Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A seven-month-old girl was admitted to the Pediatrics Department of Mackay Memorial Hospital with the following symptoms and signs: (1) high fever for more than five days; (2) injection of bilateral conjunctiva; (3) bright red lips with strawberry tongue; (4) edematous change of palms and soles, followed by digit desquamation; (5) an ill-defined, erythematous plaque on the scar of the BCG. Kawasaki disease was diagnosed, and high dose aspirin (100 mg/kg/day) and intravenous gamma-globulin (IVIG) (400 mg/kg/day) were given for four days. The patient was afebrile on the second day after IVIG infusion, and was discharged six days after admission. A small single daily dose of aspirin (10 mg/kg/day) was given after the afebrile days. Unfortunately, vomiting and consciousness disturbance were noted one day after discharge. Laboratory data showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT) and ammonia. Hypoglycemia and prolonged PT and PTT were also noted. Reye syndrome was suspected, and the patient was admitted to the intensive care unit for further management. A liver biopsy gave findings consistent with Reye syndrome. In spite of intensive treatment, the infant expired on the second day after admission. In a review of the literature, no correlation between these two syndromes was found. This rare case is presented to warn that Reye syndrome may follow Kawasaki disease when aspirin has been prescribed at a high dose.
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PMID:Kawasaki disease with Reye syndrome: report of one case. 162 54

Aspirin is commonly used as an anti-inflammatory therapy for Kawasaki syndrome. Early initiation with high dose aspirin (80 to > 100 mg/kg per day), followed by low-dose therapy at the afebrile stage, has been often used to reduce morbidity and mortality in coronary complications. We report a 10-month-old infant who was diagnosed with Kawasaki syndrome. Sudden onset of poor activity, poor appetite, lethargy, tachycardia, tachypnea, hepatomegaly, increased AST/ALT, coagulopathy and hyperammonemia developed 3 days after the high-dose aspirin therapy. His histopathological and ultrastructural findings from the liver biopsy were compatible with Reye's syndrome. He recovered completely, and there was no recurrence.
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PMID:Reye's syndrome developing in an infant on treatment of Kawasaki syndrome. 1595 35

Clinical, laboratory, and echocardiographic data were retrospectively analyzed in 112 patients with acute Kawasaki disease who received high-dose (2 g/kg) intravenous gamma-globulin (IVIG) treatment within 2 days and were compared for those who were responsive and non-responsive to initial IVIG treatment. Coronary arteries adjusted for body surface area (BSA) were evaluated quantitatively by comparison with the mean dimensions for 85 normal control subjects. The incidence of coronary abnormalities was higher in IVIG-non-responsive patients as compared to IVIG-responsive patients (71% versus 5%, p<0.0001). Univariate analysis of pre-IVIG data showed that the neutrophil count and serum levels of C-reactive protein (CRP), total bilirubin (TB), aspartate aminotransferase (AST), alanine aminotransferase, and lactate dehydrogenase (LDH) were significantly higher in IVIG-non-responsive versus responsive patients. Multivariate analysis selected CRP (p=0.009), TB (p<0.001), and AST (p=0.002) as independent predictors of non-responsiveness to initial IVIG treatment. By defining predictive values, patients with at least two of three predictors (CRP>or=7.0 mg, TB>or=0.9 mg, or AST>or=200 IU/L) are considered to be non-responsive to IVIG for acute Kawasaki disease. Alternatively, more intense initial therapy may be a promising therapeutic strategy for patients who are predicted to be IVIG-non-responsive.
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PMID:Prediction of non-responsiveness to standard high-dose gamma-globulin therapy in patients with acute Kawasaki disease before starting initial treatment. 1689 41

Clinical characteristics to predict the development of coronary artery abnormalities (CAA) in Kawasaki disease (KD) were assessed by reviewing medical records of patients diagnosed with KD at Korea University Medical Center from March 2001 to February 2005. Of the 285 patients diagnosed with KD, 19 developed CAA (6.7%). Compared with the CAA(-) group, the CAA(+) group had a longer duration of fever after intravenous gamma-globulin (IVGG) injection (2.4+/-2.9 vs. 1.5+/-1.2 days, p=0.008) and higher C-reactive protein (CRP)(12.3+/-7.8 vs. 8.7+/-7.1 mg/dL, p=0.038). In particular, the CAA(+) group tended to have more than 7 days of fever before IVGG and more than 3 days of fever after IVGG (26.3 vs. 5.3%, p<0.001; 26.3 vs. 6.4%, p=0.002). When the IVGG responsiveness was defined by the presence of defervescence within 3 days after IVGG, IVGG-non-responders showed a higher incidence of CAA (22.7 vs. 5.3%, p=0.002). Non-responders had a longer duration of fever after IVGG (5.5+/-1.9 vs. 1.2+/-0.6 days, p<0.001) and a significantly increased CRP, AST, ALT and total bilirubin. Multivariate regression analysis for CAA showed that the only factor significantly associated with the development of CAA was total fever that lasted for longer than 8 days (OR=4.052, 95% CI=1.151-14.263, p=0.0293). Conclusively, the most important predictor of CAA in KD is total duration of fever longer than 8 days. Early identification of IVGG non-responders and active therapeutic intervention for fever in KD cases might decrease the incidence of CAA.
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PMID:Predictive risk factors for coronary artery abnormalities in Kawasaki disease. 1703 7

Approximately 15-20% of patients with Kawasaki disease (KD) are not responsive to high-dose intravenous gammaglobulin (IVIG). We have previously reported a predictive method for identifying IVIG-non-responsive patients (high-risk KD patients). We determined the safety and effectiveness of pulse methylprednisolone with high-dose IVIG (mPSL+IVIG) as a primary treatment for high-risk KD patients. Sixty-two high-risk KD patients were treated with pulse methylprednisolone 30 mg/kg over 2 h, followed by IVIG 2 g/kg over 24 h (mPSL+IVIG group) and were compared with a historical control group of 32 high-risk patients treated with IVIG 2 g/kg alone at the participating hospitals before this study was opened (IVIG group). High-risk patients were identified with at least two of three predictors (C-reactive protein >or=7 mg/dL, total bilirubin >or=0.9 mg/dL or aspartate aminotransferase >or=200 IU/L). Sixty-six percent (95% confidence interval [CI] 54-78%) of patients had a prompt defervescence in the mPSL+IVIG group compared with 44% (95% CI 26-62%) for the IVIG group (p=0.048). Coronary artery lesions were observed in 24.2% (95% CI 13.2-35.2%) and 46.9% (95% CI 28.6-65.2%) of patients in the mPSL+IVIG and IVIG groups, respectively (p=0.025). This is the first report showing that mPSL+IVIG is effective and safe as a primary treatment for high-risk KD patients.
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PMID:Pulse methylprednisolone with gammaglobulin as an initial treatment for acute Kawasaki disease. 1844 65

The aims of this study were to determine the occurrence and variables associated with the initial intravenous immunoglobulin (IVIG) treatment failure in Kawasaki disease (KD) and to categorize differences in clinical characteristics between responders and nonresponders to initial IVIG treatment. Patients were classified into two groups. Group A included 33 patients who received a single dose of IVIG treatment and responded. Group B included 18 patients who received more than two doses of IVIG due to failure of the initial treatment. The mean duration of fever after initial treatment in group B was significantly longer than it was in group A. In group B, we found that higher bilirubin, aspartate aminotransferase (AST), polymorphonuclear cells (PMN) (%), and lower platelet values at baseline were independent predictors of persistent or recurrent fever in patients with KD. Coronary artery abnormalities were found in 8 patients (44.4%) in group B and in two patients (6.1%) in group A. We found that abnormal liver function tests and a lower platelet count at baseline were possible predictors of nonresponders to IVIG in patients with KD. There is a need for a prospective study focused on baseline hepatobiliary parameters.
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PMID:Risk factors for failure of initial intravenous immunoglobulin treatment in Kawasaki disease. 1875 64

We examined the serum values of high mobility group box 1 (HMGB1) in 36 patients with Kawasaki syndrome (KS) (29 responders and 7 poor-responders to initial intravenous immunoglobulin treatment). A mean value of HMGB1 of poor-responders was significantly elevated compared with those of responders (P = 0.0042). Among the 6 factors showing significant differences between responders and poor-responders including HMGB1 (admission illness day, white blood cell counts, C-reactive protein, aspartate aminotransferase, lactate dehydrogenase), values of HMGB1 showed the widest area under the receiver operating characteristic curve. In conclusion, an elevated HMGB1 value could be a potential marker for poor-responders.
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PMID:An elevated value of high mobility group box 1 is a potential marker for poor response to high-dose of intravenous immunoglobulin treatment in patients with Kawasaki syndrome. 1923 12

A 9-year-old girl developing fever and hyperemia of both bulbar conjunctiva 5 days before admission to the Saitama Children's Medical Center after antibiotics proved ineffective was found on admission to have general fatigue and a temperature of 39 degrees C. Physical examination showed hyperemia of the bulbar conjunctiva, fissures of the lips, redness of the pharynx, and swelling of the cervical lymph nodes. Laboratory tests detected neutrophilia (11,200/microL), mild anemia (11.4g/dL), thrombocytopenia (110,000/microL), and elevated serum aspartate aminotransferase (242IU/L), alanine aminotransferase (328IU/L), and C-rective protein (25.2 mg/dL). Autoantibodies such as anti-nuclear, anti-SS-A/Ro, and anti-Jo-1 were also found. Echocardiography showed no abnormality of the coronary arteries. She was diagnosed as having incomplete Kawasaki disease on day 7 of illness, necessitating that a high dose of immunoglobulin be given intravenously. Her temperature dropped temporarily to 37 degrees C, but she developed erythema of the cheek and fever. Intravenous immunoglobulin was restarted, and minocycline introduced because her daily contact with a pet cat indicated richettsial infection such as Q fever. Mild fever, muscle pain, and elevated C-reactive protein did not improve, but clinical signs and symptoms gradually lessened after ibuprofen was given, then disappeared. A definitive diagnosis of Q fever was made through an over 4-fold rise in phase II IgG antibody titers against Coxiella burnetii, titer of less than 1 : 16 on day 14 of illness, and titer of 1 : 256 on day 34. This case study describes on atypical case of Q fever with clinical manifestations mimicking Kawasaki disease.
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PMID:[A case report of acute Q fever showing Kawasaki disease-like symptoms in a 9-year-old girl]. 1952 8

It is difficult to predict the prognosis or clinical course of secondary hemophagocytic lymphohistiocytosis (HLH) due to the various underlying causes. The authors analyzed the clinical and laboratory findings and outcomes in patients with HLH who had initially been diagnosed with Kawasaki disease (KD), and evaluated the clinical significance of each factor. Among the 21 patients with HLH, 5 had initially been diagnosed with KD and 16 had other etiologies. A comparative analysis was performed for fever duration, presence of cytopenia, serum ferritin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride, fibrinogen, hyponatremia, reactivation, and survival rate in those HLH patients associated with KD (group I) and other causes (group II). In patients in group I, a higher level of reactivation (20%), a lower survival rate (P = .001), higher AST (P = .031) and ferritin (P = .005), and frequent hyponatremia (P = .000) were found compared to patients in group II. Interestingly, patients in group I was older than the average of age of most KD patients. A high index of suspicion on the progression from KD to HLH would be mandatory when the KD patients show elevated AST and ferritin and the presence of hyponatremia, and especially so if the patient is of older age.
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PMID:Clinical characteristics of hemophagocytic lymphohistiocytosis related to Kawasaki disease. 2138 68

Tuberculosis has now become a curable disease with chemotherapy. So it is natural that the present issues in tuberculosis management are focused on how to complete standard chemotherapy. In this context, management of adverse effects constitutes an essential part of antituberculosis chemotherapy, as well as directly observed therapy. In this symposium, discussions were held about three major subjects on this issue. First, hepatotoxicity develops frequently and has sometimes fatal outcome, which makes it the most problematic adverse effect. "Management of hepatotoxicity during antituberculosis chemotherapy" was published by the Japanese Society for Tuberculosis (JST) in 2006. Dr. Shinsho Yoshiba evaluated this recommendation and pointed out that the criteria for discontinuation of drug based on AST, ALT and bilirubin levels is too sensitive and the concept of predicting fulminant hepatic failure (FHF) is lacking. He stressed the importance of monitoring serum prothrombin time for predicting FHF. Next, allergic drug reaction such as fever or skin rash often causes distress, although rarely fatal. As isoniazid (INH) and rifampicin (RFP) are key drugs for the cure, readministration of these drugs is often attempted by desensitization therapy. "Recommendation about desensitization therapy of antituberculosis drugs" was also published by JST in 1997. Dr. Yoshihiro Kobashi reported high success rates of 79 percent for INH and 75 percent for RFP according to this recommendation. He also reported correlated factor with the success, such as the longer period from the discontinuation to the desensitization therapy and lower doses of drugs at starting desensitization. Finally, we sometimes experience transient worsening of radiographical findings and general symptoms during antituberculosis chemotherapy. This is presumed to be due to allergic reaction to dead bacilli without requiring discontinuation of the drug. Differential diagnosis includes drug-induced pneumonia requring discontinuation and true worsening of pulmonary tuberculosis due to drug resistance requiring change in therapy. Dr. Masanori Akira reported that presence of ground-glass attenuation and/or consolidation by HRCT suggests transient worsening or drug-induced pneumonia, whereas presence of centrilobular nodules and/or tree-in bud suggests true worsening. We believe that these findings from the symposium will add useful information for management of adverse effects and be helpful for implementation of antituberculosis chemotherapy. (1) Hepatotoxicity of antituberculosis drugs: Shinsho YOSHIBA (Sempo Tokyo Takanawa Hospital) Antituberculosis drugs are sometimes hepatotoxic. Doctors who are responsible for the treatment of patients with tuberculosis should always be aware of their hepatotoxicity, because it seldom leads to fulminant hepatic failure. The Japanese Society for Tuberculosis proposed criteria based on the levels of AST, ALT and bilirubin for the prevention of such grave hepatic injury in 2006. In recent years attempts have been made to predict fulminant hepatic failure (FHF) before patients develop coma. Yoshiba's formula using prothrombin time, etiology, cholinesterase and bilirubin is widely accepted as useful to predict FHF. Introduction of the formula to this area is recommended. (2) Desensitization therapy for allergic reactions of antituberculous drugs: Yoshihiro KOBASHI, Mikio OKA (Division of Respiratory Diseases, Department of Medicine, Kawasaki Medical School) We evaluated the usefulness of desensitization therapy for patients showing allergic reactions of INH and RFP according to the guideline proposed by the Japanese Society for Tuberculosis. Adverse reactions were 22 patients with drug eruption, 22 with drug fever and 6 with drug fever plus eruption. The clinical effect of desensitization therapy was good in 27 out of 36 patients for RFP (75%), and in 19 out of 24 patients for INH (79%). The comparative study between patient group with success desensitization therapy and that with failure desensitization therapy was not a significant difference except for initiation period of desensitization therapy. (3) The imaging features of early transient radiographic progression, true worsening of TB, and drug induced pneumonitis during TB treatment: Masanori AKIRA (Department of Radiology, NHO Kinki-chuo Chest Medical Center) HRCT findings of the new lesions in the early transient radiographic progression are enlargement or confluence of the original lesions, development of areas of ground-glass attenuation and/or consolidation ipsilateral to the original lesion, and development of areas of ground-glass attenuation and/or consolidation in the subpleural region contralateral to the lesion. These CT findings may suggest a local hypersensitivity reaction to drug or massive dead tubercle bacilli per se. In contrast, CT findings of patients with multiple drug-resistant tuberculosis and true progression are centrilobular nodules, tree-in-bud appearance, nodules, and cavitation. These CT findings may suggest a bronchogenic spread from the original tuberculous lesions.
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PMID:[Management of adverse effects with antituberculosis chemotherapy]. 2140 53


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