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)

Cocaine abuse is associated with a constellation of serious medical complications. An unrecognized and recently described complication of cocaine use is rhabdomyolysis with acute renal failure. We describe the first patient identified in our institution with this entity, admitted to the medical services with oliguric acute renal failure. Three days prior to admission the patient had a cocaine snorting binge. He presented with bilateral flank pain, gross hematuria, vomiting and chills. No history of crush injury, prolonged immobilization and or seizures was reported. On admission the vital signs were normal, physical exam revealed periorbital edema and marked soft tissue neck swelling. Lab values: Bun 120 mgs%, Creat. 10.7 mgs%, Na 132 meq/lt, Co2 13mq/lt, Cl, 103meq/lt, Co2 13meq/lt, Ca 5.3 mgs%, CPK 30,800 U/L with a MM fraction of 98%, LDH 600 U/L, SGOT 300 U/L. The urine was dark red with a ph of 6.5 and 100 rbc/hpf. The anti-GBM antibody and blood cultures were negative. An abdominal sonogram was normal. He received peritoneal dialysis and was discharged on his 14th hospital day with a CPK of 2,800 U/L and decreasing azotemia. Cocaine associated rhabdomyolysis has only been recently described in the literature (AJM April, 88). Acute myoglobinuric renal failure needs to be added to the growing list of medical complications of cocaine use.
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PMID:Cocaine and rhabdomyolysis: report of a case and review of the literature. 207 48

The spectrum of neurological complications associated with heroin addiction has changed in the past six years because of the progressive knowledge of the neurological complications related to HIV infection. We reviewed 48 heroin addicts with neurological complications and 452 heroin overdose who were seen in the Emergency Unit of our hospital during 1988 and the publications since 1967. Regarding the overdose we present the results of a prospective study leading to determine the causes. We emphasize the relationship with the level of total morphine in serum, instead of conjugate morphine, and with the presence of high levels of benzodiazepines found in the plasma rather than an hypothetic hypersensitivity phenomenon. We resume the neurological complications related with heroin addiction: spongiform leukoencephalopathy, epileptic seizures, stroke, transverse myelopathy and neuromuscular complications such mononeuropathy, plexopathy, acute inflammatory demyelinating polyradiculoneuropathy, rhabdomyolysis, fibrosing myopathy, musculoskeletal syndrome and acute bacterial myopathy. Some of such complications (i.e. transverse myelitis, polyradiculoneuropathy, leucoencephalopathy) must rise the suspicion of an HIV infection. Likewise, in patients assisted for overdosage we believe it's necessary rule out myoglobinuria by means of CPK serum levels and detection of urine hematic pigments without red blood cels in the urine sediment, in order to prevent and treat the renal failure. We report the results of muscular biopsy found in the musculoskeletal syndrome, which are similar to those found in alcoholic myopathy. Finally, we describe the clinical and diagnostic aspects in an unusually neuromuscular complication: the acute bacterial myopathy.
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PMID:[Non-infective neurologic complications associated to heroin use]. 256 83

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)
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PMID:[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case]. 263 19

In order to evaluate the enzymes CPK and LDH as potential biochemical markers of tricyclic antidepressant (TCA) cardiotoxicity, we prospectively followed 29 patients with TCA overdose. Serum CPK and LDH were obtained on all patients at admission. Population characteristics included a mean age of 33 y, a mean peak serum TCA concentration of 1190 ng/ml and mean maximal QRS interval of 0.10 sec. Seven patients (23%) had admission hypotension, 7 (23%) had severe respiratory depression, 6 (20%) had seizures and 4 (13%) had cardiac arrhythmias. One patient died. Mean admission CPK was 301 IU/L (nl less than 230 IU/L) while mean LDH was 221 IU/L (nl less than 250 IU/L). In 17 patients (57%), CPK remained in the normal range. There was no correlation between blood pressure, maximal QRS interval, serum TCA concentration, arrhythmias or seizures and CPK or LDH by regression analysis. CPK isoenzymes were obtained in 6 patients (both with and without severe myocardial dysfunction). One patient had an MB fraction of 10%; the remaining 5 had no measurable enzymes of myocardial origin. We conclude that modest elevations in CPK or LDH may occur after TCA overdose. These enzymes do not appear to originate from the myocardium and are of no utility in the assessment of antidepressant cardiotoxicity or prediction of clinical course.
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PMID:Serum enzyme disturbances after tricyclic antidepressant overdose. 292 29

A 14-year-old boy with focal seizures, syncopal attacks, and progressive intellectual deterioration had intracranial calcifications on a CT scan and hypocalcemia unresponsive to parathyroid hormone. The commonly recognized neurological manifestations of pseudohypoparathyroidism were complicated by signs of Friedreich's ataxia. A marked elevation of serum CPK was unexplained and was unrelated to seizures.
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PMID:Friedreich's ataxia forme fruste and elevated creatine phosphokinase in a child with pseudohypoparathyroidism. 737 40

An aqueous solution of norfloxacin nicotinate (NFN) was administered to donkeys (Aquus asinus) intravenously (once at 10 mg/kg), intramuscularly and orally (both routes once at 10 and 20 mg/kg, and for 5 days at 20 mg/kg/day). Blood samples were collected at predetermined times after each treatment and urine was sampled after intravenous drug administration. Serum NFN concentrations were determined by microbiological assay. Intravenous injection of NFN over 45-60 s resulted in seizures, profuse sweating and tachycardia. The intravenous half-life (t1/2 beta) was 209 +/- 36 min, the apparent volume of distribution (Vd(area)) was 3.34 +/- 0.58 L/kg, the total body clearance (ClB) was 1.092 +/- 0.123 x 10(-2) mL/min/kg and the renal clearance (C1R) was 0.411 +/- 0.057 x 10(-2) mL/min/kg. Oral bioavailability was rather poor (9.6% and 6.4% for the 10 and 20 mg/kg doses respectively). Multiple oral treatments did not result in any clinical gastrointestinal disturbances. After intramuscular administration (20 mg/kg), serum NFN concentrations > 0.25 microgram/mL (necessary to inhibit the majority of gram-negative bacteria isolated from horses) were maintained for 12 h. The intramuscular bioavailability was 31.5% and 18.8% for the 10 and 20 mg/kg doses respectively. After multiple dosing some local swelling was observed at the injection site. About 40% of the intravenous dose was recovered in the urine as parent drug. The results of comprehensive haematological and blood biochemistry tests indicated no abnormal findings except elevation in serum CPK (creatine phosphokinase) values after multiple intramuscular dosing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous disposition kinetics, oral and intramuscular bioavailability and urinary excretion of norfloxacin nicotinate in donkeys. 762 23

Legionella is a frequent etiologic agent in the development of both nosocomial and community acquired pneumonias. Involvement of the nervous system is common in Legionella infections. We present a case of Legionnaires' disease which illustrates distinctive neurologic findings including delirium and cerebellar dysfunction. Furthermore, this paper reviews the neurological and psychiatric features of 609 Legionella infected patients with involvement of the nervous system. The most common signs were disorientation (58%), headache (52.4%), and somnolence (39.7%). Less frequent or rare were: cerebellar dysfunction (11.2%), hallucinations (8.4%), agitation or stupor (4.1%), affective disorders (3.1%), peripheral neuropathy (2.8%), pyramidal disturbances (2.1%), memory loss (1.6%), seizures (1.5%), cranial nerve palsies (1.5%), incontinence (0.7%), and extrapyramidal disturbances (0.3%). Cranial CT scans, cerebrospinal fluid findings, and nerve and muscle biopsies were usually unremarkable. Neuropathologic examinations failed to demonstrate specific characteristics. Hyponatremia and serum CPK level elevation were present in up to 89% and 50% of patients, respectively. Prognosis of disturbances of the nervous system was mainly good. We conclude that in the presence of definite neurological findings, pulmonary infection, hyponatremia, and CPK elevation Legionella infection should be considered.
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PMID:[Neurologic and psychiatric symptoms of legionella infection. Case report and overview of the clinical spectrum]. 927 65

Acute renal failure is the most common complication of rhabdomyolysis, with an 8-20% reported incidence. In particular, rhabdomyolysis associated with acute renal failure is frequently observed in critically ill patients, with a 6-16% reported incidence in Intensive Care Units. Dialytic treatment is necessary to correct hydroelectrolytic imbalance and renal function alterations and it may be a pathogenetic therapy by myoglobin removal. In the present study we evaluated our experience on patients suffering from rhabdomyolysis and acute renal failure subjected to dialytic treatment. We retrospectively studied 28 patients, 17 admitted in our Intensive Care Unit (ICU-patients) and treated by continuous renal replacement therapy (particularly by continuous venovenous hemofiltration, continuous venovenous hemodialysis and continuous venovenous hemodiafiltration) and 11 admitted in our Nephrology Department (NICU-patients) and treated by high-efficiency daily hemodialysis. We excluded one ICU-patient from the study because she was affected with lung end-stage neoplasia and it would have been difficult to evaluate the effects of the dialytic treatment on RML biochemical index and on her final outcome. ICU-patients were older, with a mean age of 64 +/- 10 yrs, and were suffering from MODS and typical elderly diseases, such as cardiac and respiratory chronic failure, except from 3 patients with acute liver failure resulting from poisoning, who were relatively younger. In NICU-patients, instead, the mean age was 36 +/- 16 yrs and the causes of RML were narcotic drugs abuse, repetitive seizures and vigorous exercise, more frequently observed in young people. In three relatively older NICU-patients RML was due to lipid lowering drugs assumption. Before starting the dialytic treatment, in ICU-patients CPK plasma level was 2615 +/- 3586, while K+ was 5.10 +/- 1.08 and sCr was 5.69 +/- 4.06 In NICU-patients, on the other hand, CPK was 14273 +/- 9266, while K+ was 5.75 +/- 0.92 and sCr was 5.9 +/- 0.4. ICU-patients mortality rate was 50% (8/16 patients) in spite of the good recovery of renal function and the biochemical RML indexes improvement. In NICU-patients, instead, only one patient died for septic complications (he was a heroin-addict and suffered from overdose syndrome). Early dialytic treatment of RML allows not only to avoid life-threatening complications (first of all the acute renal failure) but moreover it's a pathogenetic treatment because it removes great amount of myoglobin from the plasma. Beside this, continuous renal replacement therapy allows a successful management of critically ill patients with severe hemodynamic conditions. Nevertheless, the final outcome may be very different between ICU- and NICU-patients, with a higher mortality rate in ICU-patients, suffering from MODS.
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PMID:Dialytic treatment of rhabdomyolysis-induced acute renal failure: our experience. 1141 50

The authors describe five pediatric cases of excessive pemoline ingestion. Based on their experience compared with previously reported cases in the literature, they describe the clinical presentation and rational treatment recommendations for acute pemoline ingestion. Overall, patients experienced a relatively benign clinical course following pemoline ingestion. Symptoms of pemoline ingestion appear to be primarily an accentuation of the drug's pharmacological effects on the central nervous and cardiovascular systems with sinus tachycardia, hypertension, hyperactivity, choreoathetoid movements, and hallucinations being most commonly observed. These findings are consistent with previously reported cases. Possible rhabdomyolysis manifested by evaluation of serum CPK was also observed in 3 of 4 patients in whom this laboratory parameter was measured and appears to be a common finding in acute pemoline poisoning. After acute ingestion, symptoms occurred within 6 hours, lasting up to 48 hours in all patients. Gastric lavage and/or activated charcoal would be effective decontamination measures, whereas ipecac-induced emesis should be avoided after massive ingestion due to the possibility of seizures. Aggressive use of a benzodiazepine appears a reasonable first choice to treat associated involuntary movements, tremor, hyperactivity, irritability, and agitation. Phenothiazines or butyrophenones may also be used especially for serious life-threatening symptoms, including hypertensive crisis and severe hyperthermia, although these serious complications of stimulant overdose have not been reported after pemoline ingestion. If a patient should experience pemoline-induced hypertensive crisis, individual dose titration of labetalol or sodium nitroprusside would appear reasonable pharmacologic approaches for rapid stabilization of blood pressure.
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PMID:Pemoline ingestion in children: a report of five cases and review of the literature. 1186 63

A 75-year-old female with history of putamenal hemorrhage 8 years earlier was admitted to our hospital with generalized convulsion lasting 40 minutes. Convulsion responded quickly to intravenous administration of diazepam, but deep coma persisted thereafter. Although renal function had normalized before this episode, urinary output was immediately estimated to be limited. Drip-infusion of Ringer's solution and the combined administration of furosemide and mannitol were started. The laboratory values 6 hours after admission demonstrated extremely elevated GOT, GPT, CPK, BUN and Cr levels, suggesting rhabdomyolysis. Urinalysis confirmed myoglobinuria. Despite massive diuretic therapy, renal dysfunction did not improve and she died on hospital day 4. The treatment outcome was probably influenced by her general condition of dehydration and acidosis at admission, as well as muscle damage caused by convulsion. Myoglobinuria can induce life-threatening renal failure, and may be caused by convulsion.
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PMID:[Acute renal failure following convulsion-induced myoglobinuria]. 1705 9


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