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"ABSTRAKPrevalensi kolitis ulseratif semakin meningkat dari tahun ketahun. Penelitian ini bertujuan untuk melihat efek Ekstrak Etanol Daun Mahkota Dewa (EEDMD) terhadap gambaran histopatologi dan  ekspresi TNF-α, COX-2, dan NF-κβ pada jaringan kolon mencit Swiss berusia 20 minggu yang diinduksi dengan Dextran Sodium Sulfat (DSS) 2% melalui air minum. EEDMD dosis 100 mg, 200 mg, 300 mg, aspirin 0,21 mg, diberikan per oral selama 2 minggu. Pemeriksaan kandungan EEDMD menunjukan kadar total fenol sebesar 4,4103% atau 44,103 mgGAE/g ekstrak, kadar flavonoid sebesar 0,3429% atau 3,429 mgQE/g ekstrak, dan memiliki aktivitas antioksidan sedang (IC₅₀ sebesar 219,716 µg/mL). Pemeriksaan histopatologi pada jaringan kolon mencit dinilai dengan mengkuantifikasi jumlah radang dan rerata sel goblet pada jaringan kolon yang diwarnai hematoksilin-eosin. Pemberian EEDMD pada semua dosis menunjukan perbedaan bermakna pada jumlah radang (p<0,00) dan rerata sel goblet (p<0,00). Pemeriksaan imunohistokimia dilakukan untuk melihat ekspresi TNF-α, COX-2. NF-κβ. Sel positif mengekspresikan TNF-α, COX-2, dan NF-κβ dihitung/1000 sel epitel. Hasil menunjukan EEDMD mampu menurunkan ekspresi TNF-α secara signifikan dibandingkan dengan kontrol negatif. Sedangkan pada COX-2 (p<0,80) dan NF-κβ (p<0,90) tidak terdapat perbedaan yang signifikan.

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ABSTRACT

Ulcerative colitis prevalence increases from year to year. The purpose of this research to see the effect of Ethanol Extract of Mahkota Dewa Leaves (EEDMD) on histopathology and expression of TNF-α, COX-2, and NF-κβ on 20-week Swiss mice tissue induced with 2% Dextran Sodium Sulfate (DSS) through drinking water. EEDMD dose 100 mg, 200 mg, 300 mg, aspirin 0.21 mg, given orally for 2 weeks. Examination of EEDMD content showed total phenol levels of 4.4103% or 44.103 mgGAE / g extract, flavonoid levels of 0.3429% or 3.429 mgQE / g extract, and had moderate antioxidant activity (IC50 of 219.716 µg / mL). Histopathological examination of mice colon tissue was assessed by quantifying the amount of inflammation and the mean of goblet cells in colon tissue stained by hematoxylin-eosin. Giving EEDMD at all doses showed a significant difference in the number of inflammation (p <0.00) and mean goblet cells (p <0.00). Immunohistochemical examination was performed to see the expression of TNF-α, COX-2. NF-κβ. Positive cells express TNF-α, COX-2, and NF-κβ counts / 1000 epithelial cells. The results showed that EEDMD significantly reduced TNF-α expression compared to negative controls. Whereas in COX-2 (p <0.80) and NF-κβ (p <0.90) there were no significant differences."

"The term "Inflammatory Bowel Disease" (IBD) is frequently used to denote two diseases, ulcerative colitis (UC) and Crohn's disease (CD). This condition is frequently recorded in the West, and along with development of diagnostic facilities, is beginning to be more commonly found in Indonesia.The etiology of this disease is still unclear, but it is suspected that environmental, geographic, and genetic factors are involved. Cytokines play a great role in the pathogenesis of IBD, where in IBD there is an unbalance of pro-inflammatory cytokines and inhibitor cytokines. In IBD, there is an increase in pro-inflammatory cytokines, such as IL-1, IL-2, IL-6, IL-8, and alpha TNF in the intestinal mucosa. Such increase significantly correlates with the activity of ulcerative colitis through endoscopic examination,At this moment, forms of therapy for IBD associated with cytokines are being developed, such as ways to inhibit cytokine synthesis, cytokine release, cytokine activity and the cytokine signaling pathway in the target cell."

"Inflammatory bowel disease (IBD) has begun to emerge in Indonesia. The disease is further classified into two types, ulcerative colitic (UC) and crohn's disease (CD). Diagnosis of IBD is initiated from symptom findings such as diarrhea, abdominal pain, bleeding diarrhea, and weight loss, and supported by physical examination and additional tests. The options for additional examinations of IBD are mainly endoscopy (esophagogastroduodenoscopy, colonoscopy, and also intestinal endoscopy), imaging the techniques and laboratory examinations either from blood or feces. The application of these modalities should be prompted by sufficient clinical suspicion to promote their efficiency as well as prevent underdiagnosis or overdiagnosis. In primary health care settings, patients with IBD are expected to be recognized for therapy or to use appropriate referral system to warrant a proper treatment."

"ABSTRAKTelah dilakukan studi radiologis secara retrospektif terhadap kolitis ulseratif yang diperiksa dengan barium enema pada dua rumah sakit, yaitu satu rumah sakit pemerintah ( RS. Umum Dadi ) dan satu rumah sakit swasta ( RS. Stella Maris ) Ujung Pandang.Tujuan penelitian ini adalah untuk mengidentifikasi kelainan radiologis yang diketemukan, menetapkan stadium berdasar gambaran radiologis oleh akibat perubahan patologis kolon yang terserang kolitis ulserativa. Selain itu penelitian ini juga bermaksud untuk mendapatkan data distribusi umur, jenis kelamin, lokasi anatomic kolitis ulserativa dan membandingkannya dengan data kepustakaan yang ada dengan harapan ini bisa digunakan dalam melacak dan mendiagnose penyakit tersebut.Penelitian dilakukan selama dua tahun ( 1988 - 1989 ) terhadap 457 pemeriksaan barium enema yang dicurigai sebagai kasus kolitis. Diketemukan 241 kolitis ulserativa yang terdiri dari 120 laki-laki dan 121 wanita ( 1 : 1 ) Tertinggi pada umur 21 - 40 tahun, gejala klinis yaitu menonjol adalah diare dengan atau tanpa darah, yang paling kurang yaitu demam dan takikardia. Kolitis fulminan diketemukan 8 penderita, hanya 14 penderita kolitis ulserativa timbul, neoplasms.Kolitis tingkat ringan terbanyak diketemukan pada penderita dirumah sakit swasta sedang yang tingkat berat terbanyak pada rumah sakit pemerintah. Penderita kolitis ulserativa terbanyak menempati ruang rawat kategori B (ekonami lemah).Lokasi anatomis kolitis ulserativa terbanyak pada kolon kiri sedang keterlibatan rectum pada penelitian ini hanya 70.5%, bandingkan dengan kepustakaan ( 95% ).Dari penelitian ini dapat ditarik kesimpulan bahwa pemeriksaan barium enema Cukup efektif untuk: mendiagnose awal kolitis ulserativa dan dapat dilakukan penetapan stadium secara radiologis, yang berquna untuk para klinikus dalam penanganan penderita kolitis ulserativa.

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Barium examination of ulcerative colitis had been studied retrospectively in two which is Dadi Goverment hospital and Stella Morris hospital ( a private one ) that located in Ujung Pandang, South of Sulawesi.

The purpose of this research was to determined radiological image of ulcerative colitis and to confirmed the stage of the disease that based on pathologic and radiological changes.

Distribution of age, sex and anatomical location were also described and compared with other articles to detect and diagnosed the disease more properly.

There were 457 barium enema examination had been performed to detect suspected cases in the period of 1933 - 1939.

From such examination, 4hc'rs were 241 cases of ulcerative colitis had been detected ( 120 men and 121 women ) with the highest age frequency was 21 till 40 years old .

The frequency clinical findings were diarrhea with or without blood staining and the lesser findings were febrile and tachycardi. There were 8 patients with fulminant stage of the disease and there were 14 patients that came up to be neoplasma.

Mild colitis were found in the private hospital but on the other hand, severe colitis were more found in the government hospital. Patients with severe colitis came from lower social economic society that they had been hospitalized in B category.

The anatomical location of ulcerative colitis were in the left side of colon and rectal involvement were only 70,5% compared to 95% from other article.

It had been concluded that barium enema examination was very effective to diagnosed the early stage of ulcerative colitis and others stage as well, that is important for clinical doctors to decide the proper management for the patients."

"Inflammatory bowel disease (IBD) in rarely found in clinical practice. However, the incidence of IBD seems to have increased recently. Generally, the patients will come to hospital with chief complain! of chronic diarrhea with or without hematochezia.We reported two cases of IBD in which they had been misdiagnosed as colitis tuberculosis based on colonoscopy examination. Treatment of anti tuberculosis drugs had made no clinical improvement. Further evaluation suggested the diagnosis of IBD. They responded very well clinically after treated as IBD. This case report reminds us to consider the diagnosis of IBD in patient with chronic diarrhea and ulceration in colonic mucosa at colonoscopy."

"The pathogenesis of inflammatory bowel disease (IBD) is not yet fully understood A genetic predisposition, some environmental factors and microbial flora of the grit are the key factors. The presence of bacteria in the intestinal lumen is a prerequisite for the development of IBD. In animal models, mice incapable of expressing IL, or IL invariably develop a colitis- or Crohn-like inflammation. No inflammation occurs if they grow up in a pathogen free environment or if they are fed with Lactobacillus sp when exposed to environmental bacteria. Thus, the absence of liminal bacteria or a different make-up there of prevents the development of inflammatory bowel disease in this model. Patients with IBD have been found to have a decreased stool excretion Lactobacillus andlor Bifidobacteria. Furthermore, an increased number of bacteria adherents to the mucosa and within the epithelium has been demonstrated in quantitative studies. It appears that these bacteria trigger a strong abnormal mucosal immunological response, leading to intestinal epithelial cell injury mediated by activated T-cells, mononuclear cells and macrophages. If this response can not be down regulated by regulatory T-cells, mononuclear inflammatory cytokines are activated by stimulation of the intracellular transcription factor NF-kB. Recently it was shown that bacterial lipopolysaccharides can activate NF-kB by binding to two specific receptors on the cell membrane (Toll-like receptors [TLR's]) or intracellular receptors (NOD's). New insights of the role of bacteria in IBD became available by identifying susceptibility genes for IBD. Several IBD susceptibility loci were recently identified. The IBD-l locus on chromosome 16 shows positive evidence for linkage in Crohn's disease and IBD-2 locus on chromosome l2 for ulcerative colitis. The evidence for' an association with Crohn's disease at the IBD-I locus have been shown to be attributed to mutations in the CARDI5/NOD2 gene. This gene is exressed in peripheral blood monocytes and in intestinal epithelial cells and serves as a key factor of innate mucosal response to luminal bacteria as an antibacterial factor. The intact intercellular NOD2 protein binds LPS and activates NF-kB. This activation of the NF-kB signalling pathway in response to bacterial components plays a protective role in the mucosal epithelial cells for the host against inviting pathogens and an increased apoptosis of infected cells. There is evidence, that the defective NOD2 protein variants increase the susceptibility to pathogen invasion and a decrease in cellular apoptosis. NF-kB plays a dual role in IBD. On the mucosal epithelial cells, bacterial components bind on NOD2 proteins and protect bacterial invasion. If this barrier mechanism is not intact, the bacterial invasion stimulates via TLR- and NOD2 receptors in immune-active cells (macrophages, T-cells and monocytes) NF-kB and triggers an aberrant inflammatory response leading to tissue damage. These new insights in the pathogenesis in IBD have led to new treatment possibilities including pre- and probiotics. These therapies are aimed at directly modulating the host immune system to suppress intestinal inflammation. This has prompted considerable interest in manipulating the enteric microenvironment as a novel therapeutic strategy Several clinical studies showed promising results rising pre- and probiotics in patients with ulcerative colitis, pouchitis and Crohn's disease. The introduction of genetically engineered probiotic organism to produce and deliver anti-inflammatory cytokines or other biological relevant molecules to the mucosa offers further new potential for the treatment of IBD."

"Latar Belakang/Tujuan: Pasien IBD berisiko terjadi defisiensi Zink. Sedangkan Zink memiliki peran dalam menstimulasi sistem imun, regenerasi sel, dan berperan sebagai koenzim yang berperan sebagai antioksidan. Pemberian suplementasi Zink diharapkan dapat menurunkan aktivitas penyakit dan meningkatkan aktivitsas antioksidan.Metode: Penelitian ini merupakan kajian sistematis dan meta-analisis. Pencarian literatur dilakukan sampai desember 2020 dengan mencari pada tiga database yaitu Cochrane central, Pubmed, dan Embase. Berdasarkan kriterian eligibilats didapatkan 9 artikel yang menilai efek Zink terhadap aktivitas penyakit IBD. Aktivitas penyakit dinilai berdasarkan skor CDAI dan skor Mayo, serta aktivitas enzim SOD.Hasil: Sebanyak 9 studi didapat dari pencarian, dilakukan analisis kualitatif dan kuantitatif. Meta-analisis dilakukan dengan membagi menjadi 3 subgrup, yaitu Zink terhadap aktivitas penyakit IBD, Zink terhadap aktivitas enzim SOD, serta aktivitas penyakit sebelum dan sesudah pemberian. Empat studi menilai efek Zink terhadap aktivitas penyakit menunjukkan tidak terdapat penutunan aktivitas penyakit IBD, dua studi menilai efek Zink terhadap aktivitas SOD menunjukkan tidak terdapat peningkatan aktivitas SOD, dua studi menilai efek Zink terhadap ekspresi metalotinonin datu studi menunjukkan peningkatan dan satu studi tidak menunjukkan peningkatan. Tiga studi pre dan post dari dua studi menunjukkan tidak terdapat penurunan aktivitas penyakit dan 1 studi menunjukkan penurunan aktivitas jika diberikan jangka panjang.Simpulan: Tidak didapatkan perbedaan aktivitas penyakit, aktivitas SOD, aktivitas metalotionin dengan suplementasi Zink jangka pendek, suplementasi jangka panjang dapat menurunkan aktivitas penyakit IBD

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Background/Aim: IBD patients are at risk of Zinc deficiency. Zinc has a role in stimulating the immune system, cell regeneration, and as a coenzyme acts as an antioxidant. Zinc supplementation will decrease disease activity and increase antioxidant activity.

Method: This research is a systematic review and meta-analysis. Literature searches are conducted until December 2020, we searched in three databases Cochrane central, Pubmed, and Embase. Based on eligibility criteria, there are 9 articles evaluate effect of Zinc on disease activity of IBD. Disease activity is assessed based on CDAI score and Mayo score, as well as SOD enzyme activity.

Result: We identified 9 studies, Of all the potentially relevant papers, 9 studies were identified. All of the studies were assessed for risk of bias along with qualitative analysis. Pre-specified outcomes were Zinc and disease activity, Zinc and SOD activity, metallothionine expression as well as disease activity before and after administration. Four studies evaluated effect of Zinc on disease activity showed no improvement in IBD disease activity, two studies evaluated effect of Zinc on SOD activity showed no increase in SOD activity, two studies evaluated effect of Zinc on metalotinonin expression, one study showed increase of expression and the other had no increase. There are 3 pre and post studies from two studies showed no decrease in disease activity and 1 study showed a decrease in activity if supplemented for long term.

Conclusion: The results of the systematic review revealed there were no difference in disease activity, SOD and methalotionen activity with short term Zinc supplementation, long term supplementation decrease disease activity of IBD"

"Latar Belakang. Vitamin D merupakan salah satu komponen regulator yang berperan dalam respons imun humoral maupun adaptif yang memiliki peranan patogenesis dalam berbagai kondisi autoimun termasuk IBD. Defisiensi vitamin D diketahui dapat mempengaruhi derajat aktivitas pada pasien dengan IBD. Beberapa studi menunjukkan terdapat peran vitamin D dalam meningkatkan angka remisi pada pasien dengan IBD. Namun studi lain menunjukkan tidak ada hubungan yang signifikan terhadap aktivitas klinis IBD dengan defisiensi vitamin D. Belum ada studi di Indonesia yang menilai hubungan kadar vitamin D dengan aktivitas klinis pada IBD.Tujuan. Mengetahui prevalensi defisiensi vitamin D pada pasien dengan IBD dan menilai perbedaan rerata kadar 25-OH D pada subjek dengan IBD aktif dengan remisi.Metode. Penelitian ini merupakan studi dengan desain potong lintang yang dilakukan di Rumah Sakit Cipto Mangunkusumo. Pasien dengan IBD yang datang ke Poliklinik Gastroenterologi dan dilakukan pemeriksaan kadar 25-OH-D. Subjek dengan kolitis ulseratif dinilai aktivitas klinisnya dengan menggunakan instrumen Simple Clinical Colitis Activity Index (SCCAI) dimana nilai <2 dikategorikan sebagai remisi, sedangkan subjek dengan penyakit Crohn dinilai aktivitas klinisnya dengan menggunakan instrumen Crohn’s Disease Activity Index (CDAI) dengan nilai <150 dikategorikan sebagai remisi. Dilakukan analisis perbedaan rerata kadar 25-OH-D antara subjek remisi dibandingkan aktif baik pada subjek dengan kolitis ulseratif dan penyakit Crohn.Hasil. Sebanyak 76 subjek memenuhi kriteria inklusi dan eksklusi, 48 subjek termasuk ke dalam kolitis ulseratif dan 28 lainnya penyakit Crohn. Sebanyak 65,3% subjek perempuan dengan rerata usia subjek adalah 46,39 (SB 16,25). Prevalensi defisiensi vitamin D pada pasien IBD adalah sebesar 46,1% dengan 32,1% pada penyakit Crohn dan 54,2% pada kolitis ulseratif. Tidak didapatkan adanya perbedaan median yang signifikan antara subjek dengan penyakit Crohn pada remisi (20,7 (12,25 – 32,55) ng/ml) dan aktif (15,7 (12,03 – 28,6) ng/ml) (p = 0,832), maupun subjek dengan kolitis ulseratif pada remisi (26,05 (19,33 – 30,73) ng/ml) dan aktif (25,05 (14,43 – 33,37) ng/ml) (p = 0,301).Kesimpulan. Prevalensi defisiensi vitamin D pada IBD adalah sebesar 46,1%. Tidak terdapat adanya perbedaan yang signifikan terhadap kadar 25-OH-D pada pasien dengan IBD yang aktif dibandingkan dengan remisi.

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Background. Vitamin D is one of the regulatory components that play a role in humoral and adaptive immune responses that have a pathogenesis role in various autoimmune conditions including IBD. Vitamin D deficiency is known to affect activity levels in patients with IBD. Several studies have shown that there is a role for vitamin D in increasing remission rates in patients with IBD. However, other studies have shown that there is no significant relationship between clinical activity of IBD and vitamin D deficiency. There are no studies in Indonesia that have assessed the relationship between vitamin D levels and clinical activity in IBD.

Aim. To determine the prevalence of vitamin D deficiency in patients with IBD and to assess the difference in mean 25-OH D levels in subjects with clinically active and remission.

Method. This is a cross-sectional study conducted at Cipto Mangunkusumo Hospital, Jakarta, Indonesia. Patients with IBD who came to the Gastroenterology Polyclinic and have their 25-OH-D levels checked. Subjects with ulcerative colitis were assessed for clinical activity using the Simple Clinical Colitis Activity Index (SCCAI) instrument where a value <2 was categorized as remission, while subjects with Crohn's disease were assessed for clinical activity using the Crohn's Disease Activity Index (CDAI) instrument with a value <150 categorized as remission. An analysis of the difference in mean 25-OH-D levels between remission versus active subjects was performed both in subjects with ulcerative colitis and Crohn's disease.

Results. A total of 76 subjects met the inclusion and exclusion criteria, 48 subjects had ulcerative colitis and 28 had Crohn's disease. A total of 65,3% of female subjects with the mean age of the subject was 46,39 (SB 16,25). The prevalence of vitamin D deficiency in IBD patients was 46,1% with 32,1% in Crohn's disease and 54,2% in ulcerative colitis. There was no significant median difference between subjects with Crohn's disease in remission (20,7 (12,25 – 32,55) ng/ml) and active (15,7 (12,03 – 28,6) ng/ml) (p = 0,832), as well as subjects with ulcerative colitis in remission (26,05 (19,33 – 30,73) ng/ml) and active (25,05 (14,43 – 33,37) ng/ml) (p = 0,301).

Conclusion. Prevalence of vitamin D deficiency in IBD is 46,1%. There was no significant difference in 25-OH-D levels in patients with active IBD compared with remission."