Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steroid withdrawal syndrome (SWS) usually refers to relapse of the disease being treated after withdrawal of glucocorticoid therapy, or the symptoms of adrenal insufficiency which occur when glucocorticoids are rapidly reduced or stopped. A less well-recognised form of SWS is that which develops when patients experience a symptom complex similar to that of adrenal insufficiency despite acceptable cortisol levels. We describe three patients who presented with this form of SWS following surgical treatment for endogenous Cushing's syndrome. All responded well to a short-term increase in the dose of glucocorticoid replacement therapy, with the median duration of the syndrome being 10 months (range 6-10 months). Trough serum cortisol levels above 100 nmol/l, with peaks between 460 and 750 nmol/l were documented in the first two patients at presentation with SWS. It is thought that the syndrome may result from development of tolerance to glucocorticoids, and mediators considered to be important in its development include interleukin-6, corticotrophin-releasing hormone, vasopressin, and central noradrenergic and dopaminergic systems. The exact underlying mechanism for SWS remains unclear. However, with increasing recommendations for use of lower doses of replacement glucocorticoids, its incidence may increase. Physicians need to be aware of this condition, which is self-limiting and easily treated by a temporary increase in the dose of glucocorticoid replacement therapy. It is possible that a slower glucocorticoid tapering regimen than that used in the standard postoperative management of patients undergoing pituitary surgery may reduce the risk of development of SWS.
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PMID:Steroid withdrawal syndrome after successful treatment of Cushing's syndrome: a reminder. 1606 25

We can define paraneoplastic syndromes as a combination of effects occurring far from the original location of the tumour and independently from the local repercussion of its metastases. Paraneoplastic hormonal syndromes depend on the secretion of hormonal peptides or their precursors, cytokines and, more rarely, thyroidal hormones and Vitamin D, which act in an endocrine, paracrine or autocrine way. Sometimes, paraneoplastic syndromes can be more serious than the consequences of the primary tumour itself and can precede, develop in parallel, or follow the manifestations of this tumour. It is important to recognise a paraneoplastic hormonal syndrome for several reasons, amongst which we would draw attention to three: 1) It can lead to the diagnosis of a previously undetected, underlying malign or benign neoplasia; 2) It can dominate the clinical picture and thus lead to errors with respect to the origin and type of primary tumour; and 3) It can follow the clinical course of the underlying tumour and thus be useful for monitoring its evolution. The molecular mechanisms responsible for the development of these syndromes are not well-known, but it is believed that they might be inherent to the mutations responsible for the primary tumour or depend on epigenetic factors such as methylation. In this review, we consider the following paraneoplastic hormonal syndromes: malign hypercalcaemia, hyponatraemia (inappropiate secretion of the antidiuretic hormone), ectopic Cushing's syndrome, ectopic acromegaly, hypoglycaemia due to tumours different from those of the islet cells and paraneoplastic gynaecomastia; we make a brief final reference to other hormones (calcitonin, somatostatin, and VIP).
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PMID:[Paraneoplastic hormonal syndromes]. 1615 18

The objective of this study was to present some clinical and radiological manifestations of PNS in relation to bronchogenic carcinoma (BC) and to evaluate the usefulness of imaging findings in the diagnosis of asymptomatic BC. In the study group of 204 patients (146 male and 58 female) with proven bronchogenic carcinoma, PNS was present in 18 (8.62%) patients. The patients with PNS were divided into two groups. The first one consisted of 13 (72.2%) patients with symptoms related to primary tumours while the second one consisted of 5 (27.7%) patients with symptoms, at initial appearance, indicative of disorders of other organs and systems. The predominant disorder was Lambert-Eaton Syndrome, associated with small-cell carcinoma. Endocrine manifestations included: inappropriate antidiuretic hormone production syndrome (small-cell carcinoma), a gonadotropin effect with gynaecomastia and testicular atrophy (planocellular carcinoma, small-cell carcinoma), a case of Cushing Syndrome (small-cell carcinoma), and hypercalcaemia, due to the production of the parathyroid hormone-related peptide, which was associated with planocellular carcinoma. A rare case of bilateral exophthalmos was found as PNS at adenocarcinoma. Digital clubbing and hypertrophic osteoarthropathy (HO) were associated with planocellular and adenocarcinoma, while clubbing was much more common than HO, especially among women. The differences between the two groups were related to the time of PNS appearance. In the first group, PNS occurred late on in the illness, while in the second group, PNS preceded the diagnosis of BC. Alternatively, the disappearance of a clinical or a radiological manifestation of PNS after surgery or chemotherapy may be an indicator of an improvement in health or PNS may be the first sign of illness recurrence. Radiological manifestations of PNS in asymptomatic patients may serve as a useful screen for identifying primary BC. In symptomatic patients, it may be an indicator of a higher likelihood of metastatic disease.
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PMID:[Clinical and radiological manifestations of paraneoplastic syndrome of bronchogenic carcinoma]. 1639 81

The major causes of central diabetes insipidus are neoplastic or infiltrative lesions of the hypothalamus or pituitary, severe head injuries and pituitary or hypothalamic surgery. Central diabetes insipidus caused by viral infections has been rarely reported in immunosuppressed patients, such as those with acquired immunodeficiency syndrome or Cushing's syndrome. We report the case of a 48-year-old woman suffering from diffuse large cell lymphoma, who developed hypotonic polyuria, hypernatriaemia and somnolence after the first course of chemotherapy with CHOEP and rituximab. Diabetes insipidus was diagnosed by low urine osmolarity and an undetectable vasopressin concentration. MRI revealed no pituitary abnormalities but encephalitis, and lumbar punction confirmed herpes zoster infection. To the best of our knowledge this is the first description of central diabetes insipidus in a lymphoma patient caused by an opportunistic CNS-infection.
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PMID:Diabetes insipidus due to herpes encephalitis in a patient with diffuse large cell lymphoma. A case report. 1645 Mar 14

Cortisol secretion in ACTH independent bilateral macronodular adrenal hyperplasia (AIMAH) can be regulated by aberrant adrenal receptors. We describe a patient with Cushing's syndrome (CS) due to AIMAH and concomitant Class IV congestive heart failure (CHF). Clinical testing for the presence of aberrant receptors revealed a pronounced serum cortisol (257%) and aldosterone response (212%) to the administration of ACTH and a partial serum cortisol (35%) and aldosterone (106%) response to upright posture. This suggested the possible presence of aberrant hormone receptors for ACTH [melanocortin 2 receptor (MC2-R)], vasopressin, catecholamines or angiotensin II (AT-II) on the patient's adrenal glands. Adrenal tissue from the patient demonstrated an eight-fold increased expression of MC2-R compared to normal adrenal tissue. This increased expression was consistent with the increase in cortisol and aldosterone seen in response to exogenous ACTH. We propose that the severe CHF resulted in activation of the renin-angiotensin system, with an increased production of AT-II. The elevated circulating levels of AT-II may have led to increased expression of MC2-R on the patient's adrenal glands and increased responsiveness to ACTH. This unusual case of CS may elucidate a heretofore unknown mechanism for the development of AIMAH.
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PMID:A case of ACTH-independent bilateral macronodular adrenal hyperplasia and severe congestive heart failure. 1718 6

ACTH-independent macronodular adrenocortical hyperplasia (AIMAH) is rare and generally presents as a sporadic disease. We describe a familial case of AIMAH with in vivo and in vitro demonstration of aberrant 5-HT4 and vasopressin adrenal receptors. Two sisters presented with clinical and biological features of mild Cushing's syndrome with bilateral macronodular adrenal enlargement on computerized tomography (CT)-scan evaluation. In vivo pharmacological tests showed a significant increase in plasma cortisol after terlipressin and metoclopramide administration. Unilateral adrenalectomy was performed in one of these patients. Reverse transcriptase-PCR analysis of the hyperplastic tissue revealed expression of 5-HT4 receptor isoforms (a), (b), (c), (i), and (n), and of vasopressin receptors, V1 and V2. Their father and brother were overweight, had easy bruisability and presented with biological features of subclinical Cushing's syndrome. CT scan showed moderate adrenal enlargement. In vivo pharmacological screening tests for the detection of adrenal aberrant receptors in the brother were negative. Finally, three out of the two sisters' children were evaluated. They had neither clinical nor biological features of Cushing's syndrome. Their adrenal glands were normal on CT-scan evaluation. In vivo evaluation for the detection of aberrant adrenocortical receptors performed in one of these subjects was negative. In conclusion, this study shows that (i) familial AIMAH could be an autosomal dominantly inherited disorder; (ii) aberrant 5-HT4 serotonin and vasopressin receptors can be expressed in familial AIMAH; and (iii) phenotypic expression of familial AIMAH could be varied in a same family and more pronounced in female than in male patients.
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PMID:Familial adrenocorticotropin-independent macronodular adrenal hyperplasia with aberrant serotonin and vasopressin adrenal receptors. 1721 22

Small cell carcinoma (SCC) of the female genital tract is rare, constituting less than 2% of all gynecologic malignancies. It occurs most frequently in the cervix but can also occur in the endometrium, ovary, fallopian tube, vagina, and vulva. SCC of the genital tract is microscopically indistinguishable from that of the lung. Neuroendocrine differentiation is often manifested by a histologic growth pattern, argyrophilia, ultrastructural demonstration of secretory granules, and expression of neuroendocrine markers. Patients with SCC of the female genital tract may be asymptomatic but usually present with localized pain, vaginal bleeding, abdominal bloating or a mass, or symptoms of metastasis disease to the liver, bone, lung, or regional lymph nodes. Ectopic Cushing's syndrome has been reported in SCC of the vagina, and hypercalcemia and inappropriate secretion of antidiuretic hormone have been noted with SCC of the ovary. In general, these tumors have an aggressive clinical course with a propensity for extensive local invasion and distant metastases. Therapy has included surgery, radiation, and chemotherapy akin to those regimens used for SCC of the lung. Although there are no randomized clinical trials, it appears that multimodality therapy is associated with the best results and is the treatment of choice for most patients. Despite aggressive therapy, however, the prognosis for SCC of the female genital tract is poor, with only a minority of patients enjoying a prolonged survival. Indeed, the majority of patients have an early demise with extensive distant disease. We review the clinical features, evaluation, and management of SCC of the female genital tract based on a comprehensive review of the literature.
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PMID:Small cell carcinoma of the female genital tract. 1727 Jun 67

Endogenous Cushing's syndrome is a clinical state resulting from prolonged, inappropriate exposure to excessive endogenous secretion of cortisol and hence excess circulating free cortisol, characterized by loss of normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and normal circadian rhythm of cortisol secretion. The etiology of Cushing's syndrome may be excessive ACTH secretion from the pituitary gland, ectopic ACTH/CRH secretion by non-pituitary tumor, or excessive autonomous secretion of cortisol from hyperfunctioning adrenal adenoma or carcinoma, PPNAD and MAH. Other than these broad ACTH-dependent and ACTH-independent categories, there are some unclassified variants as cyclical Cushing's syndrome, pituitary hyperplasia and subclinical Cushing's syndrome. In addition, variants of hypercorticism secondary to ectopic or aberrant expression of several G-protein-coupled receptors have been identified. Diagnosis of Cushing's syndrome must be made before any attempt at differential diagnosis, and key biochemical characteristics are: excess endogenous cortisol secretion; loss of normal feedback of hypothalamic-pituitary-adrenal axis; and disturbance of normal circadian rhythm of cortisol secretion. Biochemical diagnosis of Cushing's syndrome includes: urinary free cortisol determination, low-dose dexamethasone testing, circadian rhythm assessment, insulin tolerance test, and LDDST/CRH test. Differential diagnosis of Cushing's syndrome involves: plasma ACTH level determination, high dose dexamethasone testing, metyrapone testing, testing with CRH, testing with vasopressin or combination, and finally, bilateral simultaneous petrosal sinus sampling with CRH stimulation.
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PMID:[Diagnosis and differential diagnosis of Cushing's syndrome]. 1730 74

The stress response is mediated by the hypothalamo-pituitary-adrenal (HPA) system. Activity of the corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus (PVN) forms the basis of the activity of the HPA-axis. The CRH neurons induce adrenocorticotropin (ACTH) release from the pituitary, which subsequently causes cortisol release from the adrenal cortex. The CRH neurons co-express vasopressin (AVP) which potentiates the CRH effects. CRH neurons project not only to the median eminence but also into brain areas where they, e.g., regulate the adrenal innervation of the autonomic system and affect mood. The hypothalamo-neurohypophysial system is also involved in stress response. It releases AVP from the PVN and the supraoptic nucleus (SON) and oxytocin (OXT) from the PVN via the neurohypophysis into the bloodstream. The suprachiasmatic nucleus (SCN), the hypothalamic clock, is responsible for the rhythmic changes of the stress system. Both centrally released CRH and increased levels of cortisol contribute to the signs and symptoms of depression. Symptoms of depression can be induced in experimental animals by intracerebroventricular injection of CRH. Depression is also a frequent side effect of glucocorticoid treatment and of the symptoms of Cushing's syndrome. The AVP neurons in the hypothalamic PVN and SON are also activated in depression, which contributes to the increased release of ACTH from the pituitary. Increased levels of circulating AVP are also associated with the risk for suicide. The prevalence, incidence and morbidity risk for depression are higher in females than in males and fluctuations in sex hormone levels are considered to be involved in the etiology. About 40% of the activated CRH neurons in mood disorders co-express nuclear estrogen receptor (ER)-alpha in the PVN, while estrogen-responsive elements have been found in the CRH gene promoter region, and estrogens stimulate CRH production. An androgen-responsive element in the CRH gene promoter region initiates a suppressing effect on CRH expression. The decreased activity of the SCN is the basis for the disturbances of circadian and circannual fluctuations in mood, sleep and hormonal rhythms found in depression. Neuronal loss was also reported in the hippocampus of stressed or corticosteroid-treated rodents and primates. Because of the inhibitory control of the hippocampus on the HPA-axis, damage to this structure was expected to disinhibit the HPA-axis, and to cause a positive feedforward cascade of increasing glucocorticoid levels over time. This 'glucocorticoid cascade hypothesis' of stress and hippocampal damage was proposed to be causally involved in age-related accumulation of hippocampal damage in disorders like Alzheimer's disease and depression. However, in postmortem studies we could not find the presumed hippocampal damage of steroid overexposure in either depressed patients or in patients treated with synthetic steroids.
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PMID:The stress system in depression and neurodegeneration: focus on the human hypothalamus. 1752 88

Desmopressin is a synthetic analogue of the hypothalamic peptide vasopressin and binds to specific pituitary vasopressin (V3) receptors. The V3-receptor is overexpressed in pituitary corticotrope tumors and the injection of desmopressin induces a marked ACTH and cortisol release in human patients with pituitary- (PDH), but not adrenal tumor (AT) dependent hyperadrenocorticism. In this prospective study, we investigated the effects of desmopressin on serum cortisol levels in 80 dogs suspected of Cushing's syndrome. The aim was to find a sensitive and specific test to exclude AT. According to standard tests the dogs were divided into 3 groups (group 1=other disease, n=27; group 2=PDH, n=46; group 3=AT, n=7). Desmopressin was injected as an i.v. bolus of 4microg and serial blood samples were collected before and after 30, 60 and 90min. Desmopressin significantly stimulated cortisol release in dogs with PDH (median 51%, range -24 to 563%; p<0.0001), whereas no increase was seen in dogs with AT (median -12%, range -44 to 5%; p=0.063) and in controls (median +7%, range -36 to 196%; p=0.131). Using a cut off value of 10% increase over baseline, it was possible to exclude AT in 75% of patients. The results of this study suggest that the desmopressin test could be a useful tool in differentiating pituitary from adrenal dependent Cushing's syndromes. Additional dogs with adrenocortical tumor must be tested in order to recommend its use in clinical practice.
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PMID:The desmopressin stimulation test in dogs with Cushing's syndrome. 1785 Oct 17


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