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 Phase I clinical trial was performed on patients with solid tumors refractory to conventional therapy. Crotoxin was administered i.m. for 30 consecutive days at doses ranging from 0.03 to 0.22 mg/m(2). Patients entered the study after providing a written informed consent. Although 26 patients were entered only 23 were evaluated. Reversible, nonlimiting neuromuscular toxicity evidenced as diplopia because of pareses of the external ocular muscles was present in 13 patients. It started at doses of 0.18 mg/m(2) and lasted from 2 to 6 h. These episodes did not require dose adjustment and disappeared in 1-3 weeks of treatment. Three patients experienced palpebral ptosis, nystagmus (grade 2), and anxiety (grade 2-3) at the dose-limiting toxicity of 0.22 mg/m(2). Also at dose-limiting toxicity, 1 patient showed nystagmus (grade 2) and anxiety (grade 3) without evidence of palpebral ptosis. Transient increases (grades 1-3) in the levels of creatinine kinase, aspartate aminotransferase, and alanine transaminase attributed to crotoxin myotoxicity were observed but returned to normal by the last week of treatment. At 0.21 mg/m(2) there was a case of grade-3 anaphylactic reaction on day 31, which required treatment. Hypersensitivity was regarded as an adverse drug-related reaction, and the patient was removed from the protocol. Two patients at different doses (0.12 mg/m(2) and 0.22 mg/m(2)) had sialorrhea. Four patients had asymptomatic transient increase in blood pressure (up to 20 mm Hg) 12 h after the first injection, which lasted 24 h. No treatment was required and toxicity did not reappear. Six patients experienced slight eosinophilia during the first 2 weeks. The maximum tolerated dose was set at 0.21 mg/m(2). Objective measurable partial responses (>50% reduction of tumor mass) were noted in 2 patients treated at 0.21 mg/m(2) and 1 at 0.12 mg/m(2). One patient (at 0.21 mg/m(2)) presented a complete response on day 110. Crotoxin pharmacokinetics showed rapid absorption from the injection site to blood (t(1/2 A) = 5.2 +/- 0.6 min). Plasma concentration reached a peak (C(max) = 0.79 +/- 0.1 ng/ml) at tau(max) = 19 +/- 3 min. The half-life of the distribution (alpha) phase is 22 +/- 2 min. Starting at 1.5 h after injection, the decrease in plasma concentration becomes slower, reaching 14 +/- 3 pg/ml 24 h after injection. The profile is dominated by the elimination (beta) phase with a half-life of 5.2 +/- 0.6 h. Consequently, 24 h after the injection ( approximately 5 half-life) 97% of the product was eliminated. The area under plasma concentration versus time curve was 0.19 +/- 0.05 microg/min/ml. Assuming availability (F) approximately 1, the clearance is C(L) = 26.3 +/- 7 ml/min, and the apparent volume of distribution is V(d) = 12 +/- 3 liter/kg. The recommended dose for a Phase II study is 0.18 mg/m(2).
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PMID:Phase I and pharmacokinetics study of crotoxin (cytotoxic PLA(2), NSC-624244) in patients with advanced cancer. 1194 10

Serum chemistry values and complete blood counts were determined for 36 wild dusky-footed wood rats (Neotoma fuscipes) from Sonoma and western Yolo County, California (USA) in summer 1999 and spring 2001. All wood rats had adequate body condition and were hydrated. Many hematologic and biochemical values were comparable to those for house rat (Rattus rattus). There were differences between wood rats tested immediately after capture (those from Yolo County) and after a week of habituation in the laboratory (Sonoma County). Significant differences were noted in red blood cell counts, hemoglobin, hematocrit, neutrophil:lymphocyte ratio, glucose, alanine transaminase, aspartate aminotransferase, and alkaline phosphatase values. The neutrophil:lymphocyte ratio may have been iatrogenically modified in the wood rats tested immediately after capture by stress-induced neutrophilia and lymphopenia. Eosinophilia may have been associated with parasites such as botflies in four individuals, and hyperglycemia in three individuals could have been associated with stress. The cause of elevated enzymes in the animals tested after laboratory habituation is unclear. The hematologic and biochemical values of these apparently healthy wood rats provide valuable baseline information for use in further medical studies performed with this species.
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PMID:Hematology and serum biochemistry values of dusky-footed wood rat (Neotoma fuscipes). 1223 75

We experienced 4 cases of agranulocytosis due to anti-tuberculosis drugs (rifampicin [RFP], isoniazid [INH], ethambutol [EB], streptomycin [SM] or pyrazinamide [PZA]) among some 6,400 tuberculosis patients who underwent chemotherapy over the past 20 years from 1981 to 2002 in our hospital, and the incidence rate of agranulocytosis was estimated at 0.06%. The 4 cases of agranulocytosis were as follows. CASE 1: A 51-year-old woman with right chest pain and fever was admitted to our hospital on Jan 4, 2001. The white blood cell (WBC) count was 5,200/microliter. The tubercle bacilli were cultured in her sputum. The treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, allopurinol and teprenone was started on Jan 13. Pyrazinamide and allopurinol were stopped because of hyper-uric acidemia on Feb 7. Agranulocytosis and eosinophilia (WBC 1,300 [Neut 1%, Ly 57%, Eos 35%]) developed on Feb 13. All drugs were withdrawn and G-CSF drug nartograstim 100 micrograms was injected subcutaneously for 3 days. The WBC recovered to normal level and she was thereafter treated with INH, EB and Levofloxacin (LVFX) without any further trouble. Agranulocytosis in this case was supposed to be due to RFP. CASE 2: A 66-year-old man who had had nephrotic syndrome and hypothyroidism and has been treated with prednisolone 10 mg/day was admitted to our hospital on Aug 9, 2000 because of miliary tuberculosis. The tubercle bacilli were cultured in his sputum and the treatment with INH 0.3, RFP 0.45, and EB 0.75 g/day were started on Aug 10, but it was withdrawn on Aug 17 because of general skin eruption. After re-starting treatment with EB and INH on Aug 24, RFP was added in small dosage (0.05 g) on Oct 12, but agranulomatosis (WBC 2,300/microliter [Neut 2%]) developed on Nov 21, and all drugs were withdrawn again. The G-CSF drug filgrastim was used once subcutaneously, and WBC recovered immediately. He was thereafter treated with INH, EB, LVFX successfully. Agranulocytosis was supposed to be due to RFP. CASE 3: A 60-year-old woman without symptoms had abnormal chest roentgenograph, and consulted with our hospital on Aug 26, 2002. The broncho-alveolar lavage fluid was smear and culture-negative, but PCR-TB positive, and the case was diagnosed as pulmonary tuberculosis. Treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, alloprinol 300 mg and rebamipide 300 mg/day was started on Sept. 5, 2002. Late in September, she complained of appetite loss. The laboratory data on Oct 3 revealed WBC 900/microliter (Neut 1%, Ly 94%), aspartate aminotransferase (AST) 199 IU/l, and alanine aminotransferase (ALT) 253 IU/l, showing agranulocytosis and drug-induced hepatitis. The chemotherapy was immediately withdrawn and she was admitted to our hospital on the next day. Glycyrrhizin derivative (SNMC) 40 ml was injected for 5 days, and WBC recovered, and AST and ALT also became normal. CASE 4: A 60-year-old man was admitted to our hospital on March 11, 1981 because pulmonary tuberculosis had recurred. He had been treated with SM, PAS and INH in 1973 for pulmonary tuberculosis. On admission examination of blood count and blood chemistry were normal. Treatment with RFP, INH and SM was started on March 11. He stopped out from the hospital on April 17, but in a few days he returned back with sore throat, lower lip swelling and gingival bleeding. Blood cell count on April 24 showed pancytopenia with RBC 226, Hb 7.5, WBC 800 (Ly 96%, Eos 4%) and Plt 10,000/microliter. The bone-marrow showed NCC (nuceated cell count) of 5,500, and megakaryocyte 0. Thereafter ground glass appearance shadows were seen on the whole lung field, and he died May 26. Autopsy showed generalized aspergillosis. It was strongly suspected that either of RFP, INH or SM was responsible for his pancytopenia. We collected another 10 cases of agranulocytosis due to anti-tuberculosis drugs in the world wide literature, and found men/women ratio 5/8 (in one case gender was not known), the duration of chemotherapy before appearance of agranulocytosis 1-3 months, no change in the lymphocyte count of the peripheral blood, and the accompanying of another allergic signs such as skin eruption, blood eosinophilia or drug-induced hepatitis in some cases, and these findings suggest that the mechanism of agranulocytosis due to anti-tuberculosis drugs was allergic in nature.
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PMID:[Agranulocytosis due to anti-tuberculosis drugs including isoniazid (INH) and rifampicin (RFP)--a report of four cases and review of the literature]. 1467 45

SM-11355, a lipophilic platinum derivative, is a novel intra-arterial chemotherapeutic agent for hepatocellular carcinoma (HCC). A phase II study of SM-11355 was conducted to evaluate the antitumor activities and the toxicity in chemotherapy-naive patients with HCC. Sixteen patients were treated with transcatheter arterial injection of SM-11355-lipiodol emulsion (20-120 mg/body). The responses were evaluated by computed tomography 3 months after treatment. Complete response (CR) was defined as disappearance or 100% necrosis of all tumors, and lipiodol accumulation in tumors was regarded as indicating necrosis. Nine patients achieved CR (56%; 95% confidence interval, 29.9-80.2%). The grade 3 toxicities were neutropenia (19%), total bilirubin elevation (19%), AST elevation (44%), and ALT elevation (19%). None of the patients showed grade 4 toxicities or episodes of renal dysfunction. Other common adverse effects were eosinophilia (100%) and pyrexia (94%). Intra-arterial chemotherapy with SM-11355, which was well tolerated, showed promising antitumor activity in patients with HCC.
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PMID:Phase II trial of intra-arterial chemotherapy using a novel lipophilic platinum derivative (SM-11355) in patients with hepatocellular carcinoma. 1473 65

Epidemiological, clinical and laboratory data were collected during an outbreak of trichinellosis, which occurred in Izmir, Turkey, between January and March 2004. The source of the infection was raw meatballs made with a mixture of uncooked beef and pork. Of 474 persons who were admitted at the Ataturk Training and Research Hospital during this period with a history of raw meatball consumption, the diagnosis of trichinellosis was confirmed for 154 (32.5%, 87 males and 67 females; mean age 31 years, range 6-67 years). Among persons with a confirmed diagnosis, 79% had myalgia, 77% weakness and malaise, 63% arthralgia, 40% jaw pain, 68% fever, 63% periorbital and/or facial oedema, 49% oedema at the trunk and limb, 42% abdominal pain, 40% nausea and vomiting, 28% diarrhoea, 23% subconjunctival haemorrhage, 25% macular or petechial rash, 4% subungual haemorrhage, 15% cardiac complaints and 0.2% neurological complaints. Nine patients (5.8%) were hospitalised due to severe myalgia (n = 2), high fever (n = 3), neurological manifestations (n = 1), thrombophlebitis (n = 2) and palmar erythema (n = 1). Eosinophilia was present in 88% of the confirmed cases at the admission. Elevated levels of serum creatine phosphokinase, lactic dehydrogenase and aspartate aminotransferase were detected in 72%, 70% and 16% of the confirmed cases, respectively. The seroconversion occurred in most of the infected people between the 4th and 6th weeks after the infection. All of the confirmed cases were treated with mebendazole. People with severe symptoms were treated also with prednisolone (60 mg/day for three days) and those with a moderately severe clinical pattern received a non-steroid anti-inflammatory drug (naproxen sodium, 550 mg/day). All confirmed cases recovered without any clinical sequela.
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PMID:Clinical and laboratory aspects of a trichinellosis outbreak in Izmir, Turkey. 1660 69

A 3-month-old male Golden Retriever puppy was evaluated for lethargy and fever of 2-days duration. Results of a CBC and biochemical profile revealed marked eosinophilia (6.3 X 10(3)/microL; reference interval 0.1-1.2 X 10(3)/microL), moderate thrombocytopenia, and increased activities of alanine aminotransferase, aspartate aminotransferase, and creatine kinase. Hepatomegaly and peritoneal effusion were found using abdominal ultrasound. Peritoneal fluid analysis revealed eosinophilic inflammation (23,000 nucleated cells/microL with 88% eosinophils). Despite supportive treatment the puppy's condition deteriorated rapidly; euthanasia was requested, and a necropsy performed. Microscopically, there was marked necrosuppurative and eosinophilic hepatitis with vasculitis. Numerous hepatocytes contained protozoal organisms suspected to be Toxoplasma gondii or Neospora caninum. However, serum was negative for both T gondii and N caninum antibodies; polymerase chain reaction assay on hepatic tissue was negative for both organisms; and immunohistochemical evaluation of hepatic tissue using serum raised against T gondii, N caninum, and Sarcocystis neurona also was negative. Schizont morphology suggested that merozoites replicated by endopolygeny, forming rosettes around a central residual body. Transmission electron microscopy revealed that merozoites lacked rhoptries. These findings were consistent with a diagnosis of Sarcocystis canis, an apicomplexan parasite with an unknown life cycle.
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PMID:Fatal hepatic sarcocystosis in a puppy with eosinophilia and eosinophilic peritoneal effusion. 1696 26

Heartworm disease, caused by the filarial nematode, Dirofilaria immitis, is a major, potentially life-threatening disease of dogs, with worldwide distribution and global significance. It is not only of veterinary importance but it also has zoonotic potential in many regions. It is considered as an endemic disease in Thailand, although clinical data about the disease is rarely reported. The objectives of this study were to characterize the clinical hematology and the biochemistry of canine dirofilariasis cases admitted to Chulalongkorn University, Small Animal Teaching Hospital in Bangkok, Thailand, from 2001-2003. All hematology and serum biochemistry parameter interpretations were based on reference values. A total of 1023 dogs were evaluated in this study. Dogs were divided into three groups based on their heartworm classification (microfilaremic, occult and negative). The major hematological findings in microfilaremic dogs were a mild to moderate anemia, mild to severe thrombocytopenia, marked leukocytosis, moderate to marked neutrophilia, eosinophilia and monocytosis. The most common serum biochemical abnormalities in microfilaremic dogs included increased alkaline phosphatase, alanine aminotransferase and aspartate aminotransferase with a mean+/-SD of 311+/-299, 82+/-76 and 50+/-38 IU/L, respectively. It is likely that this parasitic infection led to the impairment of the hematological and biochemical status of the infected dogs. We believe that investigation of these laboratory based parameters, when associated with the clinical signs, is a very important approach to be considered in the routine clinical follow up, as well as being important for therapeutic evaluations.
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PMID:A retrospective study of the clinical hematology and the serum biochemistry tests made on canine dirofilariasis cases in an animal hospital population in Bangkok, Thailand. 1709 27

Zoonotic fascioliasis is a problem not only in Dakahlia Governorate, but also in other Egyptian Governorates. Two hundreds & twenty patients randomly selected with suggesting manifestations were examined for fascioliasis. A total of 23 (10.4%) were positive by Kato thick smears, of which 21 were from Kafr El-Hessah and two from Oweish El-Hager. The proven human fascioliasis was examined for anti-Fasciola antibodies by IHAT & ELISA (Fhes), haemoglobin level, eosinophils percent, serum bilirubin & liver function tests. IHAT gave 82.61% positive results (19/23), and ELISA gave 100% positive results (23/23). The clinical signs ranged between splenomegaly & ascitis in 4.34% for each up to hepatomegaly in 73.91% & mild fever in 78.26% but 2 cases were asymptomatic. Mild eosinophilia and moderate anaemia were recorded with means of 11 +/- 5.8 and 10 +/- 1.3 respectively. Mean serum bilirubin was not elevated (0.91 +/- 0.51 gm/dl). Liver function tests (AST within normal range in all cases; <40 unit/ml but one patient had ALT above normal; >45 unit/ml).
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PMID:Risk factors contributing to fascioliasis endemicity in a focus in Dakahlia Governorate 1-human host. 1838 7

Female Baladi goats were used for investigating the toxicological effects of dioxin. Each animal in the treated group was given an oral dose of 4 mL of stock standard solution of dioxin (labelled and native congeners) diluted in 5 mL distilled water (1/3 of LD50) for three times with 2 days interval and slaughtered 16 days post treatment. Blood and tissue samples were taken and subjected for haemogram, biochemical and pathological studies as well as for determination of dioxin residues. Results revealed that exposure of female goats to dioxin induced anemia, leucocytopenia, neutropenia and eosinophilia with non significant increases in activities of serum ALT and AST as compared with untreated group. Meanwhile, activity of ALP and BUN concentration were significantly increased. Histopathological examination showed degenerative and necrotic changes associated with inflammatory reaction in liver and kidney, in addition to cystic glandular hyperplasia and adenomyosis in uterus. In ovarian tissue, marked decrease ofpreantral follicles together with cystic atretic follicle were noticed. The average percentage residues ofpg WHO-TEQ values for dioxins (PCDDs and PCDFs) in liver, kidney, mammary gland, uterus and milk after oral dose were 0.013, 0.0012, 0.0012, 0.009 and 0.0012%, respectively. It was concluded that oral exposure to dioxin in female goats induced adverse effects on liver and kidney. Dioxins had estrogenic like effect as indicated by uterine and ovarian histopathological changes.
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PMID:Some clinico and histopathological changes in female goats experimentally exposed to dioxin. 1906 19

We encountered a 45-year-old man who presented with marked eosinophilia as the first manifestation of sclerosing cholangitis. He was found to have a liver dysfunction during a regular physical check up and thereafter consulted our hospital. The laboratory data on admission indicated an elevation of AST (96 IU/L), ALT (136 IU/L) and ALP (1,025 IU/L). Furthermore, the leukocyte count was 18,190/mm(3) and he also showed marked eosinophilia (54.5%, 9,914/mm(3)). There were no atypical findings in the eosinophils. Other diseases causing eosinophilia, including parasite infection, allergic disorders, hypereosinophilic syndromes, drug-induced eosinophilia, malignancies, etc. were all investigated and ruled out. A liver biopsy revealed marked eosinophilic infiltration in the portal area and interlobular bile duct injury. Magnetic resonance cholangiopancreatography (MRCP) demonstrated a slight dilatation of the left intrahepatic bile ducts, but no clear diagnosis could be made at that time. A follow-up liver biopsy and endoscopic retrograde cholangiopancreatography (ERCP) finally revealed a diagnosis of secondary sclerosing cholangitis due to eosinophilic cholangiopathy. According to previous Japanese reports, eosinophilia of more than 5% was reported in 39 of 142 (27.0%) primary sclerosing cholangitis (PSC) patients. Eosinophilic cholangiopathy could cause a condition mimicking PSC and it might be confused as PSC with eosinophilia. The literature contains only about 40 case reports on eosinophilic cholangiopathy, and therefore, to date little attention has been paid to this condition. We should therefore pay attention to this condition when making a differential diagnosis of either PSC or IgG4-related sclerosing cholangitis.
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PMID:Marked eosinophilia as the first manifestation of sclerosing cholangitis. 1968 82


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