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Biomedical subjects

H P Schneider

Publications and source records attributed to H P Schneider.

At least 19 recordsLinked to original sources
PubMed1992

Subnormal sperm parameters in conventional semen analysis are associated with discrepancies between fertilization and pregnancy rates in in-vitro fertilization and embryo transfer.

Three hundred and twenty-eight consecutive treatment cycles in 168 couples were analysed retrospectively in order to examine the influence of conventional semen analysis results on the outcome of in-vitro fertilization and embryo transfer with respect to the occurrence of both fertilizations and pregnancies. All treatments were performed under maximally standardized and controlled conditions. Each of the three main determinants of the spermiogram, namely the concentration, motility and morphology of sperm in seminal plasma, was of significant importance for fertilization and subsequent pregnancy. Best correlations were achieved by counting the number of progressively (a+b) motile sperm and the number of normally formed sperm in seminal plasma. The pregnancy rate was reduced significantly in cases in which the sperm concentration was < 10 x 10(6) ml-1 (P < 0.01), or in which there was < 40% progressively motile sperm (P < 0.001), or < 30% normally formed sperm (P < 0.001). If more than one parameter in the spermiogram was abnormal, the fertilization rate depended mainly on the most disturbed sperm parameter. The implantation rate as well as the pregnancy rate was reduced significantly in patients with low progressive sperm motility and normal morphology rates. The difference could only be attributed partially to the lower number of embryos replaced. In conclusion, subnormal sperm quality seems to interfere with developmental stages beyond the process of fertilization.

Adult↗
PubMed1992

[Postmenopausal osteoporosis from the viewpoint of the gynecologist].

Prophylaxis of postmenopausal osteoporosis is of major importance if estrogen replacement therapy is considered. Assessment of clinical symptoms, (standardized) x-ray analysis, and bone densitometry contribute to the final diagnosis. Incidence of osteoporotic fractures is rising due to alterations in life style and dietary habits. One out of three to four women eventually suffer from osteoporosis in the European countries, United States and Japan. Prevention of postmenopausal osteoporosis is achieved by adequate estrogen replacement therapy carried out for years, maintaining peripheral estradiol concentrations of 220 pmol/l. Doses of 2 mg estradiol or 0.625 mg of conjugated estrogen or 50-100 micrograms percutaneous estradiol/day are equally effective for prevention. The additional administration of a progestogen may be of specific value to increase the antiresorptive effect of estrogens. We distinguish between estrogen replacement in a cyclic or continuous way combined with a sequential or continuous progestogen in women with intact uterus.

Bone Density↗
PubMed1992

Identification and treatment of postmenopausal women at risk for the development of osteoporosis.

One in the three women develops osteoporosis--low bone mass and structural deterioration leading to fractures. Pre- and postmenopausal deficiency states are main causes. Estrogens prevent bone loss: Oral doses of 2 mg estradiol or 0.625 conjugated estrogens/day or 50-100 micrograms transdermal estradiol/day substantially reduce vertebral, forearm, and hip fractures. Certain progestins may enhance this effect. Calcium as a prerequisite for attainment of peak bone mass will not substitute for estrogen replacement. Selection of patients actually being at risk for postmenopausal osteoporosis needs to be improved substantially; there is no sensitive single test or testing system for osteoporosis. As individual history and physical exam or biochemical markers of bone resorption and formation rarely provide the early diagnosis of osteoporosis, prophylactic estrogen replacement therapy has to be considered in the majority of postmenopausal women to achieve prevention of postmenopausal osteoporosis. Compliance of replacement therapy in the European countries is poor, only 5-25% of postmenopausal women use estrogen replacement therapy for more than one year. Major compliance problems are alleged weight gain, resumption of withdrawal bleeding and fear to develop breast or endometrial cancer.

Aged↗
PubMed1992

[Osteoporosis from the gynecologic viewpoint].

Osteoporosis is a disease of the elderly characterized by a loss of bone mass causing fractures in presence of an inadequate trauma. Osteoporosis has to be considered as a significant ailment in our population. This review outlines epidemiology, pathogenesis and risk factors of primary osteoporosis. The physiological role of sex hormones, especially of estradiol, for the development and maintenance of skeletal bone mass is explained. Principles of preventive estrogen(-progesterone) application for the prophylaxis of postmenopausal osteoporosis are specified by several estrogen replacement studies in postmenopausal women. Individual replacement therapy for the compensation of a long-lasting estrogen deficit in the reproductive age group, in pre- and postmenopausal women is the assignment of the gynecologist in order to protect the skeletal system.

Adult↗
PubMed1979

[Familial endocrine adenomatosis (author's transl)].

The combination of pituitary and thyroid gland adenomatosis is reported in four family members of two generations. This finding of dominant inheritance is discussed with special reference to multiple familial adenomatosis, also known as Wermer's syndrome. The endocrine status including dynamic function tests is presented. It is our intention to point out that in cases of monoglandular adenomatosis clinical attention should be directed not only to anterior pituitary and thyroid gland but also to their possible incidence with tumours of the parathyroid gland and the islet cell organ.

Adenoma, Islet Cell↗
PubMed1979

[Gonadoblastoma and overgrowing dysgerminoma in Turner mosaicism [45, XO/46, Xi (Xq)] (author's transl)].

It is well established that the Y-chromosome is associated with germ cell tumor development. There is a considerable tumour risk in XY- and XY/XO-gonadal dysgenesis. In the absence of Y-chromosome germ cell tumours are extremely rare. The history of a patient with 45 XO/46 Xi (Xq)-karyotype is presented, who had a gonadoblastoma with overgrowing dysgerminoma. According to basal body temperature recordings, this patient ovulated up to the age of 22 years. After this cyclical ovarian function was exhausted; histologically no primordial follicles could be detected. Gonadotropin as well as prolactin binding sites in the tumours could not be demonstrated, suggesting hormone independency and complete malignant transformation of the tumor. In general the clinician should be aware of a possible germ cell tumour development in the absence of a Y-chromosome. However as far as the clinical management of patients with dysgenetic gonads is concerned, prophylactic gonadectomy is only indicated in the presence of a Y-chromosome.

Adult↗
PubMed1979

Sexual differentiation of the hypothalamus in gonadal agenesis and testicular feminization.

Cyclical hypothalamic function was investigated in three patients with an XY karyotype and female external genitalia; in one of them we diagnosed gonadal agenesis, and in the other two testicular feminization. We studied the effect of estradiol and progesterone on gonadotropin release. The patient with gonadal agenesis had cyclical hypothalamic function, but this cyclical function was suppressed in the patients with testicular feminization in whom no LH secretion could be provoked by steroid stimulation. These observations support the concept that hypothalamic sexual differentiation is due to testosterone (which is locally converted to estradiol in the hypothalamus).

Androgen-Insensitivity Syndrome↗
PubMed1979

Suppression of prolactin secretion by lisuride throughout the menstrual cycle and in hyperprolactinaemic menstrual disorders.

Normally menstruating volunteers as well as patients with hyperprolactinaemic menstrual disorders were treated with lisuride hydrogen maleate (200 micrograms b.i.d.), an ergoline derivative with dopaminergic properties. Within 3 h after an oral dose of 200 micrograms lisuride, PRL levels decreased significantly in all subjects to a plateau which lasted up to 3 h. Thereafter a gradual increase of serum PRL was noted. In the normally menstruating volunteers lisuride treatment did not result in any significant change of gonadotrophin or of sex steroid secretion, while both, basal as well as metoclopramide (MTCL) stimulated PRL release were significantly diminished. The inhibition of PRL secretion in patients with short luteal phases resulted in an increase of luteal progesterone output. In both treated groups ovulation occurred 1 to 5 days earlier in cycles on lisuride than in control cycles. LF-RH/MTCL tests performed in the patient bearing a pituitary prolactinoma before and after lisuride treatment revealed a continuous increase of pituitary LH pools, while PRL secretion decreased under lisuride therapy. Subsequently ovulation and menstruation occurred. The data presented demonstrate that lisuride is a potent inhibitor of PRL secretion and has proven its clinical usefulness for treatment of hyperprolactinaemic menstrual disorders. Application of lisuride resulted in an increase of luteal progesterone secretion in previously demonstrated corpus luteum insufficiency as well as in restoration of normal cyclical feedback mechanisms in tumorous hyperprolactinaemic anovulation. The MTCL-PRL stimulation test is suitable to monitor PRL suppression during lisuride treatment, while LH-RH testing reveals the effectiveness of lisuride by demonstrating an increase of pituitary gonadotrophin pools.

Adenoma↗
PubMed1978

[Tumour regression in pituitary adenoma by bromocriptin (author's transl)].

A 35 year old patient with longstanding amenorrhea-galactorrhea due to a pituitary macroadenoma has been observed for a period of more than 2 years. During this time tumour expansion was radiologically evident. A full term pregnancy was responsible for most of the tumour growth. Following postpartum period Bromocriptin treatment led to considerable regression of the adenoma. Recalcification of sella structures and an involuted sella volume was radiologically evident. With reference to the experimental investigations of Lloyd (1975) and following the suggestions of L'Hermite (1977) and Vaidya (1977) this tumour regression is interpreted as being due to the antimitotic effect of Bromocriptin via inhibition of c-AMP and DNA.

Adenoma↗