Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diseases of the central nervous system (CNS) occurring during treatment of acute lymphoblastic leukemia (ALL) may be of leukemic or nonleukemic origin. Well known examples for CNS disease of nonleukemic origin are somnolence following prophylactic CNS irradiation, methotrexate-induced encephalopathy and acute infections caused by bacteria, viruses and toxoplasma gondii. Less known is the fact that also subacute CNS infections may occur in patients undergoing cytostatic therapy. Progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis (SSPE) are examples of this category of disease. Up to now 11 well documented cases of SSPE were reported occurring during treatment of ALL. Main clinical features were disorders of behaviour, consciousness and speach, seizures, paresis and inappropriate secretion of ADH. Several authors were able to demonstrate a deficiency of cellular immunity in patients with SSPE. In some cases this deficiency was consistent with reduced reactivity of T-lymphocytes against measles antigen only. The presence of inhibiting factors may be responsible for this phenomenon. Other authors found a normal or increased function of cellular immunity in SSPE; In hamsters occurrence of SSPE is induced by the simultaneous injection of hamster-adapted SSPE virus and antihamster lymphocyte serum. We, therefore, conclude that also in humans SSPE appearing during treatment of ALL is due to immunosuppression.
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PMID:[Non-leukemic disease of the central nervous system in children with acute lymphoblastic leukemia. III. Subacute sclerosing panencephalitis (author's transl)]. 36 90

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

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

A 73-year-old man with acute adult T-cell leukemia (ATL) in remission was re-admitted to our hospital due to drowsiness, headache, and bilateral knee joint pain on May 17, 1998. On admission, examinations revealed decreased serum sodium concentration (112 mEq/l), low plasma osmotic pressure (259 mOsm/l), and elevated antidiuretic hormone(5.6 pg/ml). Cerebrospinal fluid examination showed an increased number of abnormal flower-like lymphocyte (951/microliter). Brain computed tomography and magnetic resonance imaging found no abnormality in the hypothalamus or pituitary gland. These findings yielded a diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Though ATL patients typically exhibit a variety of clinical symptoms, SIADH is rarely one of the complications. Further investigation showed that IL-1 beta and IL-6 concentrations were increased in spinal fluid but not in serum. Recently, it has been reported that exogeneous IL-6 is an inducer of ADH secretion, and that primary ATL cells and HTLV-I infected cell lines can produce IL-6. In this case, we speculated that IL-6 produced by ATL cells that infiltrated a cerebral lesion may have played an important role in the development of SIADH.
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PMID:[Syndrome of inappropriate antidiuretic hormone secretion associated with meningeal infiltration of tumor cells and elevated interleukin-1 beta and interleukin-6 in cerebrospinal fluid of a patient with adult T-cell leukemia]. 1072 44

A 74-year-old man developed fever, somnolence, hyponatremia, and life-threatening sinus bradycardia for three weeks. He showed a slight elevation of lymphocyte count and protein level in the cerebrospinal fluid. A brain CT scan revealed a diffuse low density area around the hypothalamus which was identified as a high intensity signal by flair MR imaging. Marked sinus bradycardia developed with no abnormality in the echocardiograph or cardiac enzymes. Over the next 6 weeks he became alert and normal sinus rhythm resumed. The results of endocrine tests were compatible with hypothalamic insufficiency with partial hypopituitarism and the syndrome of inappropriate secretion of ADH.
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PMID:Hypothalamic encephalitis with bradycardia. 1151 30

Alcohol consumption often leads to hangover, a condition characterized by several symptoms, characteristically headache, nausea, fatigue and drowsiness. Hangover may be alleviated by altering the rate of alcohol metabolism and facilitating elimination of acetaldehyde by affecting the activity of alcohol dehydrogenase (ADH) and/or aldehyde dehydrogenase (ALDH) enzymes. In the present study, several food commodities like fruits, vegetables, cereals, pulses, dairy products, spices and other miscellaneous products (ascorbic acid, cocoa sample, tea, coffee, egg yolk and date samples) were investigated for their effect on the in vitro activities of the enzymes and their antioxidant properties. Of the many screened food commodities, few showed an increase in the activity of either one or both the enzymes, ADH and ALDH. Studies showed no correlation between ADH and ALDH enzyme activities and antioxidant property of the selected food commodities for anti-hangover effect. Further, an anti-hangover (AHO) product was developed using pear (65%), sweet lime (25%) and coconut water (10%) and, validated for in vitro ADH and ALDH enzyme activities. AHO product was found to enhance ADH and ALDH activities by 23.31% and 70.02%, respectively.
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PMID:Influence of food commodities on hangover based on alcohol dehydrogenase and aldehyde dehydrogenase activities. 3291