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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

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Astroglial-derived factors, as transforming growth factor (TGF)alpha and TGFbeta, act in the hypothalamus to activate luteinizing hormone-releasing hormone (LHRH) secretion. Hypothalamic hamartomas (HHs) contain normal nervous tissue in a heterotopic location. When symptomatic, they cause precocious puberty and/or characteristic gelastic seizures. Thus far, the pathogenesis of these alterations remains unknown. By examining two HHs associated with sexual precocity, we found that they contained astroglial cells expressing TGFalpha, but no LHRH neurons. In a third patient with HH, only epilepsy was present, but precocious puberty developed shortly after surgery, probably as a consequence of a surgery-induced lesion. These results imply that some HHs induce sexual precocity by activating endogenous LHRH secretion via astroglial-derived factors. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065923&dopt=Abstract

Horm Res. 2002;57 Suppl 2:43.
Endocrine disrupters and testicular dysgenesis syndrome.

Skakkebaek NE.

Department of Growth and Reproduction, University of Copenhagen, Rigshospitalet, Denmark. neh.dk

Over the last couple of generations, we have been exposed to an increasing number of endocrine disrupters in our environment, including dichlorodiphenyltrichloroethane (DDT), PCB, certain pesticides, the phthalate DBP, synthetic steroids in meat and many other agents (table 1), which act as agonists or antagonists of sex steroids. Although biologists working with wildlife have been concerned about the possible effects of these chemical agents on animal reproduction, it appears that clinicians have been less concerned about possible health effects in humans. However, the increasing incidence of hormone-dependent cancers, including cancer of the breast, prostate and testis, and signs of an increasing incidence of male reproductive health problems should alert us to the possible association between exposure to endocrine disrupters and the current high frequency of reproductive problems. In Denmark, for example, 5% of all children are now born after assisted reproduction (intracytoplasmic sperm injection, in vitro fertilization, donor insemination and intrauterine insemination) and 1% of all (mostly young) men develop testicular cancer. Evidence exists to support the concept that hypospadias, undescended testis, poor semen quality and testicular cancer are symptoms of an underlying testicular dysgenesis syndrome, which may be becoming increasingly common due to adverse environmental effects. Experimental and epidemiological evidence suggests that testicular dysgenesis syndrome is a result of disruption of foetal programming and gonadal development during foetal life. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065926&dopt=Abstract

Horm Res. 2002;57 Suppl 2:66-70.
Growth prediction models, concept and use.

Kristrom B, Wikland KA.

Gothenburg Pediatric Growth Research Center, Institute for the Health of Women and Children, Department of Pediatrics, Sahlgrenska Academy at Gothenburg University, Queen Silvia Children's Hospital, Sweden. Berit.Kristroediatri.umu.se

There is a principal and qualitative difference between using regression results on data from groups of children, and using validated prediction models for individual children. Using accurate models, it is now possible to predict the growth response to growth hormone (GH) treatment in a slowly growing child with GH deficiency (GHD) or in a child with idiopathic short stature (ISS). The growth response to the standard dose of GH can be regarded as a bioassay for GH (i.e. the tissue GH responsiveness) and the information on this growth response can be used for different purposes: to decide about treatment or not, for monitoring, and for adjusting the GH dose in order to reach a defined goal for height. This last concept is now used in an ongoing prospective randomized GH dose-finding trial. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065931&dopt=Abstract

Horm Res. 2002;57 Suppl 2:88-94.
Amplitude of pubertal growth in short stature children with intrauterine growth retardation.

Lienhardt A, Carel JC, Preux PM, Coutant R, Chaussain JL.

Service d'Endocrinologie Pediatrique, Hopital Saint Vincent de Paul, Paris, France. anne.lienhardnilim.fr

OBJECTIVE: Pubertal growth contributes to 15-18% of adult height. A blunted pubertal peak could contribute to short adult height in short children born with intrauterine growth retardation (IUGR). DESIGN AND METHODS: Pubertal growth, from onset of puberty to final height, was investigated in 75 short IUGR children: 47 were treated with recombinant human growth hormone (GH) (tx) before pubertal onset (mean dose: 0.4 IU/kg/week); 28 were not treated (no-tx). They were compared with 98 normal children. RESULTS: Puberty occurred later in IUGR children than in controls (boys 14.2 +/- 1 years vs. 12.1 +/- 0.8 years; girls 12 +/- 1 years vs. 11.2 +/- 0.8 years; p < 0.0001). In girls, total pubertal growth was similar in all three groups (tx: 19.3 +/- 4.8 cm; no-tx 19.8 +/- 4.9 cm; controls 20.2 +/- 3.9 cm; non-significant). IUGR boys had a reduced pubertal growth (tx: 21.3 +/- 6.2 cm; no-tx: 23.9 +/- 6.1; controls 26.9 +/- 3.9 cm; p < 0.05). The age at puberty onset was the major determinant of pubertal growth amplitude (boys: r = 0.53, p < 0.001; girls: r = 0.45, p < 0.001). IUGR children exhibited little catch-up growth during puberty. CONCLUSIONS: In the present study, we describe a delayed onset of puberty in short children born with IUGR. Moreover, prepubertal GH treatment was associated in boys with a decrease in the amplitude of the pubertal spurt, a finding that should be further evaluated in clinical trials. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065935&dopt=Abstract

Am J Obstet Gynecol. 2002 Jun;186(6):1142-9.
Acceptance of altering the standard 21-day/7-day oral contraceptive regimen to delay menses and reduce hormone withdrawal symptoms.

Sulak PJ, Kuehl TJ, Ortiz M, Shull BL.

Department of Obstetrics and Gynecology, Scott & White Clinic, Texas A&M University System Health Science Center College of Medicine, Temple 76058, USA. psulawmail.sw.org

OBJECTIVE: Measure acceptance and use of extending the number of active oral contraceptive (OC) pills beyond 21 days and/or shortening the hormone-free interval to reduce the frequency and severity of hormone withdrawal symptoms. STUDY DESIGN: A retrospective review was performed of patients on OCs with unwanted hormone withdrawal symptoms who were counseled by one osbtetrician-gynecologist (P. J. S.) on altering their standard 21/7 regimen. All patients used a monophasic 30 to 35 microg pill and underwent an initial counseling visit between December 1993 and October 2000. RESULTS: Of 318 patients counseled on "extending the number of active pills," 292 (92%) had documented follow-up after the initial counseling session. The primary reason for extending the number of active pills was to decrease symptoms of headache (35%), dysmenorrhea (21%), hypermenorrhea (19%), and premenstrual symptoms (13%). The remaining 12% of patients cited convenience, endometriosis, and other reasons such as menstrual-associated acne. Twenty-five (9%) of 292 chose not to extend, with a preference for monthly menses as the most common reason (40%) followed by a concern that symptoms were not severe enough to warrant extension (32%). Of 267 patients who initiated an extended regimen, 57 discontinued OCs, 38 returned to a standard regimen, and 172 were extending use at the time of last follow-up. Using survival analysis methods, at 5 years 46% +/- 5% (mean +/- SE) of patients continued an extended OC pattern. The regimen of OC use by patients continuing an extended pattern was 12 +/- 12 (mean +/- SD) weeks of active pills (median of 9 weeks and range to 104 weeks) with pill-free interval of 6 +/- 2 days (median of 5 days and range of 0-7 days). CONCLUSION: The majority of patients with hormone withdrawal symptoms on OCs will initiate a regimen of extending active pills, often with a shortened hormone-free interval to reduce frequency and severity of associated symptoms.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12066088&dopt=Abstract

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