Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Furosemide is frequently used for ascites and causes adverse reactions (AR). In an intensive prospective drug monitoring study of 1,920 patients, 172 (8.9%) had cirrhosis of the liver and received furosemide. Mean age was 53 years, and 66.3% were male; and 87% had alcoholic cirrhosis. Eighty-eight (51.2%) had 221 events that by consensus of the monitoring team and attending physicians were either definitely of probably related to furosemide. No AR was fatal but 24% of patients had severe reactions. Almost all reactions were dose-related (96%). The most common were electrolyte disturbances (23.3% of patients) and volume depletion (14%). Furosemide-induced coma occurred in 20 (11.6%) patients and was more frequent in patients with prior hepatic encephalopathy (p less than 0.0005). Higher total doses (p less than 0.001), hyerbilirubinemia (p less than 0.05), prolonged prothrombin time (p less than 0.02), and longer hospital stay (p less than 0.001) were associated with higher frequencies of AR to furosemide. The frequency of hypokalemia did not decrease when potassium chloride or potassium-sparing diuretics were added to furosemide therapy. Frequdncy of AR did not correlate with age, sex, renal impairment, serum albumin, transaminase, or alkaline phosphatase.
 ...
PMID:Furosemide-induced adverse reactions in cirrhosis of the liver. 75 67

A total of 35 cases of periarticular new bone formation (PNBF) was observed among 160 patients with coma following severe craniocerebral trauma. All cases were associated with blunt trauma and none with penetrating wounds. Only 6 of 500 cases of acute non-traumatic hemiplegia developed PNBR, and all 6 of them followed craniotomy, brain surgery and coma. New bone formation first appeared mainly between 50 and 120 days after craniocerebral injury with prolonged coma. Three-quarters of the patients with PNBF showed involvement of the shoulder joint, but this was not associated with previous subluxation. Metabolic studies were done in some patients; no disturbances were found in the metabolism of calcium, phosphorus or alkaline phosphatase. The pathologic process of PNBF seemed to stabilize some 6 to 8 months following trauma, and surgery after this period produced functional improvement in the 3 patients in whom it was tried. No satisfactory pathophysiological explanation has been found for the phenomenon of PNBR. Prolonged coma is common to all patients who suffered from PNBF and is probably an etiologic factor. The absence of PNBF in cases of cerebrovascular accident with subluxations of the gleno-humeral joint and intensive physiotherapy seems to contradict the suggestion of microtrauma as an etiological factor.
 ...
PMID:Periarticular new bone formation in patients suffering from severe head injuries. 81 2

In the group of 107 patients poisoned by carbon monoxide (18 patients), ethanol (10), barbiturates (18), glutehimide (10), tranquilizers (19), organic solvents (10),salicylates (3), organochlorines (8), and sulfonamides (5)--the activities of 8 serum enzymes were determined for 6 consecutive days of treatment, the enzymes being as follows: aminotransferases, cholinesterase, alkaline phosphatase, lactate, alpha-hydroxybutyrate, glutamate, and sorbitol dehydrogenase. The antipyrine half-life was also assayed. It has been shown that the poisonings by particular groups of poisons do not bring about characteristic changes in the activity of enzymes that might be of any diagnostic value. The intensity of changes was connected withe depth and duration of toxic coma. Most frequently an increase ensued in the activity of AspAt and AlAt in the third 24-hrs period, and an increase in the activity of SDH in the first 24-hrs period. In the group under examination there were 26 drug abusers in whom a shortening of the antipyrine half-life was discovered. They were less responsive to toxic doses of drugs, and the enzymatic changes in them were less distinct. No changes in the activity of tested enzymes, which are characteristic of toxicomania, were found.
 ...
PMID:The usefulness of the enzymatic tests in acute poisonings. 124 89

Congenital hepatic fibrosis (CHF) is a recognized cause of portal hypertension with oesophageal varices, gastro-intestinal haemorrhage and cholangitis in children without significant impairment of hepatic or renal function. This report describes the varied clinical presentation of CHF as seen at King Faisal Specialist Hospital and Research Centre (KFSH & RC) and emphasizes the clinical patterns that should enable a pediatrician to consider the diagnosis. Fourteen children with CHF were diagnosed between 1981 and 1988. The age at presentation ranged from 1.8-14 years (mean: 7.5 years); clinical manifestations at diagnosis were splenomegaly (12), hepatomegaly (11), failure to thrive (10), marked abdominal distention (4), and fever (4). Liver function tests were normal except for high alkaline phosphatase. Eight patients had polycystic kidneys confirmed on ultrasound examination. Upper gastro-intestinal endoscopy showed oesophageal varices of variable severity in all eight patients examined. Splenoportography revealed splenic vein occlusion in one patient. One patient died within days of admission with convulsions, coma, and aspiration pneumonia. One patient was lost to follow-up. The remaining 12 patients are all alive and receive regular follow-up. Two patients required splenorenal shunt. In view of the prevalence of consanguinity in Saudi Arabia, the diagnosis of CHF should be considered in children with hepatomegaly despite normal liver function tests, and particularly in those with renal abnormalities and/or evidence of portal hypertension.
 ...
PMID:Congenital hepatic fibrosis in Saudi Arabia. 178 58

A 6-year-old girl with cerebral palsy developed conscious disturbance and generalized convulsion after one-hour hot herb drug bath. Physical examination on admission revealed rectal temperature 41 degrees C, hot skin, respiration 46/min, regular heart beat 98/min, BP 130/60 mmHg, Glascow coma scale 4 (E2M1V1), soft and flat abdomen, no hepatosplenomegaly, no skin rash, no focal neurological sign, increased generalized muscle ton. Laboratory data showed CBC: WBC 20400 cumm (Neutrophils 31%, Lymphocytes 69%), Hb 11.6gm%, ESR 11 mm/hr, arterial blood gas: PH 7.077, PO2 43mmHg, PCO2 57.1mmHg, HCO3- 16 mEq/L, BE-11.5mEq/L, serum sodium 143 mEq./L, potassium 5.2 mEq/L, chloride 101 mEq/L, free calcium ion 3.8mg%, GOT 63IU/L, GPT 263 IU/L, amylase 193 IU/L, alkaline phosphatase 388 IU/L, LDH 1245 IU/L, CPK 677 IU/L, total bilirubin 0.8 mg/dl, direct type 0.1 mg/dl, BUN 18 mg/dl, Glucose 35 mg/dl. Urinalysis revealed proteinuria( ) trace hematuria and pyuria, but no cast. Lumbar puncture is within normal limits. Bacteriology including blood and CSF are normal. Multiple organ failure was noted at that time. Intensive cooling methods were performed including central and peripheral cooling. We used luminal and valium to control the seizure. Condition didn't improve. Afterwards cardiopulmonary arrest developed. Patient expired 8 hours after admission despite of resuscitation. Heat stroke in infancy and childhood is different from that in adulthood. The predisposing factors are high ambient temperature, dehydration, very young baby, sweat gland dysfunction, or ectodermal dysplasia. Definition of heat stroke includes 1) rectal temperature above 41 degrees C, 2) behavioral change, 3) warm skin, wet or dry.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case]. 263 19

Zinc is essential to numerous metabolic processes in the organism, multiform symptoms being found especially in deficiencies. In addition to nutritional factors, diseases such as cirrhosis of the liver. Crohn's disease and chronic renal diseases are relevant in this context. In the present work, serum zinc levels were investigated in 109 patients with various chronic liver diseases. The lowest serum zinc concentrations were seen in patients with decompensated hepatic cirrhosis with coma. Patients with decompensated alcoholic cirrhosis had lower zinc levels as subjects with nonalcoholic cirrhosis. None of the groups exhibited a significant change in serum zinc levels during the treatment period. Laboratory data (such as transaminases, thromboplastin time, alkaline phosphatase, total proteins) did not correlate with the serum zinc concentrations. The concentration of plasma ammonia, however, appeared to be inversely related to the serum zinc levels. Thus, patients with coma had maximum ammonia and minimum zinc levels.
 ...
PMID:Clinical studies on zinc in chronic liver diseases. 321 83

The rate of perinatal encephalopathy and the nature of its outcomes in relation to the syndrome of the acute period of the disease were studied in 102 children. Also examined were the cytochemical parameters of blood leukocytes, alkaline phosphatase of neutrophils, acid phosphatase of lymphocytes, succinate and alpha-glycerophosphate dehydrogenase of lymphocytes in prematurely born infants on the 8th-15th and the 30th-45th days of life. It has been ascertained that in addition to the comatose and convulsive syndromes the prognosis of the disease is the least favourable in the syndrome of total inhibition of the CNS in the acute period. Furthermore, the findings of the conducted study open the possibility of preliminary individual prognosis of the disease on the basis of the cytochemical picture at the end of the acute period.
 ...
PMID:[Development of children with a history of perinatal encephalopathy]. 342 43

A healthy twenty-month-old boy ingested a maximal dose of valproate from which about 750 mg/kg were absorbed. Cerebral coma, which lasted for twenty hrs, was followed by an undisturbed period of approximately sixteen hrs. Death from cardiorespiratory failure due to severe bronchopneumonia occurred 46.5 hrs after the ingestion of the drug. The serum valproic acid concentration reached a peak of 1061 micrograms/ml within three hours, and fifteen minutes before death it had fallen to 187 micrograms/ml. The half-life of 16.6 hrs was within the range usually found. Metabolic acidosis, hypernatraemia and hyperosmolarity could be corrected, unlike the hypocalcaemia, which developed later. Bilirubin, GOT, GPT, gamma-GT, alkaline phosphatase, blood glucose, diastase, urea, creatinine, haemoglobin as well as PT and PTT and the platelet count were all normal. Leucopenia with 1,600 per microliter developed only during the bronchopneumonial stage. The histo-pathological findings were acute hypoxic damage of the myocardium, kidneys and certain neurones of vulnerable areas of the brain (neuronal microvesiculation and tigrolysis) in addition to a severe cerebral oedema in the final stage. A morphological substrate of an acute valproate encephalopathy was not demonstrable. The liver showed no necrosis or cholostasis. The vertebral marrow was inconspicuous. All the results indicate that liver function was not impaired in spite of the initial maximal concentration of valproic acid. In all probability the patient might have survived the acute valproate intoxication had it not been for the bronchopneumonia.
 ...
PMID:Acute valproate intoxication with fatal outcome in an infant. 393 45

A patient is presented with a postpartum hepatic artery thrombosis in association with presumed fibromuscular hyperplasia. Massive hepatic infarction developed characterized clinically by fever, coma, ascites, ileus, jaundice, and renal failure; and biochemically by markedly elevated SGOT and SGPT, alkaline phosphatase, total bilirubin levels, and decreased thromboplastin time. The diagnosis was made in vivo by computed tomography (CT). Angiography revealed thrombotic occlusion of the hepatic artery in association with presumed fibromuscular hyperplasia. Laparoscopy and biopsy confirmed the diagnosis.
 ...
PMID:In vivo diagnosis of massive hepatic infarction by computed tomography. 646 35

Effectiveness of surgically induced acute hepatic failure in pig and most suitable time to apply artificial support in hepatic coma are evaluated in this work. Five male pigs weighing about 30-35 kg are employed. Latero-lateral porto-caval shunt was performed; the vascular disconnection of liver was obtained by ligature of blood vessels. Ligature was also placed on main biliary way after cholecistectomy. Blood samples were obtained (at 0, 1, 2, 6, 12, 18, 24 hours) to essay serum bilirubin, alkaline phosphatase and GOT-GPT levels as index of cholestasis and necrosis. Porto-caval encephalopathy was evaluated by means of serum ammonium levels, aminoacid pattern and E.E.G. Serum aminoacid pattern was carefully determined; its changes were found similar in man during coma. All pigs died 24-36 hours after surgery with liver ischemic and necrosis. Clinical and laboratory data obtained in experimental conditions were found similar to picture of acute hepatic failure in man, confirming validity of our model.
 ...
PMID:[Acute experimental hepatic insufficiency in pigs. Validity of a model with biohumoral and electroencephalographic monitoring]. 667 5


1 2 Next >>