Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.1.1.1 (alcohol dehydrogenase)
9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of transient diabetes insipidus in pregnancy occurring in a 26 year-old woman is reported, and possible mechanisms leading to this disorder are considered. Delivery of a healthy boy was uneventful after induction of labor with prostin, and the condition remitted spontaneously shortly after delivery, following a short period of exogenous desmopressin administration. A water deprivation test confirmed undetectable serum ADH values, presumably due to temporary inappropriate ADH secretion or excessive vasopressinase activity.
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PMID:[Pregnancy-induced diabetes insipidus]. 825 44

A 13-year-old girl with multiple minor anomalies and severe mental retardation had recurrent episodes of severe vomiting. At each episode, marked elevations of plasma ADH, ACTH, cortisol and salivary type amylase were found with reduction of serum Na level and osmolarity. This case is similar to that with periodic ACTH-ADH discharge syndrome (Sato). However, she had underlying disease, and neither hypertension nor depressive state was observed. Latent SIADH was detected by water loading test. After DZP administration, ADH secretion was suppressed in this test, and actually the duration of each attack was shortened. We considered that her vomiting was closely related with hypothalamic dysfunction, especially latent SIADH.
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PMID:[Congenital multiple anomaly syndrome with recurrent vomiting accompanied with latent SIADH; a case report]. 828 Apr 47

We report the case of a patient with an idiopathic syndrome of inappropriate secretion of ADH for more than 6 years. Water restriction was effective only during hospital care but was socially difficult to maintain at home, so that the patient presented frequent symptoms of water intoxication. Normal natremia was also obtained with a high salt intake (9 g/day) but this induced leg edema mild dyspnea and gastric intolerance. The patient was however successfully treated for more than 5 years without any side effects with oral urea (30 g/day) allowing her a normal fluid intake (1-1.5 liters/day). Oral urea, even during long periods, is a safe and effective therapeutic approach for patients with chronic SIADH which is not controlled by water restriction alone.
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PMID:5-year treatment of the chronic syndrome of inappropriate secretion of ADH with oral urea. 845 86

A 76-year-old woman was admitted to our hospital because of productive cough, fever and anorexia in January 1995. She had suffered from bronchial asthma for 25 years. From 1983, exacerbation of PIE was recorded three times, on which occasions prednisolone and antibiotics were quite effective. On admission, marked leukocytosis (28,000/microliters) and eosinophilia (18,000/microliters) were found. However, plasma IgE level was normal, and specific antigen for eosinophilia was not detected by RAST or the skin allergic reaction test. Chest X-ray film and CT scan revealed extensive bilateral pulmonary infiltration. Increase in eosinophils (33%) was demonstrated in bronchoalveolar lavage. Furthermore, biopsy specimen of the affected lung revealed diffuse infiltration of eosinophils into alveolar septa. On the basis of these findings, the patient was diagnosed as chronic eosinophilic pneumonia (PIE syndrome). Hyponatremia (117 mEq/l) was persistent after the hydration with normal saline. Plasma ADH was not suppressed (2.29 pg/ml) in spite of hypoosmolality of plasma. Laboratory examination showed that renal, adrenal and thyroid function as well as plasma renin activity were normal. Taking these findings together, she was diagnosed as having SIADH. Treatment with prednisolone improved not only the PIE syndrome but also SIADH.
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PMID:[A case of pulmonary infiltration with eosinophilia (PIE) syndrome associated with syndrome of inappropriate secretion of ADH (SIADH) in the elderly patient]. 855 92

Polydipsia can be defined as an impulsive behavior leading to absorption of large amounts of water (4 to 20 litres a day), without any underlying organic disease. Its prevalence in a population of chronic psychiatric patients can be as high as 6 to 17%. Schizophrenia represents 80% of cases reported. Some patients with polydipsia may develop hyponatremia, leading to a PIP syndrome (Polydipsia intermittent hyponatremia and psychosis). Hyponatremia or water intoxication appears when three conditions are present: an abnormal regulation of thirst, an inappropriate ADH secretion and/or an excessive renal sensitivity to ADH, with an increased sensitivity of the central nervous system to hyponatremia. The clinician must first identify patients at risk to develop water intoxication and start treatment before any severe physical complication occurs. Pharmacological treatments aiming at an increase of renal free-water excretion--do not show a constant efficacy in the correction of hyponatremia, they have no action on polydipsia. The new atypical neuroleptics such as clozapine and risperidone seem to open new perspectives in the treatment of polydipsia. Controlled studies should be performed in this field.
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PMID:["Polydipsia, intermittent hyponatremia and psychoses" syndrome: a diagnosis and therapeutic management of a case]. 892 56

Hyponatremia is more frequently observed in elderly patients associated with exaggerated response of ADH release and attenuated response of renin-aldosterone system. Differentiation of SIADH and hyponatremia other than SIADH is essential in anticipating the therapeutic effect of water restriction to correct hyponatremia. Serum concentration of uric acid and urinary excretion of kallikrein are significant parameters in biochemical discrimination index to differentiate these two types of hyponatremia. In addition to sodium replacement, water restriction and mineral corticoid, newly developed non-peptide ADH V2 receptor antagonist, OPC-31260, seems to be a useful tool to correct hyponatremia.
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PMID:SIADH and other hyponatremic disorders: diagnosis and therapeutic problems. 894 Aug 23

An 82-year-old man with the chief complaint of anorexia was referred on suspicion of pulmonary tuberculosis. He had undergone thyroidectomy because of thyroid cancer 5 years ago, had taken levothyroxine sodium, and had kept plasma level of thyroidal hormone within normal range. He had never pointed out hyponatremia. On laboratory findings on admission, serum natrium level was 125 mEq/l. A chest X-ray film showed the infiltration in both lower lung fields, and a chest CT scan revealed a miliary pattern in both lungs. Tubercle bacilli were detected from the sputum by the Ziehl-Neelsen staining. Antituberculous drugs were started. On 5th hospital day, he developed consciousness disturbance, and the serum level of natrium and osmolarity was 103 mEq/l and 250 mOsm /kgH2O, respectively, while plasma ADH level was increased to 5.9 pg/ml, and urine level of natrium and osmolarity was 123 mEq/l and 394 mOsm/kgH2O, respectively. His mental disturbance and hyponatremia gradually improved by supplementing NaCl. We diagnosed this case as SIADH associated with miliary tuberculosis. SIADH should be considered when hyponatremia was occurred in the case of miliary tuberculosis.
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PMID:[Syndrome of inappropriate secretion of antidiuretic hormone associated with miliary tuberculosis]. 910 26

The syndrome of water intoxication, resulting from dilutional hyponatremia and characterized by lethalgy, confusion, seizures, and coma was seen in two autistic boys living in the institution for mentally retarded children. Patient 1, a 19 year-old autistic boy showed loss of attention, inactiveness, sleepiness and delirium and then followed by overbreathing, severe vomiting and finally convulsive seizures several times, or coma, since October 1985. In August 1988, he was admitted with generalized tonic clonic convulsion associated with frequent vomiting EEG showed diffuse spike and wave complex with slow background activity. Laboratory data showed inappropriately high serum ADH level (8.5 pg/ml), low sodium concentration (121 mOsm/m/l), serum osmolality (237 mOsm/l) which was lower than urine osmolality (334 mOsm/l), and remarkable body weight gain (8.5 kg). He was diagnosed as water intoxication due to compulsive water drinking and SIADH. Diminished GH secretion to insulin-induced hypoglycemia and exaggerated prolactin response to LHRH stimulation suggested a hypothalamic lesion. Patient 2, a 17-year-old autistic boy, showed essentially the same symptoms and laboratory data as Patient 1, except that he had no epileptic discharge in EEG, and curious GH response to insulin-induced hypoglycemia. A remarkable daily body weight change suggested excessive water drinking and a possible episodic release of ADH. With mild water restriction, this became smaller. Since Patient 1 had epileptic attacks several times without hyponatremia and his EEG showed epileptic discharges, he was diagnosed as having epilepsy. Patient 2 has been seizure-free until now. Abnormality of hypothalamic or pituitary defects and polydipsia and possibility of water intoxication should always be considered when an autistic patients shows recurrent epileptic attacks or episodic strange behaviors with hyponatremia.
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PMID:[Two cases of infantile autism with intermittent water intoxication due to compulsive water drinking and episodic release of antidiuretic hormone (SIADH)]. 929 11

Serum urate and sodium concentrations were measured in 23 patients with acute viral and bacterial meningitis. Serum urate level was 3.0 +/- 0.2 mg/dl (mean +/- S.D.) (3.6 +/- 1.2 mg/dl in male and 2.5 +/- 0.9 mg /dl in female) on admission, but gradually elevated with improvements of meningitis. It turned to 4.8 +/- 0.2 mg/dl after recovery, and the value on admission was significantly lower than that after recovery (p < 0.0001). Serum sodium level was 137.6 +/- 2.9 mEq/l on admission and 139.7 +/- 2.7 mEq/l after recovery; also lower in the former (p < 0.01). These results show that patients develop transient hypouricemia, which may be explained by SIADH (syndrome of inappropriate secretion of ADH), although SIADH is subclinical in most cases of meningitis.
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PMID:[Hypouricemia in patients with meningitis]. 974 83

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.
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PMID:[Hypo-osmolar hyponatremic syndromes: physiopathology and clinical aspects]. 1020 1


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