Prediction of anthracycline induced cardiotoxicity: study of thirty-one Iraqi adult patients

To look for a nearly ideal tool for prediction of anthracycline-induced cardiotoxicity. Thirty-one patients with various hematological malignancies were included in the study which was conducted from Sept. 2005 to Sept. 2006 in Baghdad Teaching Hospital - Hematology Unit. Initial cardiovascular assessment including cardiac troponin I, electrocardiography and echocardiography were done and repeated one month after the commencement of anthracycline-based regimen. Cardiotoxicity was considered present if the patient has clinical and electrocardiographic evidences, troponin positivity, echocardiographic evidence, or any combination of these. The mean age for the study sample was 34.1 +/- 17.2 years comprising of 17 male and 14 female patients. Increasing age, body surface area, anthracycline dose as well as the concomitant use of cyclophosphomide/ All Trans Retinoic were associated with increased risk of cardiotoxicity. The cut-off point of body surface area above which the risk of anthracycline-induced cardiotoxicity is increased was 1.88 m[2] while the cut-off point for anthracyclines dose was 145.5 mg/m[2]. The constellation of clinical data, ECG, and cTnI was 92% predicitive of early evidence of anthracycline-induced cardiotoxicity. More weight is added when echocardiography is used as a diagnostic tool. The incidence of cardiotoxicity attributed to treatment was 38.7%. The predictive power of cardiac troponin I alone was 58.3%, whereas it increases to 91% when combined with electrocardiography and to 95% when combined with echocardiographic study. The age, anthracyclines dose and the use of other chemotherapeutics increase the risk of anthracylince-induced cardiotoxicity. Cardiac troponin I is a simple non-invasive indicator for the presence of anthracycline- induced cardiotoxicity especially when used in combination with other parameters

Tuberculous meningitis: report of an unusual case

A patient with tuberculous meningitis is described, in whom the absence of a demonstrable tuberculous primary focus, in combination with very atypical features of the cerebrospinal fluid, resulted in a nearly fatal delay in establishing aetiologic diagnosis and providing specific treatment

New derivatives of pyrolo [3,2-e] [1,2,4] -triazolo [1,5,-c] pyrimidines

2-amino-4, 5- diphenyl-1- methylpyrrolo-3-carbonitrile [I], reacted with triethyl orthoforamte to give the 2-ethoxymethyleneamino-4, 5- diphenyl-1-methyl-pyrrole-3-carbonitrile [II]. The latter compound was converted into 5, 6-diphenyl-3H, 4H, 4-imino-7-methylpyrrolo [2, 3-d] pyrimidine-3-amine [III]

Reactions with [arylmethylene] cycloalkanones 6 Synthesis and deacetylation of 2-acetyl-5-aryl-2,3,6,7,8, 9-hexahdro-5H-thiazolo [23-b] -quinazolin-3-ones

2-[ARYLMETHYLENE] cycIohexanones condensed with thiourea to give 4-aryl-octahydrcquinazoline-2-thiones II,, which reacted with chloroacetic acid to give the title compounds III. Compounds III suffer deacetylation when reacted with aromatic aldehydes, arene-diazonium salts and also when subjected to Mannich reaction to give the following compounds, respectively; 5-aryl-2-[arylmethlene]-2, 3,6,7,8,9, hexahydro-5H - thiazolo [2,3-b] - quinazolin-3-ones [IV], 5-aryl-2-[arylhydrazono]-2,3, 6,7,8,9-hexahydro-5H-thiazolo [2,3-b] -quinazolin-3-ones [V] and 5-aryl-2 - [aminomethyl] - 23,6,7,8,9-hexahydro-5H-thiazolo[2,3-b] quinazolin-3-ones [VI]