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 68-year-old man with disturbed consciousness had repeatedly developed light-headedness and dizziness since the summer of 1996 and was admitted to a hospital for detailed examinations on October 8, 1996. On admission, he weighed 49 kg and showed subclinical hypothyroidism with low T3 syndrome. The adrenal function and serum electrolytes were normal. Since the stool samples were positive for occult blood, gastroscopy was performed. Examination of the biopsy specimens demonstrated gastric cancer. On October 21, blood examination showed hyponatremia (127 mEq/l). On October 22, marked disturbance of consciousness developed. On October 24, the serum Na level further decreased to 116 mEq/l. On November 8, he was referred to our hospital. On admission, his skin and tongue showed marked dehydration, and severe disturbance of consciousness and neck stiffness were observed. The central venous pressure was 4 cmH2O. In the cerebrospinal fluid, atypical cells were observed, and a diagnosis of meningeal carcinomatosis was made. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was excluded because of marked dehydration, a normal blood ADH level, and because plasma osmotic pressure was greater than urinary osmotic pressure. Considering the possibility of cerebral salt wasting syndrome (CSWS) or hypoadrenocorticism, Na supplementation and drip infusion of prednisolone (20 mg/day) were performed. The serum Na has normalized (140.1 mEq/l), and his consciousness improved. He died of aggravation of the general condition on December 16. Pathological examination demonstrated a small metastatic lesion in the infundibular part of the pituitary gland and a small metastatic lesion in the parenchyma of the bilateral adrenal glands. However, since neither hypotension nor hypoglycemia was observed before treatment, and the blood cortisol level and the serum K level were normal, hypoadrenocorticism was excluded. Hypoaldosteronism was also excluded because of a normal serum K level. CSWS has been reported to be caused by head trauma, subarachnoid hemorrhage, or trans-sphenoidal pituitary operation. This patient is a rare case of CSWS developed in the presence of meningeal carcinomatosis accompanied by a small pituitary metastatic lesion from gastric cancer. The aged with decreased ability to retain water and sodium in the body are more susceptible to CSWS than the young. In the aged with central hyponatremia, the possibility of CSWS should be considered, and early diagnosis and treatment are necessary.
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PMID:[A patient with meningeal carcinomatosis accompanied by a small pituitary metastatic lesion from gastric cancer who developed cerebral salt wasting syndrome]. 1057 52

Although disorders of ADH secretion associated with meningitis are usually consistent with the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), central diabetes insipidus (DI) is an exceptional complication of meningitis. Transient DI as a complication of Escherichia coli (E. coli) meningitis due to ventriculoperitoneal shunt in an 18-month-old boy is presented. Blood and spinal fluid cultures yielded E. coli, sensitive to cefotaxime. The DI arose on the day 3 after admission and continued to the day 20. Treatment comprised cefotaxime, dexamethasone, fluid adjustment and vasopressin. The course of our case supports that in cases of bacterial meningitis, initial fluid restriction may occasionally result in dangerous conditions. Therefore, all children with bacterial meningitis should be followed closely not only in terms of SIADH but also DI. To our knowledge this is the first transient DI associated with E. coli-caused meningitis case reported.
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PMID:Transient diabetes insipidus following Escherichia coli meningitis complicated by ventriculoperitoneal shunt. 1061 31

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.
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PMID:[Hyponatremia--with comments on hypernatremia]. 1089 27

Hyponatremia is a common electrolyte disturbance following intracranial disorders. Hyponatremia is of clinical significance as a rapidly decreasing serum sodium concentration as well as rapid correction of chronic hyponatremia may lead to neurological symptoms. Especially two syndromes leading to hyponatremia in intracranial disorders need to be distinguished, as they resemble each other in many, but not all ways. These are the syndrome of inappropriate ADH secretion (SIADH) and the cerebral salt wasting syndrome (CSW). The syndrome of inappropriate ADH secretion is characterized by water retention, caused by inappropriate release of ADH, leading to dilutional hyponatremia. The cerebral salt wasting syndrome on the other hand, represents primary natriuresis, leading to hypovolemia and sodium deficit. SIADH should be treated by fluid restriction, whereas the treatment of CSW consists of sodium and water administration. However, in the literature there is abundant evidence that hyponatremia in intracranial diseases is mostly caused by CSW. Therefore, treatment with fluid and salt supplementation seems indicated in patients with intracranial disorders who develop hyponatremia and natriuresis.
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PMID:Hyponatremia in intracranial disorders. 1124 11

This discussion emphasizes two aspects of hyponatremia: classification according to effective osmolality of the body fluid, and distinction between appropriate and inappropriate ADH secretion. Assessment of the effective osmolality is important because the main deleterious effect of hyponatremia is cell overhydration, which occurs only when the effective osmolality is reduced. Since most cases of hyponatremia are associated with low effective osmolality, cell overhydration is a hallmark of acute hyponatremia. On the other hand, one must be aware of other types of hyponatremia in which effective osmolality is either normal or even increased. Inappropriateness of ADH secretion is defined as ADH secretion that occurs despite low effective osmolality and normal or expanded effective vascular volume. ADH secretion that occurs in hyponatremia is deemed appropriate if the effective vascular volume is low. The use of laboratory parameters is much more reliable in determining effective vascular volume than is careful physical examination.
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PMID:Pathogenesis and diagnosis of hyponatremia. 1240 31

Immature teratoma in association with SIADH is rare. A 17-year-old patient presented with a pelvic mass and serum sodium concentration of 121 mmol/l. Subsequent investigation confirmed SIADH and grade 2 ovarian immature teratoma. No other causes of SIADH were found apart from the immature teratoma. There was no further recurrence of SIADH after the curative surgery and chemotherapy. We postulate that immature teratoma consists of neurohypophyseal structures which account for the ADH release.
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PMID:SIADH associated with ovarian immature teratoma: a case report. 1505 76

Primary small cell carcinoma of the ureter is very rare. We report a case associated with SIADH (syndrome of inappropriate secretion of ADH) -like symptoms. A 53-year-old man presented to our hospital with lower back and left lower quadrant abdominal pain. Computed tomography revealed left hydronephrosis, a peri-ureteral left lower quadrant mass, and retroperitoneal (RP) lymphadenopathy. Transduodendal biopsy of a RP lymph node revealed small cell carcinoma. He was referred to urology for further evaluation. Urography showed an obstructing mass invading the left ureter. Comprehensive metastatic evaluation revealed no other lesions. Thus, we diagnosed primary small cell carcinoma of the ureter with RP lymph node metastases. In addition, he developed SIADH-like symptoms, and we strongly suspected that it was due to ectopic production of ADH from this carcinoma. He was treated with systemic chemotherapy (methotrexate, epirubicin, and cisplatin). Following this, we performed radical nephroureterectomy with RP lymph node resection. However, he died of recurrent disease five months later.
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PMID:[A case of small cell carcinoma of the ureter with SIADH-like symptoms]. 1535 20

An 85-year-old woman with Parkinson's disease was admitted to our hospital to conduct a further work-up for progressive gait disturbance. She had been on medications for the disease for more than a decade prior to admission. In order to improve her condition, she was newly administered pramipexole, a dopamine agonist, from day 3 in addition to the preceding anti-Parkinson's therapy. However, on day 10, her consciousness level was rapidly deteriorated into delirium(JCS II-10), which was not accompanied by neurological signs and symptoms. Laboratory tests showed severe hyponatoremia with relatively increased urinary sodium excretion, and severe low serum osmolarity with an increased urinary osmolarity. Brain CT and brain MRI showed no specific abnormalities except for those related to aging. Blood concentration of ADH measured at the onset was substantially higher(39.5 pg/ml) than normal (0.3-3.5 pg/ml under normal osmolarity). Diseases causing hyponatremia, such as liver cirrhosis, congestive heart failure, hypotonic dehydration, and malignancy-associated inappropriate ADH secretion (SIADH), were all excluded. Under the suspicion of SIADH due to pramipexole, the drug was discontinued and as a result, her consciousness level improved rapidly together with a prompt reduction in ADH level (9.2 pg/ml). To the best of our knowledge, the present case is the first that demonstrates pramipexole-induced SIADH. Since pramipexole is classified as a dopaminergic receptor agonist, this case may provide new insight into a link between ADH and the dopaminergic receptor in the central nervous system.
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PMID:[Syndrome of inappropriate ADH secretion (SIADH) induced by pramipexole in a patient with Parkinson's disease]. 1613 Apr 8

An 83-year-old Japanese woman was admitted to our hospital with severe hyponatremia (sodium, 108 mEq/L [108 mmol/L]), hypokalemia, hypochloridemia, hypocalcemia, hypophosphatemia, and hypouricemia. Despite low plasma osmolarity (232 mOsm/kg [232 mmol/kg]), urine osmolarity (320 mOsm/kg) was greater than that of plasma, and she had increased urinary sodium excretion (88 mEq/L [88 mmol/L]) and an unsuppressed high plasma level of antidiuretic hormone (ADH; 5.5 pg/mL [5.1 pmol/L]). These findings indicated that she had syndrome of inappropriate ADH secretion (SIADH). In addition, she had a generalized reabsorption defect of the proximal tubules, including decreased tubular reabsorption of phosphate, increased fractional excretion of uric acid, glycosuria despite a normal blood glucose level, and panaminoaciduria. Thus, combined SIADH and Fanconi syndrome was diagnosed. The cause was thought to be the antidepressant paroxetine, which is a selective serotonin reuptake inhibitor (SSRI). Several of the abnormal values resolved within 1 week after discontinuation of this drug. Although the precise mechanism responsible was not elucidated, we report an extremely rare case of combined SIADH and Fanconi syndrome, probably caused by short-term SSRI therapy.
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PMID:A rare case of combined syndrome of inappropriate antidiuretic hormone secretion and Fanconi syndrome in an elderly woman. 1679 99

While most transsphenoidal pituitary surgery is accomplished without complication, monitoring is required postoperatively for a set of disorders that are specific to this surgery. Postoperative assessments are tailored to the early and later postoperative periods. In the early period, which spans the first few weeks after surgery, both monitoring of anterior and posterior pituitary function and managing neurosurgical issues are the focus of care. Potential disruption of pituitary-adrenal function is covered with perioperative glucocorticoids. Various strategies exist for ensuring the integrity of this axis, but typically this is done by measuring a morning cortisol on the 2nd or 3rd postoperative days. Patients with levels <10 microg/l should continue therapy with reassessment in the later postoperative period. Monitoring for water imbalances, which are due to deficiency or excess of ADH (DI or SIADH, respectively), is accomplished by continuous accounting of fluid intake, urine output and specific gravities coupled with daily serum electrolyte measurements. DI is characterized by excess volumes of inappropriately dilute urine, which can lead to hypernatremia. Most patients maintain adequate fluid intake and euvolemia, but desmopressin therapy is required for some. SIADH, which peaks in incidence on 7th postoperative day, presents with hyponatremia that can be severe and symptomatic. Management consists of fluid restriction. Neurosurgical monitoring is primarily for disturbances in vision or neurological function, and although uncommon, for CSF leak and infections such as meningitis. In the later postoperative period, the adrenal, thyroid and gonadal axes are assessed. New persistent hypopituitarism is rare when transsphenoidal surgery is performed by an experienced surgeon. Various strategies are available for assessing each axis and for providing replacement therapy in patients with deficiencies. Long term monitoring with assessments of visual, neurological and pituitary function coupled with pituitary imaging is necessary for all patients who have undergone surgery, irrespective of the hormone status of their tumors.
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PMID:Postoperative assessment of the patient after transsphenoidal pituitary surgery. 1832 Mar 27


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