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)

A 50-year-old female was admitted because of nausea, vomiting, and cerebellar ataxia. Computed tomography scan revealed an enhanced mass accompanied with a cyst in the right cerebellar hemisphere. The mass situated in the subcortical region was removed. Histologically, highly vascular tumor cells lined the cavities. Postoperative radio- and chemotherapy were administered and the clinical symptoms improved gradually. Two months later, the patient complained of dyspnea. Chest X-ray on second admission demonstrated cardiomegaly. Hemorrhagic pericardial effusion amounting to 1000 ml was aspirated by pericardial puncture. Papillary clusters of tumor cells were demonstrated in the pericardial effusion. The patient died of cardiac failure. At necropsy solid tumors were located in the heart, lung, left inguinal region, and cerebellum. Histological diagnosis was mesothelioma arising from the heart. Primary pericardial mesotheliomas are rare; approximately 106 cases have been reported. Pericardial mesothelioma frequently spreads to the adjacent pleura and mediastinum, but distant metastases are extremely rare because patients with pericardial mesothelioma tend to die early due to cardiac failure or cardiac tamponade.
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PMID:[Brain metastasis from primary pericardial mesothelioma. Case report]. 170 70

The patient presented in this paper had been stable for 3 months after the induction of hemodialysis, when nausea, vomiting and hepatomegaly suddenly developed. A chest film revealed rush cardiomegaly, and massive pericardial effusion was demonstrated by echocardiography. One liter of hemorrhagic fluid was removed by pericardiocentesis and subsequent pericardial drainage under echocardiography. The patient received chemotherapy against pulmonary tuberculosis 30 years ago and calcification on chest film was apparent. Although sputum smear and pericardial effusion was negative for acid-fast organisms, combination therapy was initiated for suspected tuberculosis. The patient recovered completely and 2 months later it was demonstrated that cultures of sputum grew mycobacterium tuberculosis. Tuberculin skin test (PPD), which was negative 2 months previously, converted to positive. Tuberculosis must be considered as a potential cause of pericardial tamponade in patients on regular hemodialysis, and prompt therapy for both cardiac tamponade and the occult infection is warranted.
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PMID:Tuberculosis on regular hemodialysis--a case of pericardial tamponade. 276 29

Four patients had pancreatitis associated with valproic acid therapy. Three patients received valproic acid at usual doses, and all were free of other symptoms of toxic reactions, with serum levels of valproic acid in the usual therapeutic range. Two patients underwent exploratory laparotomy prior to diagnosis. Complications included pseudocyst, pericardial effusion, laparotomy wound infection, and coagulopathy. All patients recovered with discontinuation of valproic acid therapy and enteral feeding and administration of intravenous fluids. After recovery, a valproic acid regimen was restarted uneventfully (in one patient). All were asymptomatic with normal serum amylase levels after five to 14 months. Pancreatitis is a serious complication of valproic acid therapy that must be considered in any patient receiving valproic acid who experiences severe abdominal pain and vomiting.
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PMID:Pancreatitis associated with valproic acid therapy. 620 16

In a survey of 15,272 canine necropsies, natural infection with Mycobacterium tuberculosis was found to have been diagnosed in eight dogs (0.05%). Clinical findings were anorexia, loss of body weight, lethargy, vomiting, and leukocytosis; radiography revealed pleural and pericardial effusion, ascites, and hepatomegaly. Granulomatous lesions with acid-fast bacilli were consistently found. Mycobacterium tuberculosis was isolated from lesions in the lungs, liver, or lymph nodes of five dogs. All eight dogs had a history of contact with human patients with tuberculosis.
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PMID:Canine tuberculosis. 742 50

The medical records of five dogs diagnosed with infectious pericardial effusion were reviewed. Clinical signs included anorexia, depression, respiratory distress, abdominal distension, collapse, coughing, and vomiting. Anemia and leukocytosis were present in three dogs. Grass awn migration was confirmed as the cause of the pericardial effusion in two dogs and suspected in the other three. Surgery, followed by continuous chest drainage, and appropriate antibiotic therapy was the treatment in four dogs. Chest drains were removed within 4 days of surgery. One dog did not have chest drainage after surgery. Antibiotic treatment was continued for up to 6 months. The dogs were monitored postsurgically for a period ranging from 3 to 24 months. All dogs recovered well without apparent complications.
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PMID:Infectious pericardial effusion in five dogs. 858 48

Pericarditis is a frequent and serious complication of chronic uremia. The uremic pericarditis can get much improvement by aggressive heparin-free hemodialysis therapy. However, the presenting symptoms and signs are too nonspecific to identify at early stage. Cardiac tamponade is the late and fatal complication, and need the immediate & adequate management. A 35-year-old female patient suffered from nausea, vomiting and right upper quadrant dull pain in November 1993, and was admitted to a local hospital. Uremia (BUN: 210 mg/dl, serum Cr.: 13.2 mg/dl) and abnormal liver function (SGOT: 330 IU/L, SGPT: 449 IU/L) were found, then she received regular hemodialysis therapy. About 10 days later, acute exacerbation of liver function (SGOT: 2,488 IU/L, SGPT: 1,048 IU/L), consciousness disturbance and hypotension occurred during hemodialysis. She was referred to our ER immediately. At ER, she had been on comatous, shock state with pulseless electric activity. After resuscitation and serial evaluation, cardiac tamponade was diagnosed. Emergent pericardiocentesis and then bilateral partial pericardiectomy were done about 2 hours later. The pericardial effusion was bloody without evidence of malignancy, bacterial or TB infection. The pathology of pericardium revealed chronic inflammation only. HBsAg, Anti-HCV Ab, and anti-HAV IgM were undetectable. So the etiology of acute hepatitis was diagnosed as ischemic hepatitis. Her general condition and vital sign became stable thereafter. The liver function also improved rapidly. She was discharged one month later and received maintainance hemodialysis therapy and no evidence of recurrence till now.
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PMID:[Acute uremic pericarditis presented as cardiac tamponade with acute ischemic hepatitis: a case report]. 904 74

A 74 year old man with chronic dysphagia acutely developed nausea, vomiting and fever, followed by abrupt, fatal brainstem stroke. Autopsy revealed an esophagoatrial fistula with multiple food emboli to visceral and cerebral arteries. Review of previous cases indicates that new onset atrial fibrillation or pericardial effusion in patients with chronic esophageal symptoms may herald fistula formation. Early recognition of such fistulas may provide an opportunity to intervene before catastrophic embolization or gastrointestinal hemorrhaging occurs.
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PMID:Food embolus. 917 28

Chronic hepatitis associated with hypereosinophilia has been very rarely reported worldwide. A 7-month-old male infant presented with a high fever, cough, non-projectile vomiting and hepatomegaly. The eosinophil count of the peripheral blood increased up to 21,500/mm3 (49% of WBC). The infant had a history of frequent contact with a neighbor keeping a pigsty. The pathologic examinations of the liver showed severe porto-periportal necroinflammation with marked eosinophilic infiltration, giant cell transformation and ballooning degeneration of hepatocytes, and degranulation of the eosinophils. Bone marrow showed increased eosinophils and decreased myeloid series. Pericardial effusion and bilateral pulmonary consolidation were noted. Corticosteroid aggravated the clinical symptoms of the infant. Anthelmintic treatment significantly normalized the eosinophil count and liver function tests, but cardiopulmonary manifestations continued.
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PMID:Eosinophil-induced chronic hepatitis. 961 Jun 27

Carbohydrate-deficient glycoprotein syndrome type 1 (CDGS-1) is an autosomal recessive hereditary metabolic disorder, the gene locus of which is chromosome 16p13. The disorder is characterised by genetic heterogeneity, and by decrease in the gene product, phosphomannomutase 2, though the heterogeneity is far less manifest in affected Swedish families. Its incidence is 1/80,000 live births, and the under-5 mortality rate over 30 per cent. The causes of death are liver failure, cardiac tamponade, haemorrhaging, and severe infection. The characteristic biochemical aberration is the occurrence of deficient carbohydrate chains in many but not all circulating glycoproteins, and the serum and blood concentrations of some glycoproteins may be above or below normal. These changes may improve over time, but never normalise. The clinical picture is generally more problematic during the first years of life when psychomotor retardation is complicated by failure to thrive, liver dysfunction, pericardial effusions, and stroke-like episodes. In addition, strabismus, lipocutaneous anomalies, and gluteal fat pads are always present, and muscular hypotonia and restricted joint mobility are common. Failure to thrive is common, with vomiting and diarrhoea and subsequent slow growth. Inflammation is a constant finding in the liver, and very common in the small bowel. Pancreatic function is also affected. Pericardial effusion has been reported in 50 per cent of the youngest children, requiring pericardectomy in 30 per cent of cases. Haemorrhaging and thromboembolic complications may occur, and the serum concentrations of several factors and inhibitors are low, particularly those of factors V and XI, protein C and antithrombin. Stroke-like episodes occur in about 30 per cent of cases, often following an infection, with coma lasting for hours to several days. Such sequelae as hemiplegia, blindness, and other focal neurological pathology have been observed transiently. Diagnosis is based on the serum carbohydrate-deficient transferrin level, verified by isoelectric focusing. Molecular genetic procedures enable point mutations to be identified and prenatal diagnosis to be performed in many families.
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PMID:[CDGS-1--a recently discovered hereditary metabolic disease. Multiple organ manifestations, incidence 1/80,000, difficult to treat]. 988 93

Cardiac toxicities in 39 consecutive patients with breast cancer receiving high-dose chemotherapy (HDC) with stem cell transplantation were reviewed. All 39 patients received various anthracycline-containing regimens in adjuvant settings and/or for metastatic disease before HDC. As a cytoreductive regimen, all received cyclophosphamide 2000 mg/m2 and thiotepa 200 mg/m2 for 3 consecutive days. No immediate fatal toxicities were observed, but one patient developed chronic congestive heart failure and two had transient left ventricular dysfunction. Pericardial effusion was observed in another three patients. ST-T abnormalities during HDC were observed in two patients and arrhythmias were observed in nine, four of which occurred during stem cell infusion (SCI). There were three atrial arrhythmias, two ventricular arrhythmias, and four atrioventricular (AV)-block episodes. Two patients developed advanced and complete AV-block with an asystolic pause. Notably, three patients experienced AV-block with uncontrolled vomiting. No relationship was observed between the cumulative dose of anthracycline and cardiac toxicities during HDC. These results suggest that abnormalities in the conduction system during HDC may be more frequent than previously reported. Vagal reflex secondary to emesis may play an important role in the development of AV-block. Bone Marrow Transplantation (2000) 25, 185-189.
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PMID:Cardiac conduction abnormalities in patients with breast cancer undergoing high-dose chemotherapy and stem cell transplantation. 1067 78


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