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PubMed1983

Postnatal developmental alterations following prenatal exposure to the herbicide 2,4-dichlorophenyl-p-nitrophenyl ether: a dose response evaluation in the mouse.

Although nitrofen, 2,4-dichlorophenyl-p-nitrophenyl ether, is a relatively nontoxic herbicide, prenatal exposure to doses considerably less than the LD50 value for adult rats and mice produces numerous developmental defects that become apparent as the animals mature. In the present study postnatal development was observed following prenatal exposure during Days 7 to 17 of gestation at doses of 0, 6.25, 12.5, 25, 50, 100, 150, and 200 mg/kg/day. These doses did not cause maternal toxicity as indicated by the viability of the dams or maternal weight gain during pregnancy. By 3 days of age all pups in the two highest dose groups were dead and 50% had died in the 100 mg/kg/day dose group. Some of the dead and moribund pups from the 200 mg/kg/day exposure group necropsied at three days of age had cleft palate (15%) or diaphragmatic hernia (6%). In addition, about 22% of the pups at 200 mg/kg/day developed a distended abdomen from gasping and swallowing air. These pups did not suckle and eventually died. Body weights of offspring were reduced at birth in the 150 and 200 mg/kg/day groups and at 3 days of age in the 100 mg/kg/day group. Growth rates were subsequently retarded at 12.5, 25, 50, and 100 mg/kg. The Harderian glands were reduced or absent in 97, 65, and 4% of the mice in the 100, 50, and 25 mg/kg dosage groups, respectively, and the gland weights were reduced at all dosages, including the lowest dose of 6.25 mg/kg/day. Weights of other organs including lung and liver (at 6.25 and above), seminal vesicle (at 12.5 and above), and testes (at 100 mg/kg/day) were also reduced by prenatal nitrofen exposure. In addition, prenatal treatment with nitrofen produced functional deficits of the reproductive system; puberty was delayed in females and litter sizes were reduced at 50 and 100 mg/kg/day. A cross-fostering experiment with 100 mg/kg/day of nitrofen demonstrated that the effects noted in the present study were produced solely by prenatal exposure; pups exposed to nitrofen in the milk alone as a consequence of any accumulation of nitrofen in the dam during gestation were unaffected.

Abnormalities, Drug-Induced↗
PubMed1984

Milk-sensitive and eosinophilic gastroenteropathy: similar clinical features with contrasting mechanisms and clinical course.

We studied 12 children with peripheral eosinophilia, iron deficiency anemia secondary to blood loss in the stools, protein-losing enteropathy, and eosinophilic infiltration of the stomach and small intestine. On the basis of immunologic features and responses to therapy, these patients could be divided into two groups. In the first group the disease was transient, presented in the first year of life, remitted on withdrawal of milk from the diet, and was not associated with IgE-mediated immediate hypersensitivity (milk-sensitive enteropathy). In contrast, the second group, which we termed eosinophilic gastroenteropathy, represented patients with a chronic disease that had its onset later in childhood, did not respond to dietary manipulations, was associated with atopy and IgE-mediated immediate hypersensitivity reactions to food, and required corticosteroid therapy to establish remission and control. The mechanism by which food causes gastrointestinal damage appears to be different in these two groups even though the clinical syndromes are similar.

Adolescent↗
PubMed1988

Diagnostic laparoscopy in apparent uterine agenesis.

We report a case of an adolescent female with apparent agenesis of the uterus with chromosomally competent ovarian dysgenesis. In our case, the apparent absence of the uterus on the laparoscopy constituted a severe hypoplasia of the organ prior to estrogen stimulation, rather than aplasia. Following a year of estrogen/progesterone replacement, an infantile but otherwise normal uterus could be demonstrated by hysterosalpinogogram. In gonadal dysgenesis, therefore, it is not possible to differentiate the absence of the uterus from severe hypoplasia using laparoscopy.

Adolescent↗
PubMed1988

Psychosocial growth retardation in adolescence. A reversible condition secondary to severe stress.

Two cases of psychosocial growth retardation in adolescents are presented, along with a brief review of the literature. Both cases were females, aged 12-13 years, who showed marked deceleration of growth and development when placed in an emotionally stressful situation. A normal pattern of growth and development ensued when the stressful situation was at least partially alleviated. To facilitate proper management, it is important to recognize those adolescents with psychosocial growth retardation. The increased availability of human growth hormone (hGH) may place more pressure on physicians to use exogenous hGH in adolescents who exhibit growth retardation. It appears that the administration of exogenous hGH is not indicated in the treatment of children with psychosocial growth retardation.

Adolescent↗
PubMed1988

Bromocriptine-unresponsive prolactin macroadenoma in a prepubertal female.

Macroprolactinomas occur rarely in prepubertal children. A prepubertal 11 10/12-year-old female with a macroprolactinoma presented with a diagnosis of anorexia nervosa. Findings included severe headaches, anorexia, weight loss, and growth failure. The initial serum prolactin level was 2,916 ng/ml. This value fell after beginning treatment with bromocriptine, but later rose despite a doubling of the dose. Transsphenoidal surgical resection was performed and postoperative radiation given. The use of bromocriptine, surgical resection, and radiation therapy in the treatment of macroprolactinomas are discussed.

Adenoma↗
PubMed1989

Hematospermia in an adolescent.

Hematospermia is an infrequent condition in adolescence. This report presents a case of hematospermia in an 15-year-old male adolescent. A relationship is postulated between hematospermia and some vascular phenomena accompanying the pubertal reproductive development.

Adolescent↗
PubMed1989

A dose-response analysis of methoxychlor-induced alterations of reproductive development and function in the rat.

In the present study rats were dosed from weaning, through puberty and gestation, to Day 15 of lactation with methoxychlor at 25, 50, 100, or 200 mg/kg/day. Morphological landmarks of puberty were measured, including the ages at vaginal opening, first estrus, and first estrous cycle in females and at preputial separation in males. In the female, estrous cyclicity, fertility, litter size, number of implantation sites, organ weights, and ovarian and uterine histology were also measured. The viability of the offspring (F1) and their fertility were evaluated using a continuous breeding protocol. Males were necropsied after breeding, the reproductive organs were weighed, and the cauda epididymal sperm counts were determined. One testis was used for histopathology, while the other was used to quantify interstitial fluid (IF) content, IF testosterone concentration, and testicular sperm production. Testosterone and androgen-binding protein were measured in the caput epididymis, and sperm motility and morphology were evaluated from a caudal sample. The serum and pituitary were saved for hormonal determinations. Methoxychlor accelerated the age at vaginal opening and first estrus, and the vaginal smears were cornified. Growth was retarded at 100 and 200 mg/kg/day and fertility was reduced when the females were bred with untreated or similarly treated males. In the highest-dose group, the mated females went from constant estrus into pseudopregnancy following mating, but they had no implants. In males, methoxychlor treatment markedly reduced growth, seminal vesicle weight, cauda epididymal weight, caudal sperm content, and pituitary weight. Puberty was delayed in the two highest-dosage groups. Testicular sperm measures were much less affected than caudal measures. Testis weight and histology were slightly affected, and testicular sperm production, sperm morphology, and motility were unaffected. Endocrine function of the testes and pituitary was altered by methoxychlor administration. Leydig cell testosterone production, in response to human chorionic gonadotropin challenge, was reduced and pituitary levels of prolactin, thyroid-stimulating hormone (TSH), and follicle-stimulating hormone (FSH) were altered. In contrast, serum levels of prolactin, FSH, and luteinizing hormone were unaffected. Serum TSH was reduced by 50% of control at 100 and 200 mg/kg/day, while pituitary levels were increased. Gonadotropin-releasing hormone concentration in the mediobasal hypothalamus was also elevated. In spite of the many reproductive alterations, the fertility of treated males was not reduced when they were mated with untreated females.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Quality of life after growth hormone therapy and induced puberty in women with Turner syndrome.

OBJECTIVE: To evaluate health-related quality of life (HRQoL) in young women with Turner syndrome (TS) after long-term growth hormone (GH) therapy and induced puberty and to analyze whether HRQoL was influenced by auxologic parameters, pubertal development, or subjective parameters. STUDY DESIGN: The study group comprised 49 women with TS, mean (standard deviation) age 19.6 (+/-3.0) years, all former participants of 2 GH studies, > or =6 months after GH discontinuation. Puberty was induced by estrogen treatment, at mean age 12.9 (+/-1.1) years. HRQoL was measured by self-reports of the 2 generic questionnaires, SF36 and TAAQOL. As an additional source of information on HRQoL, we applied parental proxy reports. RESULTS: HRQoL of the women with TS was normal. Remarkably, the women with TS had higher HRQoL scores on some of the scales, including "social functioning" and "role-emotional." Satisfaction with height and breast development had a positive influence on several HRQoL scales. CONCLUSIONS: The young women with TS who reached normal height and had age-appropriate pubertal development reported normal HRQoL. The relatively high scores on some of the HRQoL scales can be explained by an estrogen effect or by a possible response shift, indicating a different internal reference in women with TS. We hypothesize that GH and estrogen treatment positively influenced HRQoL in young women with TS.

Adolescent↗
PubMed2006

A novel form of non-X-linked hyperigm associated with growth and pubertal disturbances and with lymphoma development.

HyperIgM syndrome is a heterogenous immunodeficiency characterized by impaired class-switch recombination due to different molecular abnormalities. We report on two female patients affected by a novel syndrome associating HIGM, growth and pubertal disturbances, and severe lymphoid hyperplasia with eventual development into lymphomas, suggesting a DNA repair defect.

Adolescent↗
PubMed2006

Paediatric phenotype of Kallmann syndrome due to mutations of fibroblast growth factor receptor 1 (FGFR1).

Kallmann syndrome characterised by hypogonadotropic hypogonadism (HH) and anosmia is genetically heterogeneous with X-linked, autosomal dominant and autosomal recessive forms. The autosomal dominant form due to loss of function mutation in the fibroblast growth factor receptor 1 (FGFR1) accounts for about 10% of cases. We report here three paediatric cases of Kallmann syndrome with unusual phenotype in two unrelated patients with severe ear anomalies (hypoplasia or agenesis of external ear) associated with classical features, such as cleft palate, dental agenesis, syndactylia, micropenis and cryptorchidism. We found de novo mutation in these two patients (Cys178Ser and Arg622Gly, respectively), and one inherited Arg622Gln mutation with intrafamilial variable phenotype. These genotype-phenotype correlations indicate that paediatric phenotypic expression of FGFR1 loss of function mutations is highly variable, the severity of the oro-facial malformations at birth does not predict gonadotropic function at the puberty and that de novo mutations of FGFR1 are relatively frequent.

Adolescent↗
PubMed2004

Endocrine activity and developmental toxicity of cosmetic UV filters--an update.

UV filters represent a new class of endocrine active chemicals. In vitro, 8/9 chemicals showed estrogenic (MCF-7 cells), and 2/9 antiandrogenic activity (MDA-kb2 cells). Six/nine filters (benzophenone (Bp)-1, Bp-2, Bp-3, 3-benzylidene camphor (3-BC), 4-methylbenzylidene camphor (4-MBC), octyl-methoxycinnamate (OMC)) increased uterine weight in immature rats. 3-Benzylidene camphor and 4-MBC displaced 16alpha125I-estradiol from human estrogen receptor (ER)beta, not ERalpha. Developmental toxicity of 4-MBC (0.7-47 mg/kg body weight/day) and 3-BC (0.24-7 mg/kg), administered in chow was investigated in Long Evans (LE) rats. Weight gain of pregnant rats was reduced only by 3-BC, early postnatal survival rate and thymus weight by both compounds at higher doses. 4-Methylbenzylidene camphor and 3-BC delayed male puberty, and dose-dependently affected reproductive organ weights of adult male and female F1 offspring, with partly different effect patterns. Thyroid weight was increased by higher 4-MBC doses. Tissue-specific changes in mRNA levels of estrogen-regulated genes in prostate, uterus and brain regions, determined by real-time PCR, and in their response to acute estradiol challenge in adult gonadectomized offspring were observed. Lowest effective doses were 0.24 mg/kg/day for 3-BC and 7 mg/kg/day for 4-MBC. Fat tissue levels at 7 mg/kg 4-MBC (GC-MS) approached the range of UV filters in fish (Nagtegaal et al., 1997; Balmer et al., 2004).

Animals↗
PubMed1996

Pubarche induction with testosterone treatment in women with panhypopituitarism.

OBJECTIVE: To evaluate the efficacy and safety of T therapy in the induction of pubic hair growth in women with congenital panhypopituitarism. DESIGN: Prospective clinical study. SETTING: Patients followed at the University Endocrinology Clinic. PATIENTS: Four women with congenital panhypopituitarism, showing no pubic hair development, currently treated with substitutive therapy with L-thyroxine, cortisone acetate, and estrogen-progestin combination. INTERVENTIONS: A long-acting T preparation (25 to 50 mg) was given IM each month; serum T levels were determined before and after 12 and 24 months of therapy. MAIN OUTCOME MEASURE: Evaluation of pubarche stages (according to Tanner classification of stages). RESULTS: Patients developed pubarche (Tanner stage 3 to 5) after 3 to 18 months of T therapy. Testosterone levels were within the normal range during treatment. No hirsutism or other side effects were recorded. CONCLUSION: A cautious T treatment represents an effective and safe approach to the problem of pubarche induction in women with congenital panhypopituitarism.

Adolescent↗
PubMed1987

Induction of first cycles in primary hypothalamic amenorrhea with pulsatile luteinizing hormone-releasing hormone: a mirror of female pubertal development.

During pubertal development in girls, the attainment of regular ovulatory menstrual cycles usually is preceded by cycles that are either anovulatory or show a defective luteal phase. It is not known whether these defective cycles are caused by inadequate luteinizing hormone-releasing hormone (LH-RH) secretion or by an inadequate response of the pituitary-ovarian axis to LH-RH stimulation. To shed new light on this matter, the authors analyzed endocrine data from 12 menstrual cycles induced by pulsatile LH-RH therapy in five women with primary amenorrhea of hypothalamic origin. Anovulatory cycles occurred with and without an increase in estrogen excretion and with and without a luteinizing hormone surge. In addition, ovulatory cycles with and without deficient corpus luteum function were observed. Most of these types of anovulatory and ovulatory menstrual cycles also have been described during normal puberty. Therefore, these observations suggest that, during normal pubertal development, maturation of the pituitary gonadotropes and of the ovary occurs, as well as the increased secretion of LH-RH from the hypothalamus, which the overall process depends upon.

Adolescent↗