46 research outputs found
Hyperprolactinemia and male reproductive functions
In this thesis some effects of PRL on reproductive
functions have been investigated
PRL-secreting pituitary adenoma.
animal model has been used:
For in men with a comparison an
In. rats hyperprolactinemia has been induced by sub-cutaneous
inoculation of a PRL- and ACTH-secreting
transplantable pituitary tumor..
The local effects of PRL on testicular functions
have been studied by implantation of a pituitary
in a testis. The symptoms of hyperprolactinemia in men with a
pituitary adenoma are; as indicated ln many reports
(Chapter l), mostly due to local effects of the tumor
on para- and suprasellar tissues. Patients may present
with headache, impaired vision, visual field defects,
paresis of the eyemuscles and hypopituitarism.
Loss of libido and potency, which symptoms may retrospectively be present for a long period, are considered by many authors to be typical feattures for male hyperprolactinemia. Gynecomastia and galactorrhea are uncormnon findings,
respect to function of
triuch of the research
the hypothalamic-pituitary-
testicular axis in hyperprolactinemic uen reported
over the past few years is still controversial.
The basal serum levels of LE and FSH may be
normal or decreased and their response to LRH may be
normal or blunted. Serum testosteron levels have been found subnormal, even in the presence of normal
basal and LRH-stimulated LH and FSH levels.
Furthermore serum testosterone levels may show a normal
response to the administration of hCG. It is
difficult to draw conclusions from the data present.ed
in the various papers since most of the reported series
comprised men with macroadenomas or men who had
been treated before the time of presentatio
目次
Considerable concern has been raised in recent publications that oestrogen-lihe compounds in either food or the environment cause adverse effects on reproductive health. There is clear evidence that reproductive disruption in wildlife may be caused by environmental pollutants and more specifÌcally by endocrine-disrupting compounds. The increase in the incidence of disorders of the male reproductive tract (e.g. testicular cancer, cryptorchidisn, hypospadias) and the possible decline o[ sperm quality led to the hypothesis in 1993 that the reported increases stem from fetal or neonatal exposure of the developing male to oestrogens. Cryptorchidism, hypospadias, testicular cancer and poor semen quality have also been proposed to be symptoms of one underlying cause, the testicular dysgenesis syndrome, which may deveÌop during fetal life under the influence of environmental factors. However, there is only circumstantial evidence in humans that exposure to endocrine disrupters, especially diethylstilbestrol, during pregnancy causes problems of reproductive health. Oestrogenlike effects have been reported for a variety of naturalÌy occurring oestrogens (so-called phytoestrogens) and for numerous synthetic compounds. The critical issue is whether there are suflìciently high levels of endocrine disrupters in the ambient environment to exert adverse health effects on the general populatio
Serum inhibin B as a marker of spermatogenesis
Inhibin B is produced by Sertoli cells, provides negative feedback on FSH
secretion, and may prove to be an important marker for the functioning of
seminiferous tubules. The purpose of the present study was to examine the
relationship between the spermatogenic function of the testis of
subfertile men and the plasma concentrations of inhibin B and FSH. These
parameters were estimated in a group of 218 subfertile men. Serum inhibin
B levels were closely correlated with the serum FSH levels (r = -0.78, P <
0.001), confirming the role of inhibin B as feedback signal for FSH
production. The spermatogenic function of the testis was evaluated by
determining testicular volume and total sperm count. Inhibin B levels were
significantly correlated with the total sperm count and testicular volume
(r = 0.54 and r = 0.63, respectively; P < 0.001). Testicular biopsies were
obtained in 22 of these men. Inhibin B was significantly correlated with
the biopsy score (r = 0.76, P < 0.001). Receiver operating characteristic
analysis revealed a diagnostic accuracy of 95% for differentiating
competent from impaired spermatogenesis for inhibin B, whereas for FSH, a
value of 80% was found. We conclude that inhibin B is the best available
endocrine marker of spermatogenesis in subfertile men
Free and total insulin-like growth factor I (IGF-I), IGF-binding protein-1 (IGFBP-1), and IGFBP-3 and their relationships to the presence of diabetic retinopathy and glomerular hyperfiltration in insulin-dependent diabetes mellitus
The existing literature on serum insulin-like growth factor I (IGF-I)
levels in insulin-dependent diabetes mellitus (IDDM) is conflicting. Free
IGF-I may have greater physiological and clinical relevance than total
IGF-I. Recently, a validated method has been developed to measure free
IGF-I levels in the circulation. Serum free and total IGF-I, IGF-binding
protein-1 (IGFBP-1), and IGFBP-3 levels were measured in 56
insulin-treated IDDM patients and 52 healthy sex- and age-matched
controls. Diabetic retinopathy was established by direct fundoscopy. In 54
IDDM patients, the glomerular filtration rate (GFR) and effective renal
plasma flow were calculated from the clearance rate of [125I]iothalamate
and [131I]iodohippurate sodium. Fasting free IGF-I, total IGF-I, and
IGFBP-3 levels were significantly lower in IDDM patients than in age- and
sex-matched healthy controls (free IGF-I, P < 0.005; total IGF-I, P <
0.001; IGFBP-3, P = 0.001), whereas IGFBP-1 levels were higher (P <
0.001). In IDDM subjects, decreases in free IGF-I, total IGF-I, and
IGFBP-3 levels with age were observed (free IGF-I, r = -0.27 and P = 0.05;
total IGF-I, r = -0.52 and P < 0.001; IGFBP-3, r = -0.37 and P = 0.005).
Free IGF-I was inversely related to fasting glucose in IDDM subjects (r =
-0.35; P = 0.01), whereas the relationship between total IGF-I and fasting
glucose did not reach significance (r = -0.27; P = 0.06). Age-adjusted
free IGF-I levels were significantly higher (P < 0.05) in IDDM subjects
with retinopathy than in subjects without retinopathy after adjustment for
age. Total IGF-I and IGFBP-3 levels were positively related to GFR (total
IGF-I, r = 0.35 and P < 0.05; IGFBP-3, r = 0.28 and P < 0.05). Both of
these differences lost significance after adjustment for age. Free IGF-I,
total IGF-I, and IGFBP-3 levels were lower and IGFBP-1 levels were higher
in insulin-treated IDDM subjects compared to those in age- and sex-matched
controls. Free IGF-I, total IGF-I, and IGFBP-3 levels decreased
significantly with age in IDDM subjects. Age-adjusted free IGF-I levels in
subjects with diabetic retinopathy were higher than those in subjects
without diabetic retinopathy. Total IGF-I and IGFBP-3 levels were
positively related to GFR in IDDM subjects, but these relations were lost
after adjustment for age. Measurement of serum free IGF-I levels in IDDM
subjects did not have clear advantages compared to that of total IGF-I,
IGFBP-1, and IGFBP-3 levels. Serum IGF-I and IGFBPs reflect their tissue
concentrations to a various degree. Consequently, extrapolations
concerning the pathogenetic role of the IGF/IGFBP system in the
development of diabetic complications at the tissue level remain
speculative
Stem cell factor receptor (c-KIT) codon 816 mutations predict development of bilateral testicular germ-cell tumors
Testicular germ-cell tumors (TGCTs) of adolescents and adults originate
from intratubular germ cell neoplasia (ITGCN), which is composed of the
malignant counterparts of embryonal germ cells. ITGCN cells are
characterized, among others, by the presence of stem cell factor receptor
c-KIT. Once established, ITGCN will always progress to invasiveness.
Approximately 2.5-5% of patients with a TGCT will develop bilateral
disease and require complete castration, resulting in infertility, a need
for lifelong androgen replacement, and psychological stress. To date, the
only way to predict a contralateral tumor is surgical biopsy of the
contralateral testis to demonstrate ITGCN. We did a retrospective study of
224 unilateral and 61 proven bilateral TGCTs (from 46 patients, in three
independently collected series in Europe) for the presence of activating
c-KIT codon 816 mutations. A c-KIT codon 816 mutation was found in three
unilateral TGCT (1.3%), and in 57 bilateral TGCTs (93%; P < 0.0001). In
the two wild-type bilateral tumors for which ITGCN was available, the
preinvasive cells contained the mutation. The mutations were somatic in
origin and identical in both tumors. We conclude that somatic activating
codon 816 c-KIT mutations are associated with development of bilateral
TGCT. Detection of c-KIT codon 816 mutations in unilateral TGCT identifies
patients at risk for bilateral disease. These patients may undergo
tailored treatment to prevent the development of bilateral disease, with
retention of testicular hormonal function
POU5F1 (OCT3/4) identifies cells with pluripotent potential in human germ cell tumors
Human germ cell tumors (GCTs) may have variable histology and clinical
behavior, depending on factors such as sex of the patient, age at clinical
diagnosis, and anatomical site of the tumor. Some types of GCT, i.e., the
seminomas/germinomas/dysgerminomas and embryonal carcinomas (the stem cell
component of nonseminomas), have pluripotent potential, which is
demonstrated by their capacity to differentiate into somatic and/or
extraembryonic elements. Although embryonal carcinoma cells are
intrinsically pluripotent, seminoma/germinoma/dysgerminoma cells, as well
as their precursor carcinoma in situ/gonadoblastoma cells, have the
phenotype of early germ cells that can be activated to pluripotency. The
other types of GCT (teratomas and yolk sac tumors of infants and newborn,
dermoid cyst of the ovary, and spermatocytic seminoma of elderly) are
composed of (fully) differentiated tissues and lack the appearance of
undifferentiated and pluripotent stem cells. OCT3/4, a transcription
factor also known as OTF3 and POU5F1, is involved in regulation of
pluripotency during normal development and is detectable in embryonic stem
and germ cells. We analyzed the presence of POU5F1 in GCT and other tumor
types using immunohistochemistry. The protein was consistently detected in
carcinoma in situ/gonadoblasto
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