Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case records of and histopathologic findings in 57 dogs with nonangiogenic and nonlymphomatous splenic sarcomas were reviewed. Splenic neoplasms in these dogs included leiomyosarcoma, fibrosarcoma, undifferentiated sarcoma, liposarcoma, osteosarcoma, chondrosarcoma, myxosarcoma, rhabdomyosarcoma, and fibrous histiocytoma. The clinical signs associated with splenic sarcoma included anorexia or decreased appetite, abdominal distention, polydipsia, lethargy, vomiting, weight loss, and weakness. An abdominal mass was detected in 86% of the dogs by use of abdominal palpation (63%), and/or abdominal radiography (74%). The diagnosis was based on histopathologic findings in the spleen. Abdominal exploratory surgery was performed on 43 of the 57 dogs. Twenty-seven dogs were treated by splenectomy, and 16 were euthanatized at the time of surgery because of widespread metastatic lesions. Of the 14 dogs on which surgery was not performed, 11 were euthanatized on the basis of results of preoperative diagnostic tests, and the remaining 3 dogs had splenic neoplasms that were incidental findings at necropsy. Of the 27 surgically treated dogs, 5 died in the immediate postoperative period, 12 died or were euthanatized within 1 year after splenectomy, and only 5 dogs survived greater than or equal to 1 year. Three dogs were lost to follow-up evaluation, and 2 were still alive 6 and 7 months after surgery. The median survival time of the 22 dogs for which survival was known was 2.5 months. The median survival time for 11 dogs with no obvious metastasis at the time of splenectomy was 9 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonangiogenic and nonlymphomatous sarcomas of the canine spleen: 57 cases (1975-1987). 255 65

The three first cases of isovaleric acidemia diagnosed in Scandinavia are described. The disorder is characterized by periodic vomiting, lethargy and coma accompanied by ketoacidosis and a "sweaty feet" odour. These attacks are often triggered of by upper respiratory tract infections or by ingestion of large amounts of protein. Often there are feeding difficulties because these children have aversion to protein-containing foods. Isovaleric acidemia can be subdivided into two types: an acute neonatal form and a chronic intermittent form. The basic defect is deficient activity of isovaleryl-CoA dehydrogenase, resulting in increased urinary excretion of mainly isovaleryl-glycine and 3-hydroxy-isovaleric acid. The defective gene is assigned to the long arm of chromosome 15, and at least five different mutations among 15 patients have been demonstrated. Therapy is symptomatic with correction of the metabolic acidosis and protein restriction and long term treatment with oral glycine and possibly carnitine.
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PMID:[Isovaleric acidemia]. 258 57

The use of digoxin-specific Fab fragments (d-Fab) to treat life-threatening digitalis intoxication has been widely substantiated in adults. This reports a case of a 2-year-old girl who ingested 90-92, 0.25 mg tablets of digoxin and within four hours, developed vomiting, lethargy, tachycardia and AV block (Mobitz type I and II). These symptoms were associated with total and free serum digoxin concentrations of 17.1 and 12.4 ng/ml, respectively. Following GI decontamination, a total dFab dose of 1280 mg (32 vials) was given with resolution of electrocardiographic abnormalities within 40 minutes and a concomitant reduction in the free serum digoxin concentration to 0.11 ng/ml. Repeated blood sampling over 19 days revealed an apparent elimination half-life (t1/2) of 134.9 and 129.9 hr for total and free digoxin, respectively. The long t1/2 for digoxin corresponded to a low apparent renal clearance of total digoxin which ranged from 0.56 to 0.82 ml/minute over four separate collection intervals. The free serum digoxin concentration never exceeded 3% of the total concentration and the patient did not develop a recurrence of toxic symptoms or any adverse effects (e.g. fever) attributable to dFab. Administration of an equimolar dFab dose to children following acute, massive digoxin intoxication represents safe, effective treatment which produces a prompt, sustained reversal of toxic effects. Digoxin specific Fab fragments should be promptly administered to any infant or child with significant, life-threatening symptoms following acute digoxin intoxication.
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PMID:Pharmacokinetics and efficacy of digoxin specific Fab fragments in a child following massive digoxin overdose. 259 82

Symptoms were evaluated in 13 haemodialysis patients at dialysate temperatures between 37 and 35 degrees C. After a control period at 37 degrees C (stage 1) dialysate flow rate was increased from 300 ml/min in half the patients but no change in temperature was made (stage 2). In stage 3 dialysate temperature was reduced to 36.5 degrees C and in stage 4 to 35 degrees C. Blood pressure and temperature were measured pre- and post dialysis and patient completed a questionnaire indicating if they experienced any of nine specified symptoms: itch, restless legs, nausea, vomiting, headache, cramp, lethargy, hypotension and change in temperature. Trial stages were compared with chi 2 analysis using Yates correction. Symptoms per dialysis fell from 1.11 to 0.71 between stage 1 and 2 (p less than 0.0005). This was considered to be a trial effect. There was no further significant improvement in symptoms overall as the temperature was reduced to 35 degrees C. However, if complaints of coldness are excluded, there was a progressive reduction in symptoms from stage 1 to stage 4. Dialysate flow rate did not affect symptom reporting. There was no effect on body core temperature or blood pressure due to cool dialysate. Our results suggest there may be some benefit in lowering the dialysate temperature but this is small in relation to the placebo effect. Caution must be used in assessing similar studies using small numbers of dialyses.
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PMID:Assessment of the symptomatic benefit of cool dialysate. 266 42

Pneumatosis intestinalis (PI) is a well-recognized manifestation of necrotizing enterocolitis (NEC) in the newborn--a condition that often requires surgical intervention for infarcted bowel. However, little information is available concerning PI in older children or its management. Sixteen older infants and children (greater than 2 months) had x-ray findings of PI (intramural air). There were eight girls and eight boys ranging in age from 2 months to 8 years. Associated conditions included short bowel syndrome (SBS) (8), congenital heart disease (2), iron ingestion (1), nesidioblastosis (1), hemolytic anemia (1), rheumatoid arthritis (1), bronchopulmonary dysplasia (BPD) (1), and malrotation (1). Clinical presentation included abdominal distension (13), bloody diarrhea (12), bilious emesis (5), and lethargy (5). Two patients on steroids had unsuspected PI identified as an incidental operative finding during pancreatectomy for nesidioblastosis (1) and splenectomy for hemolytic anemia (1), respectively. Only four other children (iron toxicity, postcardiac catheterization, rheumatoid arthritis, and BPD required surgical intervention. Each manifested peritioneal irritation, acidosis, and hypotension or had pneumoperitoneum on abdominal x-ray. In ten of 14 patients, PI was managed nonoperatively with nasogastric suction, fluid resuscitation, intravenous (IV) antibiotics (seven to ten days), and repeated abdominal x-ray and physical examinations. Children with SBS comprised 50% of the total number of patients and eight of ten treated by observation. All had associated viral syndromes (rotavirus) or rhotozyme-positive stools and developed bloody diarrhea. There were two deaths (12.5%) in patients with iron toxicity and congenital heart disease who required resection of gangrenous bowel. All of the other patients survived.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pneumatosis intestinalis in children beyond the neonatal period. 267 35

The diagnosis of adrenal haemorrhage complicating heparin therapy is often delayed, despite computed tomography (CT). Moreover, its pathogenesis is not clear. Adrenal haemorrhages are often seen in cases where there is no unduly excessive anticoagulation, and can be accompanied by a paradoxical thrombosis of the central adrenal vein. Symptoms usually occur within the first 8 to 12 days after starting heparin. The difficulty in establishing the diagnosis stems from the fact that symptoms are rather nonspecific: abdominal pain and backache, nausea, vomiting, lethargy, weakness, hypotension, hyperpyrexia. To confirm the diagnosis, both hormonal proof of adrenal failure and anatomic evidence of haemorrhage must be found. Early CT scans may show the haemorrhage. Several possible causes have been put forward to account for these adrenal haemorrhages. The degree of anticoagulation did not seem to be a prerequisite, 30 to 50% of patients showing no evidence of other bleeding or coagulation tests outside the therapeutic range. Capillary fragility of old age might be a factor. Stress would seem to be an important factor predisposing to adrenal haemorrhage. Many authors consider the paradoxical central vein thrombosis as a result of the haemorrhage rather than its cause, whereas other conclude the opposite. Unfortunately, to date coagulation studies are often incomplete; platelet counts were missing in most reports published before 1985. Since that date, a heparin induced thrombosis-thrombocytopaenia syndrome (HITTS), in which thrombosis may occur in any vascular bed, has been recognized with increasing frequency. Nine cases of adrenal haemorrhage associated with HITTS have been reported. It seems highly likely that a proportion of cases of heparin-related adrenal destruction are due to HITTS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hematoma of the adrenal glands and heparin]. 269 74

Two male infants with hyperpigmentation, vomiting, lethargy and weight loss were reported. Hypoglycemia, hyponatremia, hypochloremia, hyperkalemia and metabolic acidosis were suggestive diagnosis of salt losing adrenocortical insufficiency. The absence of ambiguous genitalia, low 24 hour urinary 17 KS and pregnanetriol excretion precluded congenital adrenal hyperplasia. Low basal levels of plasma aldosterone and cortisol and low 24 hour urinary 17 OHCS excretion with disability to increase their corticosteroid secretions after ACTH stimulation as well as furosemide and theophylline infusions were supportive for the diagnosis of congenital adrenal hypoplasia. The definitive diagnosis was confirmed by ultrasonogram and computerized tomography. Family histories suggested X-linked recessive inheritance in these reported cases. Evidence of progressive postnatal adrenocortical degeneration was documented by progressive deterioration of adrenocortical functions beginning from mineralocorticoid to total corticosteroid deficiencies. The increased brain serotonin synthesis as the associated pathology of X-linked congenital adrenal hypoplasia was proposed on the basis of elevated basal plasma GH and PRL levels in the reported cases, taken together with an incidence of congenital LH deficiency and persistent ACTH hypersecretion in corticosteroid treated patients reported elsewhere.
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PMID:X-linked congenital adrenal hypoplasia: proposal pathogenesis. 273 38

We report on 10 patients between 3 and 18 years of age who had been treated in the neonatal and postneonatal period for hydrocephalus of various causes with a ventriculo-atrial or ventriculo-peritoneal shunt. Between the age of 2 and 17 years these children suffered from recurrent attacks of headache, vomiting bradycardia and lethargy suggesting shunt-obstruction. 8 children showed slowing of electrical activity in their EEG, 4 had papilledema on fundoscopy. Splayed sutures were found in one child by skull x-ray. In all the above cases the CT-headscans assessed by radiologists showed no evidence of shunt-obstruction. Only on direct comparison with previous CT-scans we were able to detect minimally dilated ventricles in 6 children. In all cases conservative treatment failed. Symptoms only ceased after surgical shunt-revision. In all children treated with shunts headache, vomiting and vegetative symptoms must be considered as signs of shunt-obstruction until proved otherwise. A negative CT-scan done while symptoms are present cannot rule out raised intracranial pressure. Only by direct comparison with previous CT-scans carried out during an asymptomatic period a minor dilatation of the ventricles can often be detected. This should be taken as a sign of shunt-obstruction.
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PMID:[Critical intracranial pressure crises in drained hydrocephalus with minimally enlarged or normal ventricles]. 273 67

A consecutive series of 385 patients with intussusception treated between January 1, 1982 and December 31, 1987 was analysed. Male patients predominated over female by a ratio of 2.2:1. Seventy nine per cent of patients were under 12 months of age. There was no seasonal variation in the incidence of intussusception. Rectal bleeding was the most common symptom, followed closely by intermittent abdominal pain and vomiting. The duration of symptoms at the time of admission was less than 24 hours in 62%. Barium enema reduction was used initially in most patients. Successful reduction by barium enema alone was obtained in 66% of patients. Thirty two patients experienced recurrence of intussusception, six following operative reduction and 26 following barium enema reduction. Five patients experienced two recurrences each. Several factors including the age of the patients, the presence of a palpable mass, lethargy and abdominal distension were identified as influencing the success rate of barium enema reduction.
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PMID:Intussusception in infancy and childhood. Analysis of 385 cases. 275 20

The medical records of 59 dogs with renal amyloidosis were reviewed. Most dogs with amyloidosis were greater than 6 years old, and females were affected more often than males. Beagles, Collies, and Walker Hounds were at increased risk, whereas German Shepherd Dogs and mixed-breed dogs were at decreased risk. Common historical findings were anorexia, polyuria, polydipsia, lethargy, vomiting, and weight loss. Common laboratory findings were leukocytosis, lymphopenia, nonregenerative anemia, hypercholesterolemia, azotemia, hyperphosphatemia, metabolic acidosis, isosthenuria, cylindruria, and proteinuria. Proteinuria was moderate to severe in most dogs, as assessed by qualitative determination of urine protein concentration, urine protein/urine creatinine ratio, and 24-hour urine protein excretion. Conservative medical management was of little value, and survival ranged from 3 to 20 months in 12 dogs for which this information was available. Moderate to severe diffuse global glomerular amyloidosis was detected in all dogs. Medullary amyloid deposition was multifocal and less severe, but was evident in most dogs. Secondary tubulointerstitial and glomerular lesions were mild or absent in most dogs. Thromboembolism was identified in approximately 14% of affected dogs, underlying inflammatory disease in 37%, and neoplasia in 20%. Laboratory indicators of renal function correlated poorly with histologic lesions, with the exception of glomerular amyloid deposition and "chronic renal disease" index with endogenous creatinine clearance.
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PMID:Clinicopathologic findings in dogs with renal amyloidosis: 59 cases (1976-1986). 276 63


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