Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Longterm use of marijuana has been found to cause physiological changes that can alter individual reproductive potential. The effects of marijuana depend on the dose and can include death from depression of the respiratory system. Longterm effects are however particularly hard to assess. Marijuana is absorbed rapidly and eliminated very slowly. The active principle, delta-9-tetrahidrocannabinol (delta-9-THC), is highly liposoluble and fixes to the serum proteins, passing to the lungs and liver for metabolization and to the kidneys and liver for excretion. As with estrogens, there is an enterohepatic circuit for reabsorption and elimination. 90% is eliminated in the feces, 65% within 48 hours. Because of the enterohepatic circuit and liposolubility, elimination requires 1 week for completion. The other important biotransformation of the active principle is hydroxilation; the hydroxilated derivatives are responsible for the psychoactivity of cannabis. Cannabis affects both neuroendocrine function and the germ cells. Studies on experimental animals have indicated that THC can cause a decline in the pituitary hormones follicle stimulating hormone, luteinizing hormone, and prolactin, and in the steroids progesterone, estrogen, and androgens. Human studies have shown that chronic users have decreased levels of serum testosterone. Because steroidogenesis can be restimulated with human chorionic gonadotropin, it appears that THC does not directly affect steroid production by the corpus luteum, but that its action is mediated by the hypothalamus. Because of its potent antigonadotropic action, THC is under study as an anovulatory agent. The same animal studies have shown that ovulation returns to normal 6 months after termination of use. High rates of anovulation and luteal insufficiency have been observed in women smoking marijuana at least 3 times weekly. THC accumulates in the milk. Animal studies have shown that THC depresses the enzymes necessary for lactation and causes a diminution in the volume of the mammary glands. In recent studies, significant amounts of the drug have been detected in both mothers' milk and the blood of newborns. Animal studies indicate that THC crosses the placenta, achieving concentrations in the fetus as high as those in the mother. Animal studies also demonstrated increasing frequency of abortions, intrauterine death, and declines in fetal weight. The effects were probably due to an alteration in placental function. A human study likewise showed that marijuana use during pregnancy was significantly related to poor fetal development, low birth weight, diminished size, and decreased cephalic circumference. Congenital malformations have been observed in experimental animals exposed to THC. Declines in sperm volume and count and abnormal sperm motility have been observed in chronic marijuana users. In vitro studies show that THC produces a marked degeneration of human sperm.
 ...
PMID:[Review and update: marijuana and reproduction]. 1228 Dec 77

We report a case of a virilized 59-yr-old woman with elevated serum testosterone levels and bilateral macronodular adrenal hyperplasia. The patient underwent laparoscopic right adrenalectomy, after which the elevated testosterone level transiently normalized. The immediate postoperative depression of the testosterone level suggested that the process was driven by gonadotropins that were suppressed by the stress of surgery. The excised right adrenal mass contained testosterone by immunohistochemistry and LH receptor mRNA by in situ hybridization. The recurrence of hyperandrogenemia suggested that the enlarged left adrenal was also secreting testosterone. The serum testosterone level increased in response to im injection of human chorionic gonadotropin, suggesting control by aberrant LH receptors. Injection of leuprolide acetate (7.5 mg im) to suppress LH levels resulted in normalization of the testosterone level 12 d later that persisted for several weeks. Ectopic receptors mediating Cushing's syndrome have been described in several cases of bilateral adrenal hyperplasia and adrenal adenoma. This is the first case to our knowledge in which pure androgen overproduction in adrenal hyperplasia has been shown to be controlled by LH receptors. In our patient, the control of androgen secretion by LH may explain the postmenopausal onset of virilization and the transient postoperative normalization of the serum testosterone level.
 ...
PMID:Virilization in bilateral macronodular adrenal hyperplasia controlled by luteinizing hormone. 1251 32

The purpose of this study was to evaluate the efficacy and safety of human chorionic gonadotropin (hCG) for patients with partial androgen deficiency of the aging male (PADAM). Twenty-one patients over 50 years of age with PADAM symptoms were included in this study. Laboratory and endocrinologic profiles were reviewed as appropriate, and PADAM symptoms were judged by means of several questionnaires such as the Aging Males' Symptoms (AMS) scale, short version of the International Index of Erectile Function (IIEF-5), and the Self-rating Depression Scale (SDS). Laboratory and endocrinologic values and symptom scores were evaluated and compared before and after treatment by hCG injection. The treatment period was 8.0 +/- 5.0 months (3.0-24.0 months). Serum concentrations of testosterone, including total testosterone, calculated free testosterone, and calculated bioavailable testosterone, increased significantly. AMS total scores and subscores decreased significantly after treatment. However, IIEF-5 and SDS scores did not improve. With respect to adverse effects, laboratory tests showed that only red blood cell count, hematocrit and hemoglobin level increased significantly after treatment, however, these values remained within the normal range. No adverse effect was identified after treatment. We conclude that hCG injection may be considered as a treatment for PADAM.
 ...
PMID:Treatment with human chorionic gonadotropin for PADAM: a preliminary report. 1639 Jul 42

A 40-year-old unmarried male was referred to our hospital with anejaculation. His secondary sex characteristics, sexual function and ejaculation were previously normal but for the last 5 years he found it impossible to ejaculate even though he could achieve an erection. His genital stage was Tanner V, and pubic hair stage was Tanner III. There were no varicoceles or chromosomal aberrations. His testis volume was 10 ml on the right side and 12 ml on the left. His hormonal data were luleinizing hormone (LH) 0.3 mIU/ml (normal: 2.2-8.4 mIU/ml), fillicle stimulating hormone (FSH) 1.5 mIU/ ml (1.8-12 mIU/ml), testosterone 0.05 ng/ml (2.01-7.5 ng/ml). A gonadtropin releasing hormone (GnRH) test and human chorionic gonadotropin (hCG) stimulation test revealed low responses of LH, FSH and a normal response of testosterone. Magnetic resonance imaging of the head revealed slight depression of the diaphragma sellae, indicating an "empty sella". We diagnosed acquired hypogonadtropic-hypogonadism related empty sella. An hCG replacement therapy was introduced and after 3 months the patient's capacity to ejaculate was restored and testis volume was 14 ml on both sides. Six months after hormone replacement therapy, semen analysis revealed azoospermia. Then we added r-hFSH to his treatment and expect his sperm to reappear.
 ...
PMID:[Acquired male hypogonadotropic hypogonadism (MHH) in a patient with empty sella: a case report]. 1917 4

The mechanism for a reported temporal association between ovulation and a transient disruption in the periovulatory increase in LH concentrations was studied in nine mares treated with human chorionic gonadotropin when the preovulatory follicle was >/=32mm. Examinations for ovulation detection and blood collection were done at 2-h intervals and the results were retrospectively centralized to ovulation (Hour 0). Concentrations of LH began to increase (P<0.03) rapidly at Hour -18, decreased (P<0.04) between Hours 0 and 6, and again increased (P<0.0001) after Hour 12. A progressive decrease (P<0.0001) in estradiol between Hours -30 and 24 was interrupted temporarily by an increase (P<0.01) between Hours -2 and 0 and a decrease (P<0.007) between Hours 0 and 2. Results indicated that a disruption and depression in the periovulatory LH surge occurred at the time of detected ovulation in mares and was temporally associated with a transient increase in estradiol during an overall progressive decline. The disruption in LH concentrations is attributable to the estradiol increase, based on a reported negative effect of estradiol on LH. The source of the circulating estradiol was likely from the discharge of estradiol-laden follicular fluid into the abdomen during ovulation and rapid absorption of estradiol into the circulation.
 ...
PMID:Disruption of the periovulatory LH surge by a transient increase in circulating 17beta-estradiol at the time of ovulation in mares. 1947 91

Human ovarian granulosa cells obtained from women undergoing in vitro fertilization were exposed to 15.6, 31.25, 62.5, 125, 250, 500, 1000 muM Ni(2+) for 48 h. To determine the site of action of Ni(2+), the granulosa cells were stimulated to produce progesterone (P) by using maximally stimulating amounts of human chorionic gonadotropin (0.1 IU/ml hCG) or dibutyryl cyclic adenosine monophosphate (1 mM db-cAMP). The luteinizing hormone (LH) analog hCG was chosen because resultant P production requires an intact membrane receptor and db-cAMP was used to test for post LH receptor defects caused by Ni(2+). Progesterone content of the culture medium was determined by radioimmunoassay (RIA), and viability of the cells was measured by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) reduction test. Concentration-dependent depression in both hGC and db-cAMP stimulated P production was seen at 15.625 muM or higher concentration of Ni(2+), which is not cytotoxic on human ovarian granulosa cells. The viability of cells was unaffected up to 31.25 muM and decreased significantly at 62.5 muM. Our results show a dose-related depression in stimulated P production of granulosa cells at a dose that does not induce significant cytotoxic action. These data indicate that the effect of Ni(2+) on P production is not due to cytotoxicity, and the cellular site(s) of inhibitory action appears to be subsequent to the membrane receptor and production of cAMP.
 ...
PMID:Effect of nickel (ni(2+)) on primary human ovarian granulosa cells in vitro. 2002 Nov 8

Currently, few users of anabolic-androgenic steroids (AAS) seek substance abuse treatment. But this picture may soon change substantially, because illicit AAS use did not become widespread until the 1980s, and consequently the older members of this AAS-using population - those who initiated AAS as youths in the 1980s - are only now reaching middle age. Members of this group, especially those who have developed AAS dependence, may therefore be entering the age of risk for cardiac and psychoneuroendocrine complications sufficient to motivate them for substance abuse treatment. We suggest that this treatment should address at least three etiologic mechanisms by which AAS dependence might develop. First, individuals with body image disorders such as "muscle dysmorphia" may become dependent on AAS for their anabolic effects; these body image disorders may respond to psychological therapies or pharmacological treatments. Second, AAS suppress the male hypothalamic-pituitary-gonadal axis via their androgenic effects, potentially causing hypogonadism during AAS withdrawal. Men experiencing prolonged dysphoric effects or frank major depression from hypogonadism may desire to resume AAS, thus contributing to AAS dependence. AAS-induced hypogonadism may require treatment with human chorionic gonadotropin or clomiphene to reactivate neuroendocrine function, and may necessitate antidepressant treatments in cases of depression inadequately responsive to endocrine therapies alone. Third, human and animal evidence indicates that AAS also possess hedonic effects, which likely promote dependence via mechanisms shared with classical addictive drugs, especially opioids. Indeed, the opioid antagonist naltrexone blocks AAS dependence in animals. By inference, pharmacological and psychosocial treatments for human opioid dependence might also benefit AAS-dependent individuals.
 ...
PMID:Treatment of anabolic-androgenic steroid dependence: Emerging evidence and its implications. 2018 94

Human chorionic gonadotropin (hCG) is as efficient as pregnancy in protecting the rat mammary gland against carcinogenesis. The effect of both pregnancy and hCG is a lasting one, without secondary effect on body weight, and endocrine related organs. The protective effect of hCG as in pregnancy is due to gland differentiation associated with depression on cell proliferation and synthesis of inhibin by the mammary epithelial cells. The protective effect of hCG is further demonstrated after carcinogen administration indicating a decrease of tumor progression. Whereas hCG action is mediated mainly through the ovary, a direct effect has been demonstrated. This data has been further confirmed by showing that hCG treatment inhibits the proliferation of human breast epithelial cells. This inhibition is associated with synthesis of new gene products, some of which have been identified by immunoprecipitation and Northern blot analysis to be alpha and beta inhibin subunits. Collectively, all these data indicate that inhibin may play an important role in cell growth and differentiation of the mammary epithelia during the physiological process of pregnancy or by the action of hCG. Further studies delineating the pathway through which hCG and inhibin modulate the fate of neoplastic cells would allow us to utilize physiologic mechanisms controlling cell proliferation in breast cancer prevention and therapy.
 ...
PMID:Role of HCG and inhibin in breast-cancer (review). 2156 23

An increasing number of young and middle-aged men are seeking treatment for symptoms related to deficient levels of androgens (hypogonadism) including depression, loss of libido, erectile dysfunction, and fatigue. The increase in prevalence of testosterone supplementation in general and anabolic steroid-induced hypogonadism specifically among younger athletes is creating a population of young men who are uniquely impacted by the testicular end-organ negative consequences of exogenous steroid use. Exogenous testosterone therapy can alter the natural regulation of the hypothalamic-pituitary-gonadal axis leading to impaired spermatogenesis with azoospermia being a serious possible result, thus rendering the individual infertile. For men of reproductive age who suffer from hypogonadal symptoms, preservation of fertility is an important aspect of their treatment paradigm. Treatment with human chorionic gonadotropin (hCG) has shown the ability not only to reverse azoospermia brought on by testosterone supplementation therapy but also to help maintain elevated intratesticular testosterone levels. In addition, selective estrogen receptor modulators, often used with hCG have been shown both to elevate total testosterone levels and to maintain spermatogenesis in hypogonadal men.
...
PMID:Preserving fertility in the hypogonadal patient: an update. 2533 50

In past few years we observed the increasing of population of men, who are treated with testosterone due to hypogonadism associated with aging but the most of them have no indications to testosterone replacement therapy. The classical symptoms of hypogonadism including depression, loss of libido, erectile dysfunction, and fatigue may be related to any others diseases. The increase in prevalence of androgenic anabolic steroids specifically among younger athletes is also observed. Exogenous testosterone and anabolic androgenic steroids can inhibit the hypothalamic-pituitary-gonadal axis leading to decreasing of endogenous testosterone synthesis and impaired spermatogenesis. In hypogonadal men who are in reproduction age the goal of therapy should be not only replacement therapy but also achiving and/or maintaining of spermatogenesis. Human chorionic gonadotropin (hCG) and selective estrogens receptor modulators (SERM) are efficacy in treatment of clinical signs and symptoms of hypoigonadism, has been shown to reverse spermatogenesis disturbances and can to maintain elevated intratesticular testosterone levels necessary to optimal spermatogenesis.
...
PMID:[The treatment of hypogonadism and maintenance of fertility in men]. 2708 5


<< Previous 1 2 3 4 Next >>