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All Journal journal of internal medicine E-Jurnal Medika Udayana Jurnal Penyakit Dalam Udayana The Indonesian Journal of Gastroenterology, Hepatology and Digestive Endoscopy
I Gusti Agung Suryadarma
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Health Professions Immunology & microbiology Medicine & Pharmacology Public Health

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Journal : journal of internal medicine

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INTERLEUKIN 8 BERHUBUNGAN DENGAN DERAJAT GASTRITIS PADA PASIEN TERINFEKSI HELICOBACTER PYLORI Mariadi, IK; Kurniari, PK; Wibawa, IDN; Purwadi, N; Suryadarma, IGA
journal of internal medicine Vol. 12, No. 2 Mei 2011
Publisher : journal of internal medicine

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Abstract

Helicobacter pylori infection induces a local pro-inflammatory cytokine response. The secretion of IL-8 by epithelialcells is probably a key factor in host defenses at mucosal sites, permitting a rapid polymorph response against infectious agents.Interleukin-8 is an important chemotactic and activating factor for neutrophils. If defense mechanisms fail and chronic infectionresults, continued up regulation of IL-8 and neutrophil activation could lead to mucosal damage and increased free radicalformation. Mucosal IL-8 production in Helicobacter pylori infection may be an important factor in the immunopathogenesisof gastritis and peptic ulcer disease. This study aim to investigate correlation between IL-8 and severity of gastritis in ourpopulation. We performed a cross-sectional analytic study in Helicobacter pylori infected patients. Severity of gastritis wasdetermined base on The Updated Sydney System. IL-8 level was analyzed from gastric mucosa biopsy using ELISA method.We included 65 samples. 31 (47.7%) men and the rest was women. Base on Kruskalwallis test we found significant associationbetween IL-8 gastric mucosa and severity of gastritis (x2 = 12.8; p = 0.002). We also found significant association between IL-8gastric mucosa and density of H pylori infection (x2 = 10.6; p = 0.01), severity of atrophy (x2 = 9.4; p = 0.02) and neutrophilscount (x2 = 11.0; p = 0.01). But notmethaplasia (x2 = 3.3; p = 0.18). Base on this study we concluded that IL-8 was associatedwith severity of gastritis in Helicobacter pylori infected patients.
ADIPONECTIN ACTIVITY IN ACUTE VIRAL HEPATTOBI Suryadarma, I Gusti Agung
journal of internal medicine Vol. 7, No. 3 September 2006
Publisher : journal of internal medicine

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Abstract

The mechanisms of hepatocellular necrosis in acute viral hepatitis, primarily through cytopathic immune mechanisms,however the processes of hepatic parenchyma necrosis also might be secondarily involved the roles of cytopathic non-immunemechanisms. Once of the defend mechanisms to the hepatic viral infection is through the releases of adiponectin. Adiponectin is ahormone secreted by adipocytes. The protective effect of adiponectin against liver injury likely involve multiple mechanisms,especially to the ability effects of adiponectin as a anti-inflammatory cytokines. Thus, decreased of the adiponectin concentration<10 mg/dl in the acute viral hepatitis, especially Hepatitis B and C perhaps as the early biomarkers of possibility progression tothe chronic hepatitis.
HUBUNGAN C-REACTIVE PROTEIN DENGAN PEMANJANGAN PROTHROMBIN TIME PADA PASIEN SIROSIS HATI YANG MENGALAMI PERDARAHAN SALURAN MAKANAN BAGIAN ATAS Mariadi, IK; Wibawa, IDN; Purwadi, N; Suryadarma, IGA
journal of internal medicine Vol. 12, No. 1 Januari 2011
Publisher : journal of internal medicine

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Bacterial infections are common complications in cirrhosis, and cause the systemic in! ammation process. The natureof the relationship between gastrointestinal bleeding and infection in cirrhosis has not been clari" ed. Infection is associatedwith failure to control variceal bleeding and early variceal rebleeding in these patients. Bacterial infections, and particularlyendotoxemia, have been shown to activate the coagulation system and generally to interfere with hemostasis. We performedcross-sectional analytic study in cirrhosis patients with upper gastrointestinal bleeding to assess whether there are any associationbetween in! ammation process (CRP) with defect in haemostatic system (prolongation in prothrombin time). Forty-nine patientswere evaluated, 37 (75.5%) out of these were male and the rest were female. Ninteen out of this with in! ammation process and30 without in! ammation process. Fourteen out of 19 patients (73.7%) in in! ammation group have prolongation on prothrombintime and 12 out of 30 patients (40%) in non in! ammation group have prolongation on prothrombin time. The difference of thisproportion statistically signi" cant (Chi-square test X2: 5.29; p = 0.021). The CRP also have positive correlation with prolongationin prothrombin time (Spearman correlation R = 0.390; p = 0.006). In conclusion there is signi" cant association between CRP andprothrombin time in cirrhosis patients with upper gastrointestinal bleeding.
HEPATIC ISCHEMIA REPERFUSION INJURY IN SEPSIS: BASIS PATHOGENIC MECHANISMS Suryadarma, I Gusti Agung
journal of internal medicine Vol. 8, No. 2 Mei 2007
Publisher : journal of internal medicine

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Abstract

Hepatic ischemia reperfusion injury is a complex patho-physiology with a number contributing factors. Ischemia insultcan lead to sublethal cell injury, which is aggravated by the formation of reactive oxygen from various intracellular sources duringreperfusion. In addition, formation of proinflammatory mediators and the recruitment and activation of macrophages, neutrophiland lymphocyte can further enhance the injury. Microcirculatory disturbances lead to underperfused areas in the liver and maycause ischemic injury. Hepatic IR injury involves interaction between different cell types and a variety of cellular and molecularmechanisms including kupffer cells activation, formation of ROS, release of cytokines and chemokines, neutrophil recruitment,mitochondrial permeability transition and pH paradox. There are two distinct phase of liver injury after warm ischemic reperfusion,such as early phases and followed by late phases. Clinical presentation of hepatic ischemic reperfusion injury in sepsis, includingsepsis-associated cholestasis, hepatitis ischemic, cholangitis lenta and progressive sclerosing cholangitis
Co-Authors Dewa Gde Agung Budiyasa Dewa Gde Agung Budiyasa Gde Somayana Hendra Koncoro Hendra Koncoro I Dewa Nyoman Wibawa I Ketut Mariadi IDN Wibawa N Purwadi Nyoman Purwadi Pande Ketut Kurniari Pande Made Aditya Saskara Putu Prathiwi Primadharsini Yuna Ariawan