Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Starvation-induced alterations of neuropeptide activity probably contribute to neuroendocrine dysfunctions in anorexia nervosa. For example, CRH alterations contribute to hypercortisolemia and NPY alterations may contribute to amenorrhea. Alterations of these peptides as well as opioids, vasopressin, and oxytocin activity could contribute to other characteristic psychophysiological disturbances, such as reduced feeding, in acutely ill anorexics. Such neuropeptide disturbances could contribute to the vicious cycle that has been hypothesized to occur in anorexia nervosa. That is, the consequences of malnutrition perpetuate pathological behavior.
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PMID:Neuropeptide abnormalities in anorexia nervosa. 873 16

The authors report the case of a 40-year-old woman with a 12-year history of irregular menses, amenorrhea, infertility, galactorrhea, a slightly elevated prolactin level, and a slowly growing pituitary adenoma. She developed recent onset of visual symptoms, prompting craniotomy for removal of an intrasellar tumor. Following surgery, her vision and prolactin levels returned to normal. Light microscopic and immunohistochemical examination of the tumor revealed it to be a neuroblastoma, which was immunohistochemically positive for synaptophysin, S-100 protein, and oxytocin. The neoplasm contained prolactin-positive neuroblastic and pituitary epithelial cells. No other pituitary hormones were found. Electron microscopy demonstrated two cell types: one with frequent neuritic processes containing neurosecretory granules and showing synaptic specialization, and another one compatible with epithelial adenohypophyseal cells. A few cells had ultrastructural features that were transitional between neuronal cells and granulated epithelial cells. Agranular folliculostellate cells were also identified. Immunoelectron microscopy demonstrated prolactin granules in the cytoplasm of the epithelial cells, in a few transitional cells, and in scattered neuritic processes. Ultrastructural and immunohistochemical features of the tumor suggested a transformation of pituitary epithelium to neuroblastic cells. Hyperprolactinemia and associated clinical symptoms may in part be attributed to selective prolactin secretion by neoplastic cells that were differentiating into adenomatous pituitary cells and, to a lesser extent, to cells differentiating into a neuroblastic line. Compression of pituitary stalk might also have been a contributory factor to the increased prolactin levels. Moreover, the oxytocin produced by the neuroblastic cells was considered an additional stimulus for prolactin secretion by neoplastic cells or by the normal pituitary.
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PMID:Differentiating neuroblastoma of pituitary gland: neuroblastic transformation of epithelial adenoma cells. Case report. 889 39

Congenital panhypopituitarism is a rare disease. It may be a complication of tumors, craniocerebral trauma, infection, granulomatous diseases, vascular pathologies, etc. In many cases no primary disease causing panhypopituitarism is found (idiopathic form). A potential reason is interruption of the pituitary stalk due to ischemic etiology in patients with cord encirclement and/or other birth injuries leading to interruption of the axonal transport of ADH and oxytocin as well as hypothalamic releasing hormones. This explains the ectopy of the neurohypophysis without diabetes insipidus and the hypoplasia of the adenohypophysis. GH-deficiency causes short stature and metabolic disturbances, LH-FSH-deficiency amenorrhoea/oligomenorrhoea, loss of libido and secondary sexual characteristics, TRH-deficiency hypothyroidism and ACTH-deficiency hypotonia, weakness, loss of pigmentation. We report a case of congenital panhypopituitarism. MR imaging of the brain revealed a hypoplastic adenohypophysis and a hypoplastic pituitary stalk which was interrupted in its superior segment. An ectopic neurohypophysis was found located in the area of the hypothalamus ("hypothalamic hot spot"). The ectopic neurohypophysis showed strong enhancement after intravenous application of Gd-DTPA. MR imaging of the hypothalamic-hypophyseal axis is well suited for the differentiation between congenital and acquired forms of panhypopituitarism in clinically uncertain cases.
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PMID:[Neuro-MR-findings in primary panhypopituitarism]. 979 7

This panel presentation consists of detailed technical descriptions of Karman aspiration and of hypertonic saline injection, a list of legal indications for abortion in France, a brief summary of how abortions are conducted in England, and a question and answer period, all following an introduction published in this journal (ibid. 1(1): 21-22, 1973.). The Karman aspiration is done only until 8 weeks of amenorrhea, with premedication only, using a polyethylene cannula and either a 50 cc syringe, a hand pump or a mechanical pump (.5-1 atmosphere vacuum). Pro fuse details of technique, treatment and complications are given, since the procedure is new to French physicians, and is currently done "semi-clandestinely." Most of the text on midtrimester abortions concerns indications and dilatation of the cervix; the hypertonic saline technique was shown in a film. The accepted indications at the Port Royal Maternity are: chromosomal or metabolic genetic defects demonstruated by amniocentesis and culture, probably severe congenital d efect indicated by elevated alpha-feto-protein, infection by German measles shown by presence of IgM in maternal serum. Every precaution is taken in such cases to guarantee the possibility of a healthy living infant in the future. Second trimester abortions in King's College Hospital, London, are usually by intraamniotic prostaglandins and iv oxytocin, and an IUD is inserted immediately. The questions concerned mainly where abortions can be performed, where techniques can be learned , and early abortion clinics in Holland.
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PMID:[Modern techniques for terminating pregnancy]. 1227 57

A prospective randomized survey of 113 abortions carried out by 1 operator using a single technique among women in the 7th-10th week of amenorrhea was undertaken to test the effectiveness of systemically administered oxytocins to reduce bleeding during therapeutic abortion by suction. General anesthesia was used in all cases. No oxytocin was used in 44 cases, an intravenous injection of .2 mg Methylergobasine was used in 36 cases, and a continuous perfusion of a solution of Syntocinan was used in 33 cases. There was no statistically significant difference in the gestational age, patient age, or parity of the 3 groups. The results indicated that bleeding is not significantly reduced as a result of the systemic use of oxytocins but blood loss is clearly associated with gestational age. There was no significant difference in the extent of digestive effects including nausea and vomiting in the 3 groups.
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PMID:[Are oxytocins safe and effective for induced abortions performed in France?]. 1233 40

The authors report their experiences in inducing labour between the 34th and the 43rd week of amenorrhea by the administration of prostaglandins. The detailed results of several series are compared: PGF2alpha by venous perfusion alone (100 cases) or associated with buccal oxytocin (100 other cases), PGE1 by perfusion (25 cases), PGF2alpha and PGE2 by intra-amniotic injection in cases of fetal death (25 cases). After an extremely detailed discussion of the maternal and fetal results and of the secondary effects, the authors explain the indications, the means of introduction, and also the dosages. Finally they compare the effects of prostaglandins in full-term inductions and in so-called therapeutic abortions.
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PMID:[Induction of labor with the help of the prostaglandins E1, E2, F1alpha, and F2alpha]. 1743 93

Lactation results in a number of physiological adaptations which exert direct effects on maternal health, some of which may confer both short and long term advantages for breast feeding mothers. Breast feeding in the early postpartum period promotes a more rapid return of the uterus to its prepregnant state through the actions of oxytocin. Breast feeding may also lead to a more rapid return to prepregnancy weight. Among studies that had good data on duration and intensity of lactation, the majority show a significant association between lactation and weight loss. However, there is no evidence that lactation prevents obesity. Lactation also affects glucose and lipid metabolism. The long term effects of these adaptations are unknown but may have implications for preventing subsequent development of diabetes and heart disease. Lactation delays the return of ovulation and significantly reduces fertility during the period of lactational amenorrhoea. This process is linked with feeding patterns and may therefore be affected by practices such as scheduled feedings and the timing of introduction of complementary foods. While the evidence from epidemiologic studies is mixed, several large studies have shown that extended lactation is associated with reduced risk of premenopausal breast, ovarian and endometrial cancers. Although bone mineralization declines during lactation, repletion takes place after weaning. As a result, breast feeding does not appear to cause long term depletion of bone nor does it increase risk of osteoporosis. Many of the physiological effects of lactation are dependent on the stimulation of the hypothalamic-pituitary axis and milk removal and thus may vary with infant feeding practices. Well controlled studies are needed that include detailed information regarding infant feeding practices in addition to the total duration of any breast feeding. Future feeding recommendations should reflect careful consideration of how such practices affect both infant and maternal health.
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PMID:Health effects of breast feeding for mothers: a critical review. 1909 57

Opioid abuse has increased in the last decade, primarily as a result of increased access to prescription opioids. Physicians are also increasingly administering opioid analgesics for noncancer chronic pain. Thus, knowledge of the long-term consequences of opioid use/abuse has important implications for fully evaluating the clinical usefulness of opioid medications. Many studies have examined the effect of opioids on the endocrine system; however, a systematic review of the endocrine actions of opioids in both humans and animals has, to our knowledge, not been published since 1984. Thus, we reviewed the literature on the effect of opioids on the endocrine system. We included both acute and chronic effects of opioids, with the majority of the studies done on the acute effects although chronic effects are more physiologically relevant. In humans and laboratory animals, opioids generally increase GH and prolactin and decrease LH, testosterone, estradiol, and oxytocin. In humans, opioids increase TSH, whereas in rodents, TSH is decreased. In both rodents and humans, the reports of effects of opioids on arginine vasopressin and ACTH are conflicting. Opioids act preferentially at different receptor sites leading to stimulatory or inhibitory effects on hormone release. Increasing opioid abuse primarily leads to hypogonadism but may also affect the secretion of other pituitary hormones. The potential consequences of hypogonadism include decreased libido and erectile dysfunction in men, oligomenorrhea or amenorrhea in women, and bone loss or infertility in both sexes. Opioids may increase or decrease food intake, depending on the type of opioid and the duration of action. Additionally, opioids may act through the sympathetic nervous system to cause hyperglycemia and impaired insulin secretion. In this review, recent information regarding endocrine disorders among opioid abusers is presented.
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PMID:The effects of opioids and opioid analogs on animal and human endocrine systems. 1990 33

With the exception of fluoxetine, all selective serotonin reuptake inhibitors (SSRIs) commonly cause hyperprolactinemia through presynaptic mechanisms indirectly via 5-hydroxytryptamine (5-HT)-mediated inhibition of tuberoinfundibular dopaminergic neurons. However, there is little insight regarding the mechanisms by which fluoxetine causes hyperprolactinemia via the postsynaptic pathway. In this text, analysis of five spontaneously reported clinical cases of hyperprolactinemia resulting in overt symptoms of amenorrhea with or without galactorrhea, were scrupulously analyzed after meticulously correlating relevant literature and an attempt was made to explore the putative postsynaptic pathway of fluoxetine inducing hyperprolactinemia. Hypothetically, serotonin regulates prolactin release either by increasing oxytocin (OT) level via direct stimulation of vasoactitive intestinal protein (VIP) or indirectly through stimulation of GABAergic neurons. The pharmacodynamic exception and pharmacokinetic aspect of fluoxetine are highlighted to address the regulation of prolactin release via serotonergic pathway, either directly through stimulation of prolactin releasing factors (PRFs) VIP and OT via 5-HT2A receptors predominantly on PVN (neurosecretory magnocellular cell) or through induction of 5-HT1A-mediated direct and indirect GABAergic actions. Prospective molecular and pharmacogenetic studies are warranted to visualize how fluoxetine regulate neuroendocrine system and cause adverse consequences, which in turn may explore new ways of approach of drug development by targeting the respective metabolic pathways to mitigate these adverse impacts.
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PMID:A new logical insight and putative mechanism behind fluoxetine-induced amenorrhea, hyperprolactinemia and galactorrhea in a case series. 2429 85

Tocolytic agents have limited efficacy, delaying preterm delivery by 48 hours to 7 days, without any neonatal benefit. Cyclo-oxygenase inhibitors and calcium canal inhibitors seem to be the most efficient. Betamimetics are tocolytic agents with the highest incidence of severe maternal side effects. Oxytocin receptors antagonists and cyclo-oxygenase inhibitors are tocolytic agents with the best maternal tolerating profile. Nifedipin is the tocolytic agent presenting the best fetal tolerating profile. However, doubts persist on fetal and neonatal tolerance for cyclo-oxygenase inhibitors and probably even for oxytocin receptors antagonists. A combined or sequential tocolytic treatment did not prove superior to a single tocolytic treatment although the former is also associated with a high incidence of severe adverse maternal effects. Nevertheless, this low efficiency should not make us forget their major interest in case of premature labour: to allow the mother's in utero transfer to a level II or III maternity following the gestational age, and moreover to gain time so as to obtain an optimal interval for the fetal lung maturation by corticoid injection. Tocolytic agents should be used between 24(+0) and 34(+6)weeks of amenorrhea. They should be used on the short term (24 to 72 hours) owing to their short period of efficacy and to the risk of side effects that increases with the duration of use.
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PMID:[A review on tocolysis]. 2614 10


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