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)

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.
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PMID:Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy. 365 42

A 65-year-old female with general malaise, anorexia and marked emaciation was studied by secretion stimulation tests on 6 anterior pituitary hormones. Only ACTH showed no response and the other 5 hormones responded normally. The basal value of antidiuretic hormone was normal. She was found to be suffered from primary hypothyroidism. Though neither antithyroid antibodies nor other autoantibodies were found, Hashimoto's thyroiditis was confirmed by a thyroid open biopsy. Neoplastic lesions of the hypophysis were ruled out by various X-ray and CT examinations of the sella turcica as well as the brain. The case was concluded to be isolated ACTH deficiency associated with Hashimoto's thyroiditis. The substitution therapy using small doses of adrenocortical hormone and thyroid hormone has kept her well and she has been living normally for these five years.
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PMID:Isolated ACTH deficiency associated with Hashimoto's thyroiditis: report of a case. 608 96

6 patients with amyotrophic lateral sclerosis were treated with intravenous infusion of 100-200 million IU per day of human leukocyte interferon. Side effects of treatment included fever, chills, malaise, nausea, marked leukopenia, mild anemia, and thrombocytopenia. Tiredness, confusion, papilledema, and overall signs of acute encephalitis were observed. Tendon reflexes and muscle force decreased. EEG activity was slowed, and evoked potentials showed significant slowing of conduction times. Neuropsychological tests revealed congitive dysfunction. The syndrome of inappropriate antidiuretic hormone secretion developed in all patients. All side effects were reversible with cessation of interferon treatment.
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PMID:Neurotoxic and other side effects of high-dose interferon in amyotrophic lateral sclerosis. 620 81

Stimulation of the abdominal vagus nerve increases arterial pressure and causes secretion of vasopressin. We have shown in rabbits that the arterial pressure increases are mediated by activation of barosensitive bulbospinal neurons in the C1 region of the rostral medulla. Secretion of vasopressin involves activation of neurons in the A1 region of the caudal ventrolateral medulla. Neuroanatomical studies with Fos indicate that approximately 50% of the C1 area cells are C1 neurons. Approximately 70% of the A1 area cells are A1 neurons. These neurons may mediate physiological responses occurring during abdominal malaise resulting from ingestion of toxins. Our discovery of a major excitatory input to A1 and C1 neurons from the abdominal vagus should prove useful in studies of the function of these neurons.
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PMID:Abdominal vagal inputs to catecholamine neurons in the ventrolateral medulla. 773 72

Pituitary apoplexy is a neuroendocrine emergency produced by hemorrhage or infarction of pituitary tumors, and its accurate diagnosis has relied mainly on clinical manifestations and computed tomography (CT) scan of sella in the past. A case is reported of pituitary apoplexy which was demonstrated on magnetic resonance imaging (MRI). The 72-year-old male patient was admitted to the Nephrology Section of VGH-Taipei with symptoms of general malaise, poor appetite for four months and apparent hyponatremia (Na 102 mEq/L) on laboratory findings. Under the impression of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), fluid restriction and infusion of isotonic saline were prescribed, but in vain. The patient was transferred to the Endocrinology Section because of lowered serum cortisol, T3, T4, and hs-TSH levels. Dynamic pituitary function tests confirmed the diagnosis of panhypopituitarism. Contrast enhanced CT scan of sella revealed displacement of the pituitary stalk to the right side. T1-weighted MRI showed persistent high intensity in left sella and T2-weighted MRI showed persisting isointense to white matter. The hyponatremia and clinical symptoms resolved within a few days after replacement therapy with glucocorticoid and thyroid hormone. It was concluded that MRI is more sensitive than CT scan for detecting subacute or chronic pituitary apoplexy.
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PMID:Pituitary apoplexy diagnosed by magnetic resonance imaging: a case report. 775 60

Hyponatremia is rarely reported as a delayed complication of transsphenoidal resection of pituitary adenoma. Usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), hyponatremia causes nonspecific symptoms, often after hospital discharge. To clarify the frequency, presentation, and outcome of this poorly understood complication, we reviewed our database of 2297 patients who underwent transsphenoidal pituitary surgery between February 1971 and June 1993. Of 53 patients (2.3%) treated for symptomatic hyponatremia, 11 were excluded (2 received arginine vasopressin within 24 hours, 1 had untreated hypothyroidism, 4 had untreated adrenal insufficiency, and 4 had incomplete records). The remaining 42 patients (1.8%), 11 men and 31 women aged 21 to 79 years, presented 4 to 13 days (mean, 8 d) postoperatively with nausea and vomiting (20 patients), headache (18 patients), malaise (12 patients), dizziness (4 patients), anorexia (2 patients), and seizures (1 patient). Hyponatremia was unrelated to sex, age, adenoma type, tumor size, or glucocorticoid tapering. Although the clinical picture in our patients is consistent with SIADH, this was not supported by the antidiuretic hormone levels, which were normal or low-normal in the two patients in whom they were measured, suggesting the possibility that low serum sodium may not reflect SIADH. In all patients, hyponatremia resolved within 6 days (mean, 2 d); treatment consisted of salt replacement and mild fluid restriction in 37 patients and fluid restriction only in 4 (treatment unknown in 1). Delayed hyponatremia after transsphenoidal resection of pituitary adenoma is not as rare as previously thought, nor is it necessarily associated with SIADH or with hypoadrenalism during glucocorticoid tapering.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delayed onset of hyponatremia after transsphenoidal surgery for pituitary adenomas. 855 92

Hemorrhage and nonhypotensive hypovolemia are known to increase plasma levels of oxytocin (OT) and vasopressin (VP) in rats. The present experiments demonstrated that secretion of OT and VP also are stimulated by acute drug-induced hypotension. Injection of hydralazine abruptly decreased arterial blood pressure in conscious rats and induced Fos expression, a marker of neuronal activation, within OT and VP neurons in the hypothalamus. Hydralazine also elicited substantial increases in plasma levels of both OT and VP. Injection of chlorisondamine similarly elicited acute hypotension and increased plasma levels of OT and VP. Furthermore, when the hypotensive effect of chlorisondamine was blunted by coinfusion of phenylephrine, the induced increases in OT and VP were markedly attenuated. Across all treatments, arterial blood pressure was inversely related to plasma levels of OT and VP. Plasma osmolality was not increased by hydralazine, nor was there evidence of gastric malaise, two known stimuli for OT secretion in rats. These results suggest that arterial hypotension increases neurohypophysial release of OT and VP in conscious rats.
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PMID:Decreases in arterial pressure activate oxytocin neurons in conscious rats. 936 14

Rathke's cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernig's sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. Magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.
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PMID:Hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report. 1046 7

We report a 47-year-old man with multiple sclerosis (MS) with previous history of recurrent sensorimotor disturbance and visual deficit. The patient developed bilateral motor weakness in the upper limbs, and systemic malaise. An administration of 20 mg/day of prednisolone was ineffective for his symptoms and he complained dyspnea a week later. On admission, his clinical findings included brainstem dysfunction with optic nerve atrophy, motor disturbance in the bilateral upper limbs, hyperreflexia, and superficial sensory disturbance. Biochemical examination revealed marked reduction in serum Na (117 mEq/l) and C1 (85 mEq/l) with increased urinary Na excretion. Although his plasma osmotic pressure decreased to 233 mOsm/kg, urinary osmotic pressure increased to 409 mOsm/kg. Serum antidiuretic hormone (ADH) concentration was 26.1 pg/ml and plasma renin activity was 0.1 ng/ml/ hour. Renal function and adrenal function were normal. Cerebrospinal fluid contained increased protein concentration, IgG, and myelin basic protein. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with MS was diagnosed. Intravenous Na infusion with restricted supplemental fluid and serial administration of methylprednisolone (1,000 mg/day for three days) improved his neurological abnormalities and normalized his serum serum Na level and plasma osmotic pressure. This suggests that demyelinating lesions in the hypothalamus due to MS may cause the transient increased ADH secretion.
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PMID:[Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with relapsing multiple sclerosis]. 1578 1

Adenoid cystic carcinoma is a tumor of exocrine glands originating primarily from the minor and major salivary glands, lacrimal gland, bronchus, breast, and intestinal and genital tracts. Intracranial remote metastasis from adenoid cystic carcinoma in salivary gland is quite rare. The authors encountered a case of intrasellar remote metastasis from an adenoid cystic carcinoma of parotid gland origin, presenting with hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). To our knowledge, this is the first reported case of metastasis from an adenoid cystic carcinoma to intrasellar area. A 78-year-old woman had an adenoid cystic carcinoma in the left parotid gland, which was resected surgically followed by local radiation therapy of 60 Gy. After 4 years, the patient presented with general malaise, followed by disturbed consciousness caused by hyponatremia. The clinical data showed severe hyponatremia induced by SIADH. An intrasellar heterogenous mass lesion compressing the optic chiasm was resected subtotally via an endonasal transsphenoidal approach. Histopathological examination of the tumor specimens revealed adenoid cystic carcinoma, which had identical histological findings as those of the painful superficial cervical lymph nodes resected in the same operation. Tumors such as the present case are easily confused with pituitary adenoma or craniopharyngioma. Although rare, metastasis from tumors including those of salivary gland origin should be considered in the differential diagnosis of unusual pituitary tumors.
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PMID:Intrasellar remote metastasis from adenoid cystic carcinoma of parotid gland: case report. 1690 61


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