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)

Serum hyperviscosity syndrome was diagnosed in 2 cats with multiple myeloma. Clinical signs included pale mucous membranes, dehydration, retinal hemorrhages, dilated and tortuous retinal vessels, seizures, head-tilt, nystagmus, systolic murmur, and gallop rhythm. Laboratory abnormalities included hyperglobulinemia, azotemia, hyperphosphatemia, nonregenerative anemia, and thrombocytopenia. Both cats had IgG monoclonal gammopathy, Bence Jones proteinuria, increased numbers of bone marrow plasma cells, and high values for relative serum viscosity. Renal disease was suspected in both cats. Cardiac hypertrophy was documented in 1 cat and was suspected in the other cat. Chemotherapy, using melphalan, prednisone, and vincristine, caused short-term remission in both cats, and plasmapheresis was used to lower serum protein concentration in 1 cat. Serum hyperviscosity syndrome rarely develops in cats, but should be suspected when monoclonal gammopathy exists with signs of neurologic, cardiac, or retinal disease.
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PMID:Serum hyperviscosity syndrome associated with multiple myeloma in two cats. 153 97

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

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.
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PMID:Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog. 226 50

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

The systemic manifestations of "asphyxia" were evaluated prospectively in 35 consecutively intubated term newborn infants. The following systemic organ injuries were identified most often: (1) renal, ie, oliguria less than 1 mL/kg per hour for at lest 24 hours (40%), an elevated urinary beta-2-microglobulin concentration (57%), azotemia (11%), and an elevated serum creatinine level (17%); (2) central nervous system, ie, hypoxic-ischemic encephalopathy (including seizures) (31%) or an abnormal cranial ultrasound scan, ie, diffuse parenchymal echogenicity, slitlike ventricles, and poor visualization of the sulci, and/or intracranial hemorrhage (26%); (3) cardiovascular, ie, an abnormal echocardiogram (25%) or abnormal electrocardiogram (11%); (4) pulmonary complications, including persistent pulmonary hypertension (23%); and (5) gastrointestinal complications, which were rare. Traditional markers of fetal distress were not related to the frequency and/or distribution of systemic organ injury. An important implication of this study relates to the recognition of the extent and distribution of organ injury in the "asphyxiated" infant.
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PMID:Acute systemic organ injury in term infants after asphyxia. 271 98

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.
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PMID:Significance of megamitochondria in alcoholic liver disease. 369 4

We studied three boys who had a similar encephalopathy develop during moderate chronic renal failure. The features included cerebellar system dysfunction, seizures, and intellectual and motor retardation. Extensive laboratory investigation failed to disclose an etiology other than chronic azotemia. These cases suggest that the developing nervous system is particularly sensitive to the effects of chronic azotemia. Early dialysis and/or transplantation should be considered in such children in an attempt to modify the serious nervous system abnormalities.
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PMID:Encephalopathy in young children with moderate chronic renal failure. 738 32

To define the CNS manifestations of the hemolytic-uremic syndrome (HUS), the records of 61 consecutive episodes of HUS in 60 patients were reviewed. Major CNS signs (seizures and/or coma) occurred in 30 of the 61 episodes. Twenty-four children had seizures. Analysis of blood pressure and metabolic parameters or admission to the hospital did not predict which child would exhibit CNS signs. However, during the subsequent course of the illness, children with CNS dysfunction had lower minimum serum sodium concentrations and more severe azotemia and were more likely to require dialysis than children without CNS signs. Of the 61 episodes, there were three deaths, and three children suffered major CNS sequelae. Coma at the time of admission and elevated CSF protein levels were features associated with poor outcome.
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PMID:CNS manifestations of the hemolytic-uremic syndrome. Relationship to metabolic alterations and prognosis. 741 14

A postpartum mare and foal were presented for evaluation of fever and lethargy in the mare. The mare was diagnosed with endometritis and initially responded well to treatment. On the second day of hospitalization, the mare developed renal insufficiency characterized by oliguria, azotemia, hemolysis, and thrombocytopenia. Concurrently, the foal developed rapidly progressive central nervous system signs culminating in refractory seizures. Both animals failed to respond to treatment and were euthanized. Thrombotic microangiopathy involving glomeruli was evident on microscopic examination of the mare's kidneys. Microscopic evidence of brain edema was the principal postmortem finding in the foal. No specific etiology was confirmed in either case. Notably, Escherichia coli 0103:H2 was isolated from the mare's uterus and the gastrointestinal tracts of both animals. To the authors' knowledge, this is the first report in which an organism implicated as a cause of hemolytic-uremic syndrome was isolated from an animal with clinical signs and postmortem findings consistent with the disease.
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PMID:Hemolytic-uremic syndrome in a postpartum mare concurrent with encephalopathy in the neonatal foal. 1831 42


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