Articles
<![CDATA[APLIKASI KLINIS RETIKULOSIT ]]>
<![CDATA[Suega, Ketut]]>
<![CDATA[ journal of internal medicine Vol. 11, No. 3 September 2010 ]]>
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<![CDATA[Reticulocytes are immature nonnucleated erythrocytes that are released from the bone marrow following enucleation ofthe normoblast. Under the in! uence of erythropoietin, committed erythroid progenitor cells divide and differentiate through aseries of stages, giving rise basophilic normoblasts, polychromatophilic normoblasts, and orthochromic normoblastsin sequence.Reticulocytes are similar to mature red blood cells, except that they retain functioning polyribosomes and continue to synthesizehemoglobin. Because the reticulocyte stage of erythroid differentiation only lasts a few days, the number of reticulocytes in theblood is a useful clinical indicator of the rate of erythropoiesis. Reticulocytes exist in the circulation for only 1 ? 2 days and signalthe marrow erythropoietic activity 3 ? 4 days after iron was actively incorporated into haemoglobin. Early changes in reticulocytecount may simply re! ect the release of immature reticulocytes from the marrow rather than the true expansion of erythropoiesis.Reticulocyte counts have once again acquired great interest and importance following the introduction of instruments that usedyes speci" c for RNA. This has resulted in precise and accurate counts even at low reticulocyte concentrations The latestgeneration of automated analyzer provides additional information on reticulocytes, such as the immature reticulocyte fraction(IRF) and other reticulocyt indices, eg, mean reticulocyte volume (MCVr) and mean reticulocyte haemoglobin content (CHr).To date, the most widely studied of the reticulocyte indices is the CHr. The hemoglobin content is considered to be constantthroughout the lifetime of erythrocytes and circulating reticulocytes1 unless structural changes take place that compromise theamount of cytoplasm or cause cellular fragmentation. The normal value for the ! owcytometry method can range from 1% to2% depending on the cut off point used to separate reticulocytes from the normal red blood cell population. Since reticulocyteenumeration provides information about the bone marrow activity and the effectiveness of red blood cell production, it is crucialin the clinical application of reticulocytes parameters to aid the diagnosis of anemic patients, and for monitoring bone marrowtransplantation patients, patients undergoing therapy with marrow toxic drugs, and patients being treated for anemia]]>
<![CDATA[HEPCIDIN PADA ANEMIA OF CHRONIC DISEASE ]]>
<![CDATA[Agustriadi, Ommy]]>;
<![CDATA[Suega, Ketut]]>
<![CDATA[ journal of internal medicine Vol. 7, No. 2 Mei 2006 ]]>
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<![CDATA[Anemia of chronic disease (ACD) induce dysregulation of iron homeostasis. A hallmark of anemia of chronic disease is thedevelopment of disturbances of iron homeostasis, with increased uptake and retention of iron within cells of thereticuloendothelial system (RES), that leads to a diversion of iron from the circulation into storage sites of RES, and decreasedintestinal iron absorption, subsequent limitation of the availability of iron for erythroid progenitor cells, and iron-restrictederythropoiesis. A new small peptide called hepcidin was found. It is strongly suggest that hepcidin play role on the pathogenesisof ACD. Hepcidin expression is induced by inflammation/infection (by lipopolysaccharide and interleukin-6) and iron overloadcondition, it is strongly suggest that hepcidin induced dysregulation of iron homeostasis by inhibit iron efflux from macrophagedan RES (causing iron retention in turn) and decrease intestinal iron absorption. In the aggregate, the increase of hepcidinproduction suppress erythropoiesis by iron starvation strongly suggest that hepcidin is the key mediator of ACD. If hepcidinfollows the pattern of other peptide hormones or cytokines, its actions will be mediated by cell surface receptors. Elucidation ofthe receptor and its transduction pathways should lead to the development of hepcidin antagonists, some of which could be usefulin treatment of ACD, along with it's underlying disease.]]>
<![CDATA[THROMBOPHILIA KARENA DEFISIENSI PROTEIN C DAN PROTEIN S ]]>
<![CDATA[Rama Putra, I Made]]>;
<![CDATA[Suega, Ketut]]>
<![CDATA[ journal of internal medicine Vol. 11, No. 2 Mei 2010 ]]>
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<![CDATA[Protein C is a natural anticoagulant, inhibits thrombin generation. Protein C de! ciency, is associated with a variablyincreased risk of thrombosis. Incidence of symptomatic protein C de! ciency is approximately 1 in 16,000 to 1 in 32,000 persons,similar in men and women. Morbidity in protein C de! ciency greatly increases with advancing age, when patients are at greaterrisk for thrombotic events such DVT, PE, postphlebitic and blindness secondary to vitreous hemorrhages may occur in patientswith these severe conditions. The etiology can be inherited and acquired in a number of clinical scenarios include meningococcalseptic shock; DIC; liver disease; or chemotherapy. Diagnostic base on personal history of venous thrombosis, thromboembolicevents, abnormal laboratory coagulation tests. The laboratory workup should include haemostatic parameters, coagulationsystem such aPTT, PT, ! brinogen level and D-dimer test. A decreased protein C activity level is required. Imaging studies areappropriate for assessing the presence of thrombotic disease in a particular vessel. The treatment depends largely on a particularpatient?s disease manifestations. Surgical treatment may be appropriate in some circumstances.We reported, a male Balinese 62 years old came with complain red vision and dull feeling since a moth prior toadmission. No historical medical problem found. Physical exam found hypertension and laboratory ! nding showed slightdyslipidemia. Ophthalmologic examination revealed BRVO (Branch Retinal Vein Occlusion) ocular sinistra. Hypercoagulablaestate are suspected. Hematologic exam revealed light hyperagregation and low level of protein C and protein S. Treated withheparin 5000 unit intravenously followed by drip 1000 unit per hour for 3 day continued with warfarin 4 mg OD reach INR 1.5? 2.5. Good resulted base on patient?s good compliance.]]>
<![CDATA[PERUBAHAN GOLONGAN DARAH PADA PENDERITA LEUKEMIA MIELOBLASTIK AKUT ]]>
<![CDATA[Losen Adnyana, IW]]>;
<![CDATA[Suega, K]]>
<![CDATA[ journal of internal medicine Vol. 12, No. 1 Januari 2011 ]]>
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<![CDATA[We reported a case of acute leucemia (AML-M6) that experienced change of blood group. Leukemia is hematologicmalignancy with differentiation abnormality at grades haematopoetic stem cell that can make progressive expansión frommalignant clone cell in bone marrow and than spread to systemic circulation. In ABO blood system, group A with A antigenand anti B antibody, group B with B antigen and A antibody, O group without AB antigen and antibody. In this case, acuteleukemia be con! rmed with blood smear and bone marrow puncture. Changes of blood group known after remission inductionchemotherapy accordng to AML-M6 regiment. Post chemotherapy, there was changes O to A blood group according to ABOsystem. On family examination showed result of subgroup A of blood group previously. On acute leucemia or other hematopoiticdisease, there are two mechanism for explanation change of ABO blood system. The ! rst hematologic malignancy induced lossof ABO antigen due to inactivity of transferae A and B as the result was loss or decreased of antigen A and or B with simultantincrease of H antigen. Second, loss of ABH antigen in certain type of leucemia preceeding by loss of heterogenicity. ABO antigenwill reversed after proper treatment of leucemiaitself.]]>
<![CDATA[PERBANDINGAN BEBERAPA METODE DIAGNOSIS ANEMIA DEFISIENSI BESI: usaha mencari cara diagnosis yang tepat untuk penggunaan klinik ]]>
<![CDATA[Suega, Ketu]]>;
<![CDATA[Bakta, I Made]]>;
<![CDATA[Adnyan, Losen]]>;
<![CDATA[Darmayuda, Tjok]]>
<![CDATA[ journal of internal medicine Vol. 8, No. 1 Januari 2007 ]]>
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<![CDATA[Iron deficiency anemia (IDA) is the most widespread public health problems. In 1989 WHO report more than one third ofworlds population suffered from anemia and half of them with iron deficiency anemia. Iron deficiency anemia can cause reducedwork capacity in adults and impact motor and metal devolepment in children and adolescents. It also can increase risk of infection,mother mortality rate, affects cognition in adulescents girls and causes fatique in adult women. IDA may affect visual andauditory functioning and is weakly associated with poor cognitive development in children. The diagnosis of IDA requires properclinical manifestation, laboratory evidence and also others diagnostic test that support iron deficiency. There are some diagnostictests frequently use in clinical practice to diagnose IDA, such as the morphology of erytrosite, examination of serum iron andtotal iron binding capacity, examination of feritin serum, and bone marrow staining. Knowing the best of diagnostic methods canuse in clinical practice and also knowing the profile of IDA, can leads into better management of IDA in population. A diagnostictest was done in order to know the sensitivity and spesifity of erytrosite index, serum iron, TIBC, and feritin serum in dignosticIDA. The study was done at Internal Departement, Sanglah Hospital for 6 months, start from March 2003 until October 2003.The result is Feritin has the best sensitivity (90.6%) and specificity (90.6%) , with cut off point 35.4 µg/l. MCH as erytrosite indexhas sensitivity (84.4%) and specificity (75%) to diagnose IDA, the cut off point is 21.8 pg . Sensitivity and specificity of TIBC is81.3% and 83.8% with cutt off point 282 µg/l. Sensitivity and specificity saturation of transferin is 84.4% and 79.7% with cuttoff point 6%. Serum iron has sensitivity 75.0% and specificity 68.7% with cut off point 17 µg/l.]]>
<![CDATA[TERAPI TERKINI MULTIPLE MYELOMA ]]>
<![CDATA[Suega, Ketut]]>;
<![CDATA[Sripurnama Sjah, Yunny]]>
<![CDATA[ journal of internal medicine Vol. 10, No. 3 September 2009 ]]>
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<![CDATA[Management strategies for Multiple Myeloma (MM) have continued to evolve as the result of innovative treatmentmodalities and efÞ cacy data used in establishing new standard of care. In 2004, multiple myeloma was diagnosed in more than15.000 people in the United States and will account for approximately 20% of deaths due to hematologic malignancies. Mostcommonly diagnosed in the growing elderly population.Until recently, few effective treatment existed. The use of alkylating agents and corticosteroid had remained the treatmentof choice for almost four decades. On a cellular level, the disease is characterized by complex interactions between tumor cellsand the surrounding bone marrow microenvironment. Understanding of the relationship between malignant plasma cells andthe microenvironment has sparked ongoing efforts to develop targeted therapeutic agents for treatment of this disease. Recentadvances in its treatment including using of the immunomodulatory drugs such as thalidomide and lenalidomide as well as theproteasome inhibitor bortezomib. Each of these agents is undergoing extensive clinical evaluation in combination with othertherapies to produce unprecedented response rates in newly diagnosed and relapsed MM. They have each improved the responseto therapy, but they are expensive. In recent years, evidence supporting a survival beneÞ t for three new drugs have resulted intheir inclusion, in combination with older drugs, in the management of younger and older patients. Each of these new drugs hasmultiple mechanisms of action, targeting both intracellular signaling pathways and tumor microenvironment. This review focuson the newer agents such as thalidomide, bortezomib, and lenalidomide in treatment of patient with newly diagnosed MM andrelapsed MM, treatment-related side effect, and future using of these agent including new combination therapy]]>
<![CDATA[SEORANG PENDERITA HEMOFILIA RINGAN DENGAN PERDARAHAN MASIF ]]>
<![CDATA[Renny A.R, Ni Made]]>;
<![CDATA[Suega, Ketut]]>
<![CDATA[ journal of internal medicine Vol. 7, No. 2 Mei 2006 ]]>
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<![CDATA[Haemophilia A is the most common of the hereditary clotting factor deficiencies, which have defect of absence or lowlevel factor VIII in the plasma. It is a X-linked recessive inheritance disease, with incidence approximately 1 per 10.000 malebirth. In the middle of the year 2001,it were reported 314 cases in Indonesia. The clinical features of the bleeding may be shownmany various severity, and classified into mild, moderate and severe disease. The clinical severity of the disease correlates withthe extent of the factor VIII deficiencies. Diagnostic confirm by specific clinical features, there is a history of the bleeding in thefamily, and laboratorium examination to measure the factor VIII level in the plasma. We reported a case, male, 46 years old,Balinese, reffered from private hospital with complaining profuse bloody vomiting and blackish stool and has been done bloodtransfusion for 15 bags, with history of haemophilia confirmed. The history of bleeding before classified patients into a milddisease, but in the present the patient suffered from chronic liver disease and erosive gastritis, that can lead patients has moreprofuse bleeding. A good respons shown by giving the transfusion of the cryopresipitate and packed red cell.]]>
<![CDATA[SEORANG PENDERITA DENGAN LEUKEMIA MIELOID KRONIK DAN MIELOMA MULTIPEL ]]>
<![CDATA[Suega, Ketut]]>
<![CDATA[ journal of internal medicine Vol. 11, No. 3 September 2010 ]]>
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<![CDATA[Chronic Myeloid Leukemia (CML) and Multiple Myeloma (MM) are two chronic progressive diseases characterizedby neoplastic proliferation of myeloid cell and monoclonal plasma cell. Chronic myeloid leukemia was recognized as a distinctentity, associated with massive splenomegaly and as ! rst malignant disease found to be constitutively associated with spesi! ccytogenetic abnormality the Philadelphia oncogene. Whereas MM is frequently recognized by monoclonal protein productionand either difuse osteoporosis or lytic bone lesion. Clinical manifestation are consequence of marrow in! ltration of plasma cells,production of M protein in blood or urine and immune de! ciency. Coincidence of these two diseases in one particular patient is avery rare occasion. Herewith we reported a woman 42 years old Balinese presented of abdominal enlargement without symptomof bone pain, anemic syndrome. After complete examination supporting by ! nding on bone marrow examination this patient! nally diagnosed of having chronic phase of CML and MM stage IIIB as well. Treatment was given with hydroxy urea andother supported measures and we planned to continue with melphalan and prednisone. There were no clear explanation for thiscondition whether it occur concomitantly or one disease follow with the other. Several reports found that in quite similar occasionMelphalan was the agent of suspected with induced secondary malignancy. Others also found twenty MDS patient togetherwith lymphoid malignancy and plasma cell. Tanaka et.al., noted that a more satisfactory explanation is that both disorders arefrom malignant transformation of a precursor cell capable of differentiating into both lymphoid and myeloid lines. In our casemore likely that CML concomitantly found with MM because there were no previous history of having chemotherapy norradiotherapy.]]>
<![CDATA[HUBUNGAN BESI DAN PRODUKSI SITOKIN ]]>
<![CDATA[Suega, Ketut]]>
<![CDATA[ journal of internal medicine Vol. 7, No. 2 Mei 2006 ]]>
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<![CDATA[Iron deficiency is a widespread nutritional disorder in infant, children and women of reproductive age especially indeveloping countries where almost 2 billion individuals are concerned, particularly infant and children. The absorption ofintestinal iron as regulated in several ways such as dietary regulator, stores regulator and erythropoietic regulator. The negativeconsequence iron deficiency anemia on behavior, psychomotor development and growth rate are well established and underlinedthe need to control iron deficiency anemia. Iron supplementation has proven to be useful, particularly in infant and children,when iron deficiency is important and has to be corrected rapidly. However several studies have indicated that iron deficiencyprotects against infection and other studies show the opposite where morbidity is higher in iron deficient children. Iron deficiencywould decrease the resistance to infection through impairment of immune competence of the individual especially cell-mediatedimmunity. The mechanisms of impairment are very likely multifactorial and may include but not be limited to a reduction in theactivity of certain iron-dependent enzymes such as ribonucleated reductase. Other mechanism may include a defect in one orseveral of the early events of lymphocyte activation and cytokine productions such as IL-2. The main cellular source of IL-2 isactivated lymphocyte and TCR/CD3 actvation leads to autocrine IL-2/high affinity receptor signal transduction, resulting in cellproliferation. Iron deficiency may inactivated T cell proliferation and decreasing IL-2 production.]]>
<![CDATA[HUBUNGAN FERITIN SERUM DENGAN KADAR IL-2 PADA PENDERITA ANEMIA DEFISIENSI BESI ]]>
<![CDATA[Losen Adnyan, I Wayan]]>;
<![CDATA[Bakta, I Made]]>;
<![CDATA[Suega, Ketut]]>;
<![CDATA[Darmayuda, Tjok Gde]]>
<![CDATA[ journal of internal medicine Vol. 8, No. 1 Januari 2007 ]]>
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<![CDATA[Iron deficiency anemia is one of the most common single nutrient deficiency in the world, impairs lymphocyte proliferationin humans and laboratory animals. The mechanisms are not fully understood. Cellular iron availability modulates the differentiationand proliferation of Th-1 and Th-2 subsets. Th-1 clones are very sensitive to treatment with antitransferrin receptor antibodies,resulting in inhibition of their DNA synthesis. Th-1-mediated immune effector function may be much more sensitive to changesin iron homeostasis in vivo. Th-1 produce IFN- and IL-2. The effects of iron deficiency on immunity remain controversial. Crosssectional study was performed to determine the relationship between iron status (serum ferritin) and IL-2 production in patientswith iron deficiency anemia. This relationship was assessed in 33 adult patients. Infection, malnutrition, malignancy, acute bleedingand using immunosuppressive medicines were excluded. Iron deficiency anemia was defined by Kerlin et al criteria. Serumferritin was measured by immunometric assay and IL-2 was measured by immunoassay solid phase ELISA. The mean of Hb was6.27 ± 2.19 g/dL, serum ferritin 30.07 ± 49.41, IL-2 2.26 ± 1.30. The most causes of this anemia were chronic bleeding i.e. pepticulcer, ancylostomiasis, menorrhagia, hemorrhoid and hematuria. There was not correlation between serum ferritin and IL-2 (r =0.118; p = 0.512). There was not correlation between Hb and IL-2 too (r = 0.220; p = 0.219). Lack of the correlation may be causedby some conditions i.e. without activated T cell, inadequately controlled the other trace elements or co-morbid diseases. Our datasupport that there is not correlation between serum ferritin, Hb and IL-2 production by lymphocyte without stimulation. Furtherprospective studies are needed to determine relationship between iron status and immune function.]]>
