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KAJIAN KELUARGA tHALAssEMIA b-HEMOGLOBIN E Nurul A; Adi K Aman; Ratna A G
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 13, No 3 (2007)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v13i3.911

Abstract

HbE-b thalassemia is an inherited hemoglobin disorder of gene combination b thalassemia and HbE. It is caused by thalassemia and hemoglobinopathy gene,which acting as the allele in the same locus of chromosome. The clinical presentation is more severe than HbEhomozygote and almost similar to b thalassemia major. This disease is found predominantly in South East Asia, including Indonesia.The family study is very needed in order to genetic screening to prevent hemoglobinopathy and thalassemia homozygote. The objective ofthis study is to know the pedigree from the daughter who suffer from HbE- b thalassemia which is taken care in the children ward at H.Adam Malik Top Refferal Hospital, Medan. The family study was also done to both father and mother, one sister and to both grandparent.An examination was carried ,which include physical examination, complete cell blood count, peripheral blood morphology, hemoglobinanalysis with Hb-electroforese pH 8.5 agarose medium and read with densitometri, and osmotic fragility examination. From the familystudy was found that her father suffer from HbE heterozygote while the mother suffer from b thalassemia trait and sister got HbE- bthalassemia. The father and mother have no relative acceptance and there is no any blood linkage. Her grandparent could not performthe blood sample because they were have already passed away .
PENERIMA ASAM RETINOID a (a RETINOID ACID RECEPTOR) DI LEUKEMIA AKUT PROMYELOSITIK DENGAN BATANGAN (ROD) AUER Adi K Aman; Tonny .
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 15, No 3 (2009)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v15i3.966

Abstract

Acute Promyelocytic Leukemia (APL) is a subtype of AML with a defined clinical course and biology that is distinct from otherforms of AML. The term M3-AML was assigned to the hyper granular promyelocytic leukaemia that is characterized by blast cells withazurophilic granules, bundles of auer rods and reniform or bilobed nucleus. Clinically, APL is related to disseminate intravascularcoagulation and abnormal fibrinolysis. Cytogenetically, APL may cause translocation on the promyelocytic leukaemia (PML) gene,and chromosome 15 and with the retinoic acid receptor α (RARA) gene, on chromosome 17. The diagnosis of APL is shown by bonemarrow morphologically The majority of cells in the bone marrow are abnormal, having some similarities with promyelocytes. Themalignant cells bear numerous large granules and several auer rods. Aspirates of bone marrow are also taken for cytogenesis evaluationand for detecting the translocation. A twelve years girl was admitted to the hospital with haemorrhage from the gums during 5 dayafter extraction of a tooth. On physical examination there is no organomegaly shown. The laboratory examination found normocyticnormochromic anaemia, leucopoenia and thrombocytopenia with 15% blast cell and 5% promyelocytes with multiple auer rods. Thebone marrow aspirates showed predominant of promyelocyte cells (70%) with multiple auer rods.
PLATELET AGGREGATION IN ACUTE CORONARY SYNDROME Sulianty .; Adi K Aman
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 17, No 3 (2011)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v17i3.1167

Abstract

Haemostatic system is the mechanism that controls response of bleeding or thrombosis, so that thrombogenesis and fibrinolysis are inbalance. Obstruction of brain and heart vascular system often occurred, because of the hyperactivity of thromboses function that causesthrombosis. CBC, blood glucose, lipid profile and cardiac enzyme assay were performed on acute coronary syndrome patients at theEmergency Department as well as at the normal control. In this study, each group consist of 10 patients. Platelet aggregation test wasmeasured with turbidimetric method using Helena Agram aggregometer. ADP and epinephrine 5 and 10 µM were used as the agonists.There was significant difference in the mean total cholesterol, LDL and blood sugar level in the acute coronary syndrome patients thanthe control group. Platelet aggregations with ADP 1 and 5 µM were significantly different in the acute coronary syndrome patients thanthe control one. In this study were found patients aged above 50 years old have platelet aggregation with ADP 10 µM, which differsignificantly than the control group.