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

Sulfites are widely used as preservatives in the food and pharmaceutical industries. In the United States more than 250 cases of sulfite-related adverse reactions, including anaphylactic shock, asthmatic attacks, urticaria and angioedema, nausea, abdominal pain and diarrhea, seizures and death, have been reported, including 6 deaths allegedly associated with restaurant food containing sulfites. In Canada 10 sulfite-related adverse reactions have been documented, and 1 death suspected to be sulfite-related has occurred. The exact mechanism of sulfite-induced reactions is unknown. Practising physicians should be aware of the clinical manifestations of sulfite-related adverse reactions as well as which foods and pharmaceuticals contain sulfites. Cases should be reported to health officials and proper advice given to the victims to prevent further exposure to sulfites. The food industry, including beer and wine manufacturers, and the pharmaceutical industry should consider using alternative preservatives. In the interim, they should list any sulfites in their products.
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PMID:Adverse reactions to sulfites. 405 97

Thirty-six patients with measurable or evaluable advanced soft tissue sarcoma were entered in a phase II trial with PALA. Among the 27 evaluable patients, 15 were men, the median age was 55 yr (16-69) and the median performance status (Karnofsky) was 80 (50-100). Most patients had leiomyosarcoma (8), liposarcoma (3), neurofibrosarcoma (3), synovial cell sarcoma (3), or undifferentiated sarcoma (3). Indicator lesions consisted essentially of lung metastases (21) and/or soft tissue lesions (14). All patients had received prior chemotherapy with 1-5 regimens and 6 had achieved objective response with these previous treatments. PALA was given as a 60-min i.v. infusion at a daily dose of 2.5 g/m2 for two consecutive days. Courses were repeated every two weeks. A median number of 3 courses (2-17) were administered. Partial remission (greater than 50%) was obtained in one patient with a liposarcoma who had also responded to prior combination chemotherapy. This single response to PALA lasted 6 weeks from initiation of therapy. Four patients had unchanged disease after 6+ courses of PALA and 22 had progressive disease. Toxic effects were generally mild to moderate and included cutaneous toxicity (17), diarrhea (14), stomatitis (13), ocular manifestations, consisting of conjunctivitis, corneal ulceration and/or photophobia (11), nausea and vomiting (6) and, possibly, seizures (2). There was no evidence of drug-related myelosuppression. It is concluded that PALA given at the dose schedule selected for this trial has no significant antitumor activity in advanced soft tissue sarcoma previously treated with chemotherapy.
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PMID:N-(phosphonacetyl)-L-aspartate (PALA) in advanced soft tissue sarcoma: a phase II trial of the EORTC soft tissue sarcoma group. 621 62

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

A new essential hypereosinophilic syndrome has been reported in a 53 years old man who presented an important blood and bone marrow hypereosinophilia of unknown etiology since 5 years. The evolution of the clinical course included neurological accidents (hemiplegia, spasmodic quadriplegia, seizures) congestive heart failure, hepatomegaly, transient renal involvement, pulmonary infiltrates with pleural hemorrhage, episodes of diarrhea and fever with weight loss. The cytological study of the eosinophiles showed the existence of abnormal inclusions which were confirmed by the electron microscope. These and cytoenzymological abnormalities led to discussion of the relationship between the essential hypereosinophilic syndrome and eosinophilic leukemia.
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PMID:[An essential hypereosinophilic syndrome. Cytological, cyto-enzymological and ultrastructural studies (author's transl)]. 645 47

In 19 children with acute infantile hemiplegia an ischemic cerebral infarct was found clinically and by serial computertomography. In 11 patients an angiography has been performed in addition. 9 of the children had chronic diseases which are known as predisposing factors for cerebrovascular disease (congenital heart disease in 7 and chronic renal failure with hypertension in 2). One child had a severe hypernatremic dehydration due to infantile diarrhea and in 1 child thrombosis of the internal carotid artery occurred 3 days after a perforating trauma of the soft palate. No obvious reason for the ischemic stroke could be evaluated in 8 children. The onset of symptoms was either acute or slowly progressive. An altered state of consciousness was present in 11 children. Hemiparesis was found in 18 patients (13 right, 5 left) accompanied by facial palsy in 12 and aphasia in 6. Seizures occurred in 6 patients. One patient with incomplete occlusion of a vertebral artery showed acute cerebellar ataxia. In children without predisposing factors the prevalence of girls was higher (2 : 6) and there was a history of a preceding acute febrile illness in 5 of 8 patients. Laboratory investigations showed polycythemia in 4 children with cyanotic heart disease and additional hypochromia in two. Blood sedimentation rate was increased in 6 out of 8 patients without a known predisposing factor. Cerebrospinal fluid (CSF) showed a slight increase of erythrocytes (36-88/cmm) in 4 children, in two others purulent CSF was obtained after the infarct had developed into a brain abscess. The etiology of ischemic stroke in childhood and the possibility of an inflammatory vascular disease are discussed.
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PMID:Acute infantile hemiplegia caused by cerebral ischemic infarction. Etiology, clinical features and investigations. 647 69

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
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PMID:Practical toxicologic diagnosis. 649 3

This report describes a patient who accidentally ingested 215 g of chlordane in a liquid pesticide formulation. The patient experienced multiple acute clinical sequellae attributable to his acute intoxication, including vomiting, diarrhea, seizures, coma and respiratory failure. Upon initial presentation and during the recovery phase, blood and urine specimens were collected to measure the disposition and elimination of chlordane and its metabolites. Whole blood chlordane concentrations measured over the subsequent 49 days suggested a multicompartmental kinetic profile of chlordane distribution, with an approximate terminal elimination half-life of 34 days. Tissue samples obtained from this patient, during elective surgery 58 days post chlordane ingestion, revealed persistent high levels of chlordane related metabolites. This case illustrates the physiological distribution and elimination of chlordane and its related metabolite residues after acute intoxication in an adult patient. Such information is important to improve the clinical management of patients acutely exposed to potentially lethal levels of pesticides.
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PMID:Acute chlordane intoxication. 665 71

Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
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PMID:Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome. 677 12

Two siblings with a congenital syndrome of secretory diarrhea and seizures developed progressive skin rash, alopecia, and mucocutaneous candidiasis while receiving biotin-free total parenteral nutrition. Abnormally low urinary biotin excretion was associated with these clinical findings, but the serum concentration of biotin was within the normal range. There was also increased urinary excretion of lactic acid, 3-hydroxyisovaleric acid, 3-hydroxypropionic acid, and 3-methylcrotonylglycine. The younger of the two children subsequently died with severe metabolic acidosis. In the oder sibling, intravenous treatment with biotin (200 micrograms/day) resulted in resolution of the organic aciduria. A larger dose (10 mg/day) appeared to be required for rapid improvement in the skin lesions. These cases suggest that clinically significant biotin deficiency can occur in patients with chronic diarrhea receiving biotin-free total parenteral nutrition.
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PMID:Biotin-responsive in vivo carboxylase deficiency in two siblings with secretory diarrhea receiving total parenteral nutrition. 679 36

Two male newborns developed severe life threatening hypernatremia with serum sodium levels of 181 and 196 meq/l respectively. Both children were fed a two-to fivefold concentrated powdered infant formula since birth. Shortly before admission diarrhea developed in both patients. The children were admitted during the third week and fourth week respectively, of their lifes with clinical signs of severe hyperosmolar dehydration. In both, treatment of shock was instituted and was followed by rehydration therapy. Great care was taken to lower serum sodium by not more than 15 meq/l/day in order to prevent cerebral edema. Inspite of these measures, the first patient developed cerebral seizures 5 hours after initiation of fluid replacement. The patient was intubated, and measures aimed at prevention of cerebral edema were started (hyperventilation). The eventual outcome was satisfactory, on follow up the patient showed no signs of persistent cerebral damage. In the second patient the same management was started from the beginning and no cerebral problems occurred. Restoration of stable body functions with a normal electrolyte status was achieved within five days.
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PMID:[Life-threatening hypernatremia caused by faulty preparation of fully adapted infant formula]. 683 43


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