted.