Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of warfarin-induced intramural hematoma and hemorrhagic infarction of the small intestine is described, and the literature on this adverse effect is reviewed. A 32-year-old white woman who had been receiving warfarin and carbamazepine came to a clinic complaining of lower back and stomach pain. She had a history of iliofemoral deep venous thromboses and seizures. A pelvic sonogram showed a large quantity of fluid present. Her prothrombin time (PT) was 29.2 sec. Her hemoglobin concentration and hematocrit were within the normal ranges. The patient was admitted to the hospital when her back pain increased and she vomited. The warfarin was discontinued. On day 5 the patient was still having abdominal pain and nausea. Her hemoglobin concentration and hematocrit had fallen to 6.6 g/dL and 20%, although her PT had decreased to 12.5 sec. On the same day, the patient underwent an exploratory laparotomy, and an indurated and ischemic area of jejunum was found and resected. The pathology report indicated the presence of hemorrhage and infarction consistent with an anticoagulant-related disorder. About 100 cases of intramural hematoma of the small intestine induced by anticoagulant therapy have been reported. Most patients are white males about 60 years of age. The sites most frequently involved are the duodenum and proximal jejunum. Symptoms include constipation, nausea, vomiting, and abdominal pain. Laboratory test and radiological findings are fairly nonspecific, but when found together in a patient receiving an anticoagulant, the diagnosis can be made with some confidence. Management may be complicated by the bleeding disorder, the intestinal obstruction if present, and the original indication for warfarin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Warfarin-induced intramural hematoma of the small intestine. 161 15

We have established an improved model of fulminant hepatic failure in dogs. Buthionine sulfoximine is used to inactivate glutathione synthesis, and small increments of acetaminophen are given intravenously to maintain the plasma level at approximately 200 micrograms/ml for 20 hr. This regimen produces severe liver injury along with many of the features seen in humans with acetaminophen poisoning. The first sign of impending liver failure is hypoglycemia. This occurs about 15 hr into the experiment and requires treatment with a continuous infusion of glucose. Between 15 and 20 hr, serum ALT activity begins to rise, indicating the onset of liver necrosis. Over the following 15 to 20 hr ALT activity continues to rise and is accompanied by an increase in bilirubin, a prolongation of the prothrombin time and the development of fetor hepaticus. Thirty to 48 hr after the initial acetaminophen dose, the animals begin to exhibit symptoms of encephalopathy and progress from lethargy to the inability to maintain posture and then coma, seizures and death. Liver biopsy specimens obtained at several stages throughout the study showed progressive necrosis, ultimately resulting in the complete destruction of zones 2 and 3.
 ...
PMID:An improved model of acetaminophen-induced fulminant hepatic failure in dogs. 173 38

Although valproic acid as well as its derivatives are effective in the treatment of some epileptic seizures, they are not free of adverse side effects. The purpose of this work was to describe the collateral clinical effects of valproic acid, the associated changes that take place in some serum laboratory parameters, and correlations among these adverse clinical effects, drug serum level and therapeutic response. One hundred patients aged 7 months to 19 years (average 5 year and 6 month old) were followed for at least 13 months. Clinical collateral effects were observed in 14% patients, anorexia and hair loss being the most frequent. One third of patients showed raised serum alkaline phosphatase and transaminases values, while lower than normal prothrombin time and platelet counts were detected in 4% and 1% of patients, respectively. In one patient treatment was interrupted because of low platelet counts which persisted in spite of drug withdrawal, but basal counts were not done, so it is not possible to establish causal relationships between both events. No correlation between adverse clinical symptoms and valproic acid plasma levels was observed. In spite of the fact that basal laboratory values were not known and that abnormal tests were not repeated for confirmation, collateral clinical effects and laboratory findings associated to treatment with valproic acid seemed not severe in this series. Anyway, taking into account drug characteristics, it should always be used with caution.
 ...
PMID:[Adverse effects of valproic acid in epileptic infants and adolescents]. 184 42

We have identified an inhibitor of the protein C anticoagulant pathway in the plasma of a patient with systemic lupus erythematosus and a history of recurrent deep vein thrombosis, fetal wastage, and seizures. The patient's plasma contained anticardiolipin antibodies as well as a weak lupus anticoagulant. Examination of this patient's plasma revealed normal levels of protein C and protein S antigen, normal levels of functional protein C, as well as essentially normal levels of every blood coagulation factor. In a modified prothrombin time assay, the activated protein C-mediated prolongation of the clotting time observed in normal plasma was not observed in this patient's plasma. Gel permeation chromatography of the patient's plasma revealed that the inhibitory material was a high molecular weight protein that coeluted with the IgM peak. The inhibitor did not appear to circulate as a complex with protein C, since the inhibitor could easily be separated from protein C during fractionation procedures, and did not interfere with the activation of protein C in plasma as assessed by a functional amidolytic assay. Our findings suggest that the recurrent thrombotic episodes observed in this patient may have occurred as a result of the patient's antiphospholipid antibody neutralizing specific phospholipids essential for the full expression of the anticoagulant activity of activated protein C.
 ...
PMID:Impairment of the protein C anticoagulant pathway in a patient with systemic lupus erythematosus, anticardiolipin antibodies and thrombosis. 210 91

We report the clinical characteristics and course of 38 children with fulminant liver failure. A viral etiology was demonstrated in 19 patients out of 25 with serologic screening (virus A in 17 patients, B in 2 patients). One patient had toxic liver damage from ingestion of a caustic substance. Mean age was 4 years and 6 months. Jaundice was present in all but 2 patients at admission. Encephalopathy developed at a mean of 13 days and 17 children were admitted with stage 3 or 4 coma. Evidence of severe liver failure was present in every patient. A lower prothrombin time and higher bilirrubin concentration were shown by non survivors. Hypoglycemia developed in 37% of patients, seizures in 37%, gastrointestinal bleeding in 45%, respiratory failure in 32% and severe infection in 32%. Overall mortality rate was 42% raising to 83% in patients with stage 3 coma at admission. Thus, although the etiology of fulminant liver failure differs in children as compared to adults, mortality rate and complications are similar.
 ...
PMID:[Fulminant hepatic failure in children]. 213 23

Six alcoholic patients developed extensive cerebral hemispheric hemorrhages with both intraventricular and subarachnoid blood. All patients had evidence of liver damage, low platelet counts, and abnormal prothrombin and partial thromboplastin times. Four patients presented with seizures; in two of the four, these seizures were initially diagnosed as alcohol withdrawal seizures. Four patients were comatose with lateralizing neurologic deficit; two patients were comatose without lateralizing neurologic deficit, suggesting a metabolic encephalopathy. In one patient there was delayed neurologic deterioration. In all six patients, computed tomography showed large diffuse cerebral hemispheric hemorrhages, prominent intraventricular blood, and breakthrough into the subarachnoid spaces, which was confirmed by necropsy findings. There was marked mass effect but minimal surrounding edema. All six patients died. In three, autopsy showed no evidence of aneurysm, vascular malformation, neoplasm, or amyloid angiopathy and no arteriolar hypertensive changes.
 ...
PMID:Alcoholic intracerebral hemorrhage. 320 17

Cases of intraventricular haemorrhage in full term newborn reported in the literature are scarce and etiopathological factors responsive remain unclear. Authors report a series of four full term infants weighting normal for their gestational age, who developed intraventricular hemorrhage, without any previous etiological factor. Seizures were the onset in all the newborns and, two of them prothrombin test was decreased. Diagnosis was confirmed by cranial ultrasonographic and CT scan after Papilla's classification. Haemorrhage was grade IV in two cases, grade III in another and grade I in the last case. One of the patients died in neonatal period, and the three others developed hydrocephalus. Two of them required ventriculo peritoneal shunt. Follow-up was carried from 14 months to 4 years. Authors found that infants who developed widespread haemorrhage had a poor neurologic outcome.
 ...
PMID:[Intraventricular hemorrhage in healthy newborn infants at term]. 366 64

The significance of megamitochondria in the alcoholic liver injury of humans was investigated as part of a large Veterans Administration cooperative study of the natural history of alcoholic hepatitis. Two hundred twenty patients were clinically stratified into the following three groups according to disease severity using serum bilirubin and prothrombin time as indicators: Group 1 (mild disease), serum bilirubin levels less than 5 mg/dl and prothrombin time prolonged for less than 4 s; group 2 (moderate disease), serum bilirubin levels greater than 5 mg/dl but prothrombin time prolonged for less than 4 s; and group 3 (severe disease), serum bilirubin levels greater than 5 mg/dl and prothrombin time prolonged for greater than 4 s. Megamitochondria were observed in 20% of the patients (45 of 220). Of these, 43 patients were in groups 1 and 2 of severity and only 1 patient belonged in group 3. The association of megamitochondria with cirrhosis was infrequent (33%, 15 of 45 patients). The differences in severity correlated with the differences in mortality: in patients with megamitochondria, only 1 had died at 6 mo compared with 40 deaths in patients without megamitochondria. By 12 mo, there were two deaths in patients with megamitochondria versus 51 deaths in those patients without. No complications were present in 72% of patients with megamitochondria versus 39% for those without. Infection, gastrointestinal bleeding, pancreatitis, hyperglycemia, azotemia, delirium tremens, seizures, and hepatic encephalopathy were all more common in patients without megamitochondria. The patients with megamitochondria appear to represent a subcategory of alcoholic hepatitis with a milder degree of clinical severity, lower incidence of cirrhosis, fewer complications, and good long-term survival.
 ...
PMID:Significance of megamitochondria in alcoholic liver disease. 369 4

Twenty-four patients had intracerebral hemorrhage while they were being treated with anticoagulants. Hypertension was present in 67% of the cases, head trauma was an uncommon preceding event, and simultaneous bleeding in other organs occurred in only one instance. Neurologic abnormalities progressed for several hours in 58%. Seizures occurred at onset in 12.5%. The location of the hemorrhage was as follows: cerebellum (nine cases), lobar white matter (six), basal ganglia (five), thalamus (two), and hemisphere, unspecified (two). In 61%, the hemorrhages occurred within 6 months of therapy. In 75%, the prothrombin time was beyond 1 1/2 times the control value. Mortality was 62.5%. Survivors had smaller hematomas than did patients with fatal hemorrhage.
 ...
PMID:Anticoagulant-related intracerebral hemorrhage. 401 Sep 61

Changes in the coagulation system due to steroids and asparaginase during treatment for acute lymphoblastic leukemia (ALL) are well known side effects and may cause bleeding or thrombosis. We report the case history of a 7-year old girl who developed thrombosis of the sinus sagittalis superior during ALL-treatment. Diagnosis was made by computed tomography and magnetic resonance imaging after the child became symptomatic with seizure. Until this event the girl had been treated already for two weeks with prednisone and E. coli-asparaginase (4 infusions). This medication caused distinct hypofibrinogenemia (Fibrinogen 53 mg/dl), prothrombin time expressed as percent of normal values of 58% was also pathological, activated partial thromboplastin time of 35 sec, antithrombin III 120% and thrombocyte count 178 G/l were in normal range. We were not successful in the attempt to adjust the imbalance in the coagulation system by transfusion of fresh frozen plasma (FFP)--seizure happened during FFP-infusion, fibrinogen blood level could be elevated only slightly. Our patient stayed consequently asymptomatic, the clinical recovery was confirmed radiologically.
 ...
PMID:[Venous thrombosis of cranial sinuses in asparaginase therapy. A case report]. 796 36


1 2 3 4 5 Next >>