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\u003C\u002Fjats:bold> The similarity between poison and antidote was known to the ancient Greeks who used the same word, pharmakon, for both. This paper presents evidence that aniline (the toxin) and methylene blue (the therapy) are in fact remarkably similar and additive in some of their effects on erythrocytes. Studies were prompted by a case of aniline‐induced methaemoglobinaemia in which two injections of methylene blue did not rapidly eliminate cyanosis and were followed by severe, delayed haemolysis. Interactions between aniline and methylene blue were studied in cats which, although showing important differences from man in their haemoglobin and splenic vasculature, represent a useful model. Methylene blue potentiated the oxidative denaturation of haemoglobin by aniline as judged by the size and number of Heinz bodies and their turbidity in haemolysate. It also aggravated and prolonged the fall in erythrocyte reduced glutathione content which occurred at a time of maximum Heinz body production. While methylene blue in judicious dosage will reduce the content of methaemoglobin after aniline exposure, it may not eliminate visible cyanosis. Repeated injections of methylene blue can markedly aggravate subsequent haemolysis without further lowering methaemoglobin content.\u003C\u002Fjats:p>",{"EN":805},"Studies of the efficacy and potential hazards of methylene blue therapy in aniline‐induced methaemoglobinaemia",{"VOID":807},"6849836",{"VOID":809},"10.1111\u002Fj.1365-2141.1983.tb02064.x",[252],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1365-2141.1983.tb02064.x",[813,834],{"id":814,"sortIndex":25,"researcher":24,"roles":815,"affiliations":816,"properties":827},"6315ade3-5e91-46e6-862d-1109668c1246",[],[817],{"id":818,"sortIndex":25,"affiliation":819,"properties":24},"69a42566-6fd0-4bcc-872d-2f169a43ff00",{"id":820,"createTime":821,"updateTime":821,"relativeEntities":822,"slug":823,"properties":824,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"a3f706d5-4157-4571-a0f9-48f70bce5eac","2025-01-04T23:38:18.013+00:00",[],"Department-of-Physiological-Sciences-College-of-Veterinary-Medicine-and-Departments-of-Pathology-and-Medicine-College-of-Medicine-J-Hillis-Miller-Health-Center-University-of-Florida-Gainesville-Florida",{"title":825},{"EN":826},"Department of Physiological Sciences, College of Veterinary Medicine, and Departments of Pathology and Medicine, College of Medicine, J. 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Loundes, F. Coceani, L. Kelsey, and P.M. Olley (1986 ) Evidence against a role of thromboxane A2and leukotrienes in the pulmonary constriction response to hypoxia in the newborn lamb. (Abstract) . Proceedings of the Sixth International Conference on Prostaglandins and Related Compounds, p. 453 .",{},{"id":24,"text":2513,"url":24,"identifiers":2514},"Lu L., 1985, Experimental Hematology, 13, 989",{},{"id":24,"text":2516,"url":24,"identifiers":2517},"Miller A.M., 1986, Experimental Hematology, 14, 760",{},{"id":24,"text":2519,"url":24,"identifiers":2520},"10.1084\u002Fjem.158.2.393",{"doi":2519},{"id":24,"text":2522,"url":24,"identifiers":2523},"Payan D.G., 1983, Journal of Immunology, 131, 551, 10.4049\u002Fjimmunol.131.2.551",{"doi":2524},"10.4049\u002Fjimmunol.131.2.551",{"id":24,"text":2526,"url":24,"identifiers":2527},"10.1016\u002F0091-6749(84)90138-6",{"doi":2526},{"id":24,"text":2529,"url":24,"identifiers":2530},"10.1073\u002Fpnas.81.11.3501",{"doi":2529},{"id":24,"text":2532,"url":24,"identifiers":2533},"10.1084\u002Fjem.156.3.756",{"doi":2532},{"id":24,"text":2535,"url":24,"identifiers":2536},"Piper P.J., 1983, British Medical Bulletin, 39, 255, 10.1093\u002Foxfordjournals.bmb.a071829",{"doi":2537},"10.1093\u002Foxfordjournals.bmb.a071829",{"id":24,"text":2539,"url":24,"identifiers":2540},"10.1084\u002Fjem.154.5.1455",{"doi":2539},{"id":24,"text":2542,"url":24,"identifiers":2543},"10.1016\u002FS0006-291X(82)80081-8",{"doi":2542},{"id":24,"text":2545,"url":24,"identifiers":2546},"10.1016\u002F0006-291X(83)91758-8",{"doi":2545},{"id":24,"text":2548,"url":24,"identifiers":2549},"Shaw G.M., 1978, Journal of Clinical Investigation, 62, 1172, 10.1172\u002FJCI109236",{"doi":2550},"10.1172\u002FJCI109236",{"id":24,"text":2552,"url":24,"identifiers":2553},"Sheard P., 1982, Leukotrienes and other Lipoxygenase Products, 229",{},{"id":24,"text":2555,"url":24,"identifiers":2556},"Snyder D.S., 1984, Blood, 64, 135a",{},{"id":24,"text":2558,"url":24,"identifiers":2559},"Snyder D.S., 1986, Blood, 67, 1675, 10.1182\u002Fblood.V67.6.1675.1675",{"doi":2560},"10.1182\u002Fblood.V67.6.1675.1675",{"id":24,"text":2562,"url":24,"identifiers":2563},"Sun F.F., 1984, Biochimica et Biophysica Acta, 794, 56, 10.1016\u002F0005-2760(84)90297-2",{"doi":2564},"10.1016\u002F0005-2760(84)90297-2",{"id":24,"text":2566,"url":24,"identifiers":2567},"10.1016\u002F0022-1759(77)90137-5",{"doi":2566},{"id":24,"text":2569,"url":24,"identifiers":2570},"10.1016\u002FS0140-6736(84)92564-9",{"doi":2569},{"id":24,"text":2572,"url":24,"identifiers":2573},"10.1016\u002F0006-291X(82)91438-3",{"doi":2572},{"id":24,"text":2575,"url":24,"identifiers":2576},"Ziboh V.A., 1986, Cancer Research, 46, 600",{},{"id":2578,"createTime":2579,"updateTime":2579,"relativeEntities":2580,"slug":2581,"properties":2582,"entityType":248,"verifyStatus":249,"verifyTime":2579,"verifyNote":250,"syncStatus":23,"languages":2596,"translateLanguages":24,"viewCount":25,"primaryUrl":2597,"fullTextUrl":24,"authors":2598,"publicationType":362,"publisherRelationship":2727,"citationCount":2764,"citationInfo":2765,"publishDate":2767,"publishYear":2768,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":2769,"isForceReanalyzing":790},"a5ea3bc8-522a-4161-9434-145a8d911d8b","2024-09-25T23:33:39.075+00:00",[],"Increased-incidence-of-scp-VTE-scp-in-sickle-cell-disease-patients-risk-factors-recurrence-and-impact-on-mortality",{"mag":2583,"keywords":2585,"openalex":2586,"abstract":2588,"title":2590,"pm":2592,"doi":2594},{"VOID":2584},"2605277819",{},{"VOID":2587},"W2605277819",{"EN":2589},"\u003Cjats:title>Summary\u003C\u002Fjats:title>\u003Cjats:p>Previous reports show increased incidence of venous thromboembolism [\u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content>, deep‐vein thrombosis (\u003Cjats:styled-content style=\"fixed-case\">DVT\u003C\u002Fjats:styled-content>) and pulmonary embolus (\u003Cjats:styled-content style=\"fixed-case\">PE\u003C\u002Fjats:styled-content>)] in sickle cell disease (\u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content>) patients but did not account for frequency of hospitalization. We determined the incidence of \u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content> in a \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content> cohort versus matched controls. For \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content> patients, risk factors for incident \u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content>, recurrence and the impact on mortality were also determined. Among 6237 patients with \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content>, 696 patients (11·2%) developed incident‐\u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content>: 358 (51·6%) had \u003Cjats:styled-content style=\"fixed-case\">PE\u003C\u002Fjats:styled-content> (±\u003Cjats:styled-content style=\"fixed-case\">DVT\u003C\u002Fjats:styled-content>); 179 (25·7%) had lower‐extremity \u003Cjats:styled-content style=\"fixed-case\">DVT\u003C\u002Fjats:styled-content> only and 158 (22·7%) had upper‐extremity \u003Cjats:styled-content style=\"fixed-case\">DVT\u003C\u002Fjats:styled-content>. By 40 years of age, the cumulative incidence of \u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content> was 17·1% for severe \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content> patients (hospitalized ≥3 times a year) \u003Cjats:italic>versus\u003C\u002Fjats:italic> 8·0% for the matched asthma controls. Amongst \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content> patients, women (Hazard ratio [\u003Cjats:styled-content style=\"fixed-case\">HR\u003C\u002Fjats:styled-content>] = 1·22; 95% confidence interval [\u003Cjats:styled-content style=\"fixed-case\">CI\u003C\u002Fjats:styled-content>]: 1·05–1·43) and those with severe disease (\u003Cjats:styled-content style=\"fixed-case\">HR\u003C\u002Fjats:styled-content> = 2·86; 95% \u003Cjats:styled-content style=\"fixed-case\">CI\u003C\u002Fjats:styled-content>: 2·42–3·37) had an increased risk of \u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content>. Five‐year recurrence was 36·8% in patients with severe \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content>. \u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content> was associated with increased risk of death (\u003Cjats:styled-content style=\"fixed-case\">HR\u003C\u002Fjats:styled-content> = 2·88, 95% \u003Cjats:styled-content style=\"fixed-case\">CI\u003C\u002Fjats:styled-content>: 2·35–3·52). In this population‐based study, the incidence of \u003Cjats:styled-content style=\"fixed-case\">VTE\u003C\u002Fjats:styled-content> was higher in \u003Cjats:styled-content style=\"fixed-case\">SCD\u003C\u002Fjats:styled-content> patients than matched controls and was associated with increased mortality. 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