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)

Pregnancy after complete loss of pituitary function is uncommon. However, advances in fertility treatment have led to increased pregnancy rates in hypopituitary women. We hereby present a literature review of pregnancies affected by hypopituitarism, including a comparison with published controls; further, we add one case report of severe hypopituitarism where third-trimester oxytocin supplementation was performed. As only limited information is available on management and outcome, our purpose was to determine obstetric complications associated with deficiency of pituitary hormones. The analysis of 31 pregnancies in 27 women revealed that hypopituitary women are at increased risk: postpartum hemorrhage occurred in 8.7%, transverse lie in 16%; 42.4% of the newborns were small for gestational age. These findings are supposedly the result of uterine dysfunction caused by hormone deficiency. Oxytocin supplementation was performed with the aim to establish physiologic conditions and to prevent postpartum uterine inertia. In this case substitution may have contributed to correct fetal presentation but did not prevent postpartum hemorrhage. Further investigations into both oxytocin-dependent and -independent mechanisms regulating uterine contractions and contractility are necessary to develop strategies for prevention of uterine inertia in oxytocin-deficient pregnancies.
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PMID:High-risk pregnancy management in women with hypopituitarism. 1917 43

Diabetes mellitus, widely known to the ancients for polyuria and glycosuria, budded off diabetes insipidus (DI) about 200 years ago, based on the glucose-free polyuria that characterized a subset of patients. In the late 19th century, clinicians identified the posterior pituitary as the site of pathology, and pharmacologists found multiple bioactivities there. Early in the 20th century, the amelioration of the polyuria with extracts of the posterior pituitary inaugurated a new era in therapy and advanced the hypothesis that DI was due to a hormone deficiency. Decades later, a subset of patients with polyuria unresponsive to therapy were recognized, leading to the distinction between central DI and nephrogenic DI, an early example of a hormone-resistant condition. Recognition that the posterior pituitary had 2 hormones was followed by du Vigneaud's Nobel Prize winning isolation, sequencing, and chemical synthesis of oxytocin and vasopressin. The pure hormones accelerated the development of bioassays and immunoassays that confirmed the hormone deficiency in vasopressin-sensitive DI and abundant levels of hormone in patients with the nephrogenic disorder. With both forms of the disease, acquired and inborn defects were recognized. Emerging concepts of receptors and of genetic analysis led to the recognition of patients with mutations in the genes for 1) arginine vasopressin (AVP), 2) the AVP receptor 2 (AVPR2), and 3) the aquaporin 2 water channel (AQP2). We recount here the multiple skeins of clinical and laboratory research that intersected frequently over the centuries since the first recognition of DI.
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PMID:Diabetes insipidus: celebrating a century of vasopressin therapy. 2521 89