Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Described are the susceptibility of the Indian langur (Presbytis entellus) to Leishmania donovani and the consequent haematological and serum biochemical changes. The host response to antileishmanial chemotherapy and the immunological profile were also examined. Each langur was inoculated intravenously with 1 x 10(8) amastigotes; a spleen biopsy carried out on day 35 post-infection (p.i.) revealed 10-13 L. donovani bodies per 500 cell nuclei, which reached a maximum of 130-195 at death (day 105-110 p.i.). The infected monkeys lost body weight, developed severe anaemia, lymphocytosis, hyperproteinaemia, hypergammaglobulinaemia, hypoalbuminaemia and an increase in the level of alkaline phosphatase and alanine aminotransferase (AAT). Treatment with sodium stibogluconate (60 mg Sb5+ per kg body weight intramuscularly for 10 days) reduced the number of spleen parasites (0-1 amastigotes per 500 cell nuclei) but after the therapy the parasites appeared in the skin, which had previously been free of infection. Relapse occurred on day 30 post-treatment (10-24 amastigotes per 500 cell nuclei) and the parasites were resistant to repeat intensive therapy (120 mg Sb5+ per kg per day x 30 days). The stibogluconate treatment caused a proportionate reduction in the haematological and biochemical parameters to normal values except for alkaline phosphatase and AAT, which remained elevated. The level of IgG antibodies, which rose during the infection, rapidly fell to the pretreatment value following the first therapeutic schedule and then increased a second time coinciding with relapse. Our findings suggest that langurs could serve as acceptable models for human visceral leishmaniasis.
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PMID:The Indian langur: preliminary report of a new nonhuman primate host for visceral leishmaniasis. 131 9

A 27-year-old woman who acquired cutaneous leishmaniasis in Central America was inadvertently treated with 10 times the intended daily dose of the pentavalent antimonial compound sodium stibogluconate (Pentostam): 8500 mg (143 mg/kg) instead of 850 mg. The patient felt "wiped out" during the 4-h infusion of the drug. After the mistake in dosing was discovered, she was vigorously hydrated and carefully monitored in an intensive care unit for greater than 48 h. Her vital signs were stable, and no arrhythmias were noted. Her alanine aminotransferase level rose briefly to 2.4 times the upper limit of normal, and her white blood cell count briefly fell 43% to a low of 3700/microliter. Her skin lesions subsequently healed without further therapy. Although sodium stibogluconate has been associated with a variety of side effects, in this case, a single high dose of the drug was tolerated without serious toxicity.
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PMID:Sodium stibogluconate (Pentostam) overdose during treatment of American cutaneous leishmaniasis. 131 73

Adult wild-trapped opossums were infected with Leishmania donovani (Khartoum strain, WR 378) and evaluated as an animal model of visceral leishmaniasis. All infected opossums died within 32 days. Loss of body fat, hepatomegaly, and petechiae of skin and abdominal musculature were seen at necropsy. Microscopically, numerous amastigote-laden macrophages were seen in histologic sections of liver, spleen, and lymph nodes; fewer parasite-laden macrophages were in the bronchial-associated lymphoid tissues and renal glomeruli. Hematological findings included thrombocytopenia (terminal), neutropenia, and lymphopenia. Blood lymphocyte blastogenesis in response to concanavalin A and phytohemagglutinin was decreased markedly at day 24 post-infection (PI). Serum antibodies (1:40 dilution) to promastigotes of L. donovani were detected in five of eight infected opossums tested on days 10 and 24 PI. Total bilirubin concentrations and alanine aminotransferase and aspartate aminotransferase activities were increased after day 25 PI. Activated partial thromboplastin times and one-stage prothrombin times were prolonged before death. Concurrently, factors V, VIII, and XII activities were decreased.
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PMID:Experimental visceral leishmaniasis in the opossum. 276 21

Leishmania donovani organisms isolated from 10 children coming from different districts in Iraq, were compared between themselves, with Leishmania donovani isolated in Iran and the Sudan, and with a Leishmania sp. isolated from the viscera of a rat caught in Baghdad. The comparison was made by examination of the electrophoretic mobilities of seven soluble enzymes: malic enzyme E.C.1.1.1.40; glucose phosphate isomerase E.C.5.3.1.9; glucose-6-phosphate dehydrogenase E.C.1.1.1.49; phosphoglucomutase E.C.2.7.5.1.; malate dehydrogenase E.C.1.1.1.37; aspartate aminotransferase E.C.2.6.1.1 and alanine aminotransferase E.C.2.6.1.2 following thin-layer starch-gel electrophoresis. The Iraqi isolations of L. donovani fell clearly into three groups. Group A contained the organisms from seven children, six from the Wasit district and one from the outskirts of Baghdad; Group B, the organism from one child from the Hilla district (100 km south of Baghdad) with severe visceral leishmaniasis which relapsed following chemotherapy; Group C, the organisms from two children from Suaira in the Wasit district. The Iranian and Sudanese isolations gave patterns different from each other and from those from Iran. The Leishmania sp. isolated from the viscera of the rat gave a pattern identical to that of L. tropica.
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PMID:Leishmania spp. in Iraq. Electrophoretic isoenzyme patterns. I. Visceral leishmaniasis. 738 96

Leishmania organisms isolated from the sores of patients in Iraq suffering from cutaneous leishmaniasis were compared between themselves and with Leishmania major, L. tropica and L. donovani, all of which had been identified on clinical and geographical grounds. The comparisons were made by examination of the electrophoretic mobilities of seven soluble enzymes: malic enzyme E.C.1.1.1.40; glucose phosphate isomerase E.C.5.3.1.9; glucose-6-phosphate dehydrogenase E.C.1.1.1.49; phosphoglucomutase E.C.2.7.5.1; malate dehydrogenase E.C.1.1.1.37; aspartate aminotransferase E.C.2.6.1.1 and alanine aminotransferase E.C.2.6.1.2. following thin-layer starch-gel electrophoresis. The Iraqi isolations of Leishmania spp. from cutaneous lesions fell clearly into two groups, one of which gave isoenzyme patterns identical to those of a marker stock of L. major isolated in the USSR, and the other which gave patterns identical to those given by L. tropica also from the USSR. Previously it had been thought that L. tropica alone was responsible for cutaneous leishmaniasis in Iraq. The L. tropica and L. major isoenzyme patterns clearly differentiated these organisms from L. donovani.
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PMID:Leishmania spp. in Iraq. Electrophoretic isoenzyme patterns. II. Cutaneous leishmaniasis. 738 97

Sodium stibogluconate is the mainstay of treatment for all forms of leishmaniasis. Therapy is associated with an increase in serum aminotransferases. In this study liver damage was assessed during treatment of American cutaneous leishmaniasis with sodium stibogluconate and also in a control group given aminosidine. In addition to standard liver function tests, acute hepatocellular damage was assessed by measuring plasma glutathione S-transferase B1 (GST), and hepatic metabolic capacity was assessed by a caffeine clearance (CCL) test, before, during and after treatment. Thirteen patients were treated; 5 received sodium stibogluconate, 6 received aminosidine and a further 2 patients received aminosidine followed by sodium stibogluconate. Treatment with sodium stibogluconate was associated with an increase in both alanine aminotransferase (ALT) and GST and a fall in the CCL, indicating both hepatocellular damage and functional impairment. Six weeks after treatment had stopped ALT and GST had returned to pre-treatment levels and the CCL remained depressed in only one patient. Patients given aminosidine did not show any evidence of liver damage. Sodium stibogluconate is associated with significant hepatocellular damage and hepatic functional impairment. However, this is rapidly reversible on drug withdrawal. We suggest that liver function is monitored throughout treatment and that patients with pre-existing liver disease receive alternative treatment.
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PMID:Hepatotoxicity of sodium stibogluconate therapy for American cutaneous leishmaniasis. 757 Aug 43

Leishmania parasites isolated from two patients with cutaneous leishmaniasis from geographically different localities in Paraguay have been characterized by enzyme electrophoresis (zymodeme) and digestion profiles of kinetoplast DNA with restriction enzymes (schizodeme). Both Paraguayan isolates showed identical zymodeme profiles to each other using 14 enzymes (glutamic pyruvate transaminase, glutamic oxaloacetic transaminase, enolase, fumarate hydratase, glucose phosphate isomerase, glucose-6-phosphate dehydrogenase, malate dehydrogenase, malic enzyme, mannose phosphate isomerase, nucleoside phosphorylase, peptidase-D, 6-phosphogluconate dehydrogenase, phosphoglucomutase, and pyruvate kinase). Although two Paraguayan isolates showed different zymodeme profiles from those of six Leishmania reference strains of Old and New World Leishmania species, they showed identical zymodeme profiles to those of an L. major-like parasite from Ecuador. These observations were confirmed by schizodeme analysis using three restriction endonucleases (Msp I, Hae III, and Taq I). These results indicate that Leishmania parasites isolated in Paraguay are identified as an L. major-like parasite, and it is necessary to consider the existence of L. major-like parasites when classifying Leishmania isolates from the New World.
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PMID:Leishmania major-like parasite, a pathogenic agent of cutaneous leishmaniasis in Paraguay. 781 Aug 7

Secondary haemostasis was evaluated in 26 dogs with leishmaniasis and 10 normal dogs by measurements of modified one-stage prothrombin time (m-OSPT), activated partial thromboplastin time (APTT), thrombin time, fibrinogen concentration and fibrin degradation products. There were no significant differences between the groups in the m-OSPT, fibrinogen concentration, or levels of fibrin degradation products. The APTT was significantly (P = 0.006) longer in the infected dogs than in the control group, and in infected dogs with alanine aminotransferase (ALT) activities > 50 U/litre. There was a significant linear regression between ALT and APTT. Thrombin time was significantly (P = 0.003) longer in the infected dogs than in the normal dogs. There were no significant differences between the thrombin times of sick dogs with different levels of creatinine or activities of ALT, or between male and female dogs, whether diseased or normal.
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PMID:Evaluation of secondary haemostasis in canine leishmaniasis. 1009 24

A 69-year-old male was hospitalized in January 1999 because of visceral leishmaniasis. He had also suffered from anti-hepatitis C virus (HCV)-positive chronic hepatitis for years. All serum hepatitis B virus (HBV) antigens and antibodies were negative except for anti-HBc. The patient was treated with amphotericin B cholesteryl sulfate (2 mg/kg twice a day for 7 days, iv). Fever disappeared on the 3rd day of treatment, the clinical condition improved rapidly and the patient recovered. In May 1999 the patient developed icteric HBsAg-negative acute hepatitis (aspartate aminotransferase 722 U/l; alanine aminotransferase 988 U/l). Anti-HBc IgM was positive and HBV-DNA was detected in serum by PCR. Anti-HAV IgM was negative. A serum sample obtained on presentation and stored at -80 degrees C was retrospectively tested and found positive for HBV-DNA. In July 1999, complete remission of acute hepatitis and seroconversion to anti-HBs was observed. We suppose that a moderate depression of the immune system, probably associated with leishmaniasis, may have enhanced HBV replication in the patient who had an HBsAg-negative 'silent' HBV infection. Restoration of the immune system after successful antiprotozoan therapy might have induced cell-mediated necrosis of the HBV-infected hepatocytes and seroconversion to anti-HBs.
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PMID:Clinical expression of 'silent' hepatitis B virus infection in a patient with visceral leishmaniasis. 1144 Mar 89

Although the lesions, clinical signs and biochemical alterations observed in the course of canine leishmaniasis have been amply described a thorough definition and characterisation of the affected populations is important in order to detect relationships between parameters which may be involved in the development of this disease and to correctly assess further studies. This study included 61 dogs diagnosed with naturally acquired canine leishmaniasis by means of indirect immunofluorescence assay (IFA). At diagnosis, dogs were classified according to the following qualitative and quantitative variables: gender, breed, age, clinical picture, antibody titre, serum protein electrophoretogram, haemogram (CBC), urea, creatinine and ALT. Our population included dogs of 24 breeds, both sexes and different ages indicating no sex, age or breed predilection. In relation to the clinical picture, eight dogs were asymptomatic, 16 displayed mainly cutaneous signs, 18 presented primarily visceral signs and 19 displayed both cutaneous and visceral signs. Our results indicate that the clinical picture is significantly related to electrophoretogram and to RBC, PCV and haemoglobin. Dogs with mainly cutaneous signs showed the highest eosinophil mean values and those with mainly visceral signs showed the highest alpha-globulin mean values. This study confirms that the antibody titre is highly correlated with electrophoretogram and with RBC, PCV and haemoglobin. Lymphocytes were not associated or correlated with any other variable considered. PMNC, monocytes and eosinophils, as well as WBC, showed a significant correlation with beta-globulins, which is difficult to interpret.
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PMID:Distribution and relationships between clinical and biopathological parameters in canine leishmaniasis. 1273 37


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