+90 (312) 472 17 69

ULCERATIVE COLITIS

ULCERATIVE COLITIS / INFLAMMATORY BOWEL DISEASE

Classical Definition

Inflammation of the layer on the inner surface of the large intestine, manifested by complaints such as fever, abdominal pain, diarrhea, rectal bleeding, in which genetic background and environmental factors play a role in the formation of the disease.

EPIDEMIOLOGY

Ulcerative colitis can be seen at any age. However, it usually starts between the ages of 15 and 30, and is less frequent in the fifties and seventies. The frequency of incidence in men and women is considered equal. It is more frequent in white race than in blacks.

ETIOLOGY (CAUSALITIES) AND PATHOPHYSIOLOGY (FORMATION MECHANISM)

Classical Approach

Reason cannot be explained. It is thought to be connected to environmental and genetic infrastructure. One of the theories that is emphasized is the triggering of inflammation by constantly stimulating the immune system of a virus or bacterium in the intestinal wall. It is thought that an excessive reaction of the immune system constitutes complaints, but it is not known how this develops.

 

Ulcerative colitis can be seen along the inflammatory colon (limited to the large intestine).

Dr. Ceyhun NURI’s Approach to Formation Mechanism:

  1. Effect on the environment of physiology

Unconscious drug use such as Aspirin, Antibiotic, Cigarette, Alcohol, Stress, Blood Transfusion, Tonsillectomy, Appendectomy, Appendicitis, Nontosteroid anti-inflammatory drugs (Painkillers), The Frequent, Confused, Mixed intake of added foodstuffs that cannot be consumed causes the intestinal wall surface to be covered with an indigestible waste layer. Intestinal probiotic flora begins to be affected in the worst way. As a result, the intestinal surface protection shield is removed. This process forces the regeneration process of the intestinal surface epithelium. The bowel surface begins to lose its property (it turns into fibrous tissue).

In Ulcerative colitis, inflammation of the intestinal mucus is seen as a cause of the growth of some microorganisms under the development of inflammation. Ulcerative colitis, inflammation of the intestinal mucus is seen as a cause of the growth of some microorganisms under the development of inflammation. As the intestinal natural flora is destroyed for some reason as mentioned above, the pathogenic microorganisms start to settle here, and these microorganisms start intense immune reaction against themselves or the toxic factor, cytokine, enzymes they secrete. (Th1 begins to increase further in the inflammatory response and releases the proinflammatory IL2 ITF-Gamma cytokines, which maintain the response). If inflammation is persistent, epithelium, mucous membrane destruction and ulceration begin to develop. Some of these pathogenic microorganisms are: Salmonella, E. coli, Campylobacter, Yersinia, E.Hysterica, measles virus. Maybe it is the microorganism that initiates damage on the intestinal wall, but it cannot be named because it cannot be produced in culture.

  1. The effect of the environment on genetic structure

There are microRNAs carried by each food, plant, and nutrient item. As an example, the genetic information that passes through the rice leads to an increase in the level of LDL that plays a role in cardiovascular diseases. Once the RNA in the food structure is absorbed in the gut, it is transported to the tissues of your body and begins to interfere with human genes. Changes in the DNA or RNA sequence begin. With the change of genetic information, the structure of proteins and enzymes encoded by DNA starts to change. This change results in disruption of structure and metabolism. The mutated genetic information begins to be transmitted. But let’s not forget that there are DNA repair mechanisms in our bodies that will correct genetic mutations. It is sufficient to support them!

As a result, when the DNA changes, it encodes it and starts to change in the proteins and enzymes that it sets its functionality. The enzyme either completely loses its function or causes incorrect metabolic processes. Here, some of the enzymes necessary for digestion (lipase, peptidase, amylase, lactase, etc.) lose their functional activity and the food taken into the intestines cannot be digested. There is a dense immune response to toxins that accumulate in the gut surface and in the gut lumen. If this process is prolonged (if the attack takes a long time) surface damage is inevitable. If, over time, it does not interfere with the course (wrong feeding, uncontrolled drug use, etc.), it is inevitable that the inflammatory process on the surface of the intestine changes direction to colon cancer. Do not forget that a certain structure of the cell is enough to create some conditions to destroy DNA (acid shift of ph balance, decrease in oxygen reaching the cell, deterioration of blood quality which removes toxins from the cell and nutrient accumulation etc.). Also, in this process, DNA synthesis and repair stops (Prostaglandin, Prostasiclines, IL-1, TNF-gamma and bacterial lipopolysaccharides stop Nitric Oxide inducers (triggers), NO stops mitochondria functions (a building block of cells) and inhibits DNA synthesis).

Ulcerative colitis is one of the most important risk factors of positive family history. In other words, it is the existence of the disease in the close family members like parents. The important thing to keep in mind is that due to the mistakes made by your parents, the DNA structure changes and the mutation is transferred to the child.

There are some genetic reading errors detected in the frame of our current knowledge. Chromosome 3,6,7,12 susceptibility locus, polymorphism in cytokine genes (TNFalpha, IL-1RA). HLA-DR2 is considered to be an important factor in susceptibility to the disease. These are the genetic reading mistakes that are transmitted from parents to children.

CHRONIC

The severity of the disease varies from person to person. It manifests itself in a one-to-one following of exacerbation and goodness.

The most common symptoms of ulcerative colitis are cramp-shaped abdominal pain and bloody diarrhea. In addition, stool and mucus discharge can be seen. As the inflammation of the region close to the intestinal outlet increases, the stooling impulse increases, but the stool passage becomes smaller or lesser as the outlet region contracts with the cause of edema and inflammation. Symptoms that can be seen as inflammation and ulcers, as areas become more severe are:

 Fatigue

 Nausea / Vomiting

Loss of appetite

 Weight loss

 Rectal Bleeding

 Frequent bowel movements (if the inflammation affects the rectum area)

 Liquid, nutrient, elemental loss (Diarrhea Iron, B12 Vit, Ca malabsorption)

 Frequent fever

 Bloody Diarrhea

 Constipation (from complaints seen in older ages, preventing the emergence of rectal spasms)

Outside the intestinal system, the most common symptom in the UC is the musculoskeletal system.

 Arthritis

 Sacroileite (Continuous pain in the lower part of the belly, very mixed with spinal disc herniation)

 Ankylosing Spondylitis (morning dysfunction, moving back / back pain)

 Osteoporosis

 Aseptic Necrosis

Hippocratic fingers

 Polymyositis

Other autoimmune diseases can be seen together:

 Uveitis, Retinal hemorrhages, Cataracts

 Hepatitis

 Cirrhosis

 Primer sclerosing cholangitis

 Pericolinite

 Psoriasis, Vitiligo, Pyoderma Gangrenosum, Erythema Nodosum

 Nephrotic Syndrome, Glomerulonephritis

In addition, involvement and problems related to some circulatory system and neurological system can be seen in the UC.

 Uveitis, Retinal hemorrhages, Cataracts

 Hepatitis

 Cirrhosis

 Primer sclerosing cholangitis

 Pericolinite

 Psoriasis, Vitiligo, Pyoderma Gangrenosum, Erythema Nodosum

 Nephrotic Syndrome, Glomerulonephritis

In addition, involvement and problems related to some circulatory system and neurological system can be seen in the UC.

 Anemia (anemia due to chronic bleeding due to frequent bleeding)

 Thrombocytosis, Thrombophlebitis (Vein Occlusion)

 Thromboembolism (embolism)

 Thrombocytopenic purpura (slight bumps or unexplained bruises)

 Pericarditis (inflammation of the heart membrane)

 Bronchopulmonary involvement (Respiratory system involvement)

 Peripheral neuropathy (especially pain in feet, manifested by pain)

 Myasthenia gravis, cerebrovascular blindness (some neurological problems)

DIAGNOSIS

The first step to progression is to apply the physical examination without skipping any detailed history and no phase. (Including rectal touch)

Ulcerative colitis is among the diseases that should come to our attention if we have intestinal complaints (nausea, abdominal pain, diarrhea etc.), joint pain, general fatigue, increased gastrointestinal complaints, frequent fever and similar complaints.

The laboratory tests to be requested are:

– Whole Blood Count

 

-Iron, Ferritin, Iron

Bonding Capacity

 

– Zinc, Zinc binding

its capacity

-Vitamin B12

 

-Insulin (Hunger), Hunger- blood sugar

 

-CRP, RF, ES Speed

 

– Calcium, Phosphorus

-Magnesium

-Alkaline Phosphatase

 

– Liver enzymes

 

-Total protein, albumin

 

-Electrolytes

 

– microscopic inspection of stool

 

-PTH, vitamin D

 

-Hand-wrist graphy

 

-Bone densitometry

 

-IgA, IgG, IgM

-PT, PTT

-Thyroid function tests

 

– Thyroid antibodies (TG, Anti Tg, Anti TPO)

 

— Autoantibodies (ANA, dsDNA, AMA, ASMA, LKM 1)

 

-EEG

 

– Cranial MR

 

– Tissue group

Stool Microscopy and Culture:

Eosinophils, erythrocytes, inflammatory cells can be seen. Amoeba, Salmonella, Shigella, Yersinia, E. coli, Clostridium difficile, Campylobacterium.

Imaging

The most valuable diagnostic method in UC is colonoscopy and biopsy results obtained during this procedure. But the following imaging methods can also be used.

  • Barium Column Graphic
  • Computerized Tomography
  • Magnetic Resonance
  • Ultrasonography (Fistula, abscess, valuable in detecting fluid accumulations)
  • Standing Direct abdomen Graph

Biopsy

Although the involvement is observed in many parts of the large intestine, the most common involvement is rectum (area near the anus). Inflammation usually involves mucosa and submucosa in the UC. So the involvement is usually superficial.

DIFFERENTIAL DIAGNOSIS

Diseases with ulcerative colitis

• Crohn

 

• Celiac

 

• Bacterial infections (Shigella,

Yersinia, Campylobacter, ameba, Escherichia coli, Clostridium difficile)

 

• Hemorrhoids

 

• Anal Fissure

 

 

• Collagenous colitis

 

• Ischemic Colitis

 

• Intestinal tuberculosis

 

• Amyloidosis

 

• Cecal Diverticulitis

 

• Acute appendicitis

 

• Tubo-ovarian disease

 

• Pelvic Inflammatory Disease

 

• Ectopic Pregnancy

• Systemic vasculitis

 

TREATMENT

Classical Treatment Approach

THERE IS NO DEFINITIVE TREATMENT.

The purpose of the treatment is to improve the quality of life of the patient, to control the inflammatory damage (naturally not possible to eradicate the cause as it is not known exactly), to reduce symptoms (such as abdominal pain, diarrhea, correction of malnutrition). The approach to this is shown as follows:

  1. Drug Treatment

Expectations from Treatment: the provision of remission and improvement of patients’ quality of life. To this end, medicines containing 5-aminosalicylic acid (5-ASA) for controlling inflammation. Sulfasalazine sulfapyridine is also used in remission. However, many side effects such as nausea, vomiting, heart attack, diarrhea, and headache can be seen in these drugs. In addition, drugs such as corticosteroids such as prednisone, hydrocortisone and drugs used to reduce inflammation. Side effects such as weight gain, acne, hypertension, increased risk of infection can be seen. Therefore, prolonged use is not recommended.

If the complaints are not taken under control and the drugs above are not responded, some immunosuppressive medicines have to be applied. Immunomodulators such as azathioprine and 6-mercaptopurine (6MP), cyclosporine A try to reduce inflammation by influencing the immune system. These drugs also have many side effects such as pancreatitis, hepatitis, leukopenia (reduction of immune cells), and increased risk of infection.

  1. Surgery

In cases where the drugs cannot be suppressed and cannot be controlled, surgical procedures are called for, which is called proctocolectomy, resulting in removal of the rectum and large intestine, if necessary, insertion of the intestines into the abdomen wall with a bag (Colostomy).

  1. CEYHUN NURI’S APPROACH TO THE TREATMENT
  2. Trying to suppress a condition whose reason you cannot detect on your body with anti-inflammatory (anti-inflammatory), immunosuppressive (immunosuppressive) drugs, is actually the biggest evil done to the patient without realizing. Although recourse to irreversible pathways (bowel removal) is done with the intention of improving the quality of life of the patient, extinguish the love of life of man, maybe kill the human!!!

IT IS POSSIBLE TO COMPLETELY ELIMINATE THE DISEASE AS WE DO KNOW THE REASON OF IT.

  1. The detox program, which will help repair the intestinal sealing wall and cleanse the liver system, should be applied quickly.
  2. Now that food and nutrients are influencing the structure of DNA and RNA then it is necessary to keep away from processed, added, misplaced and structurally altered foods (fried, roasted cookies, processed drinks, stale foods etc.). It is essential to resort to phytotherapeutic solutions that will activate DNA repair mechanisms and assist in the correct coding of genetic material and regeneration of ulcer sites (seeds that do not deteriorate structure)
  3. Absent, missing elements and other deficiencies should be rapidly resolved (Iron, B12Vit, Ca, Mg, P, Na, K, etc.)
  4. When complaints are flare up, besides the main treatment we apply, the most important additional measure is the rest of the intestines. So it would be right to feed light foods that support the intestinal biological life, keeping the intestines away from heavy foods.

COMPLICATIONS THAT CAN BE DEVELOPED IF NOT TREATED

  • Toxic megacolon is one of the most dangerous outcomes that Ulcerative Colitis can cause (enlargement process without any blockage in the intestines)
  • Dangerous conditions such as perforation may occur in the intestines.
  • The UC should be taken seriously and the development of intestinal ulcers, fluid, nutrients, elemental loss, permanent blood loss and other autoimmune problems are inevitable if the underlying cause is not treated.
  • The anemia that can be seen in the UC may be due to the loss of many substances such as chronic disease, loss of blood, deterioration of intestinal absorption, removal of the intestines by surgery. Drugs that suppress the immune system, which are used for a long time, cause the bone marrow to shrink and reduce the production of blood cells.
  • Additional complaints such as fistula, anal fissure, abscess, hemorrhoids may occur in the intestine.
  • If chronic, pseudo-polyps may develop on the intestinal wall.
  • Inflammation can spread to the liver, gallbladder, joints.
  • Clotting disorder may develop
  • Colon cancer develops in about 5% of Ulcerative Colitis patients (the longer the period of retention in the disease and the greater the intestinal area, the greater the risk increases).

RECOMMENDATIONS OF DR.CEYHUN NURI:

Besides the main treatment that we apply, patients can get nutritional and herbal supplements that can help reduce the symptoms of UC at home:

  • As feeding on probiotics (Kefir, Yogurt) rises intestinal beneficial biological flora (Lactobacilli, Bifidobacteria etc.), it helps to reduce complaints.
  • Cesarean birth that destroys the bowel flora, unnecessary use of medication, wrong nutrition style should be abandoned
  • Smoking should definitely be abandoned (exacerbation and recurrences increase).
  • Omega 3 fatty acids help relieve inflammation, relieve symptoms of UC, and prevent the recurrence of the condition. These patients should use at least 2-3 grams of Omega 3 preparation per day.
  • Evening primrose oil is very useful in resolving the UC complaints. We recommend consuming a sweet spoon, on an empty stomach, three times a day.
  • Plantaginis ovatae Yellow semen psyllii are also useful herbal supplements in addition to the main treatment. Prolongation of the remission and prevention of relapses (Repeat) have been shown to be as effective as this drug in comparison with mesalazine.
  • In the UK, patients often lose many nutrients, minerals, and elements with blood loss, malabsorption, frequent diarrhea and dehydration. For this reason, many minerals such as folic acid, B12, D, E vitamins, Magnesium, Iron, and Calcium will be correct.
  • Aloe Vera containing various enzymes (protease, lipase, amylase, catalase, Carboxypeptidase etc.), polysaccharides, vitamins (A, B1, B2, B12, E, Choline), minerals (Iron, Na, Manganese, is useful for the regeneration of the colon mucosa structure in the UC with the reason of its viscous structure. We recommend consuming 1 or 2 tablespoons on empty stomach a day.

Dr. Ceyhun NURİ

For more information, please contact us at our contact details.

 

RESOURCES

  1. Friedman SL. McQuaid KR. Grendell JH. Current Diagnosis and Treatment in Gastroenterology. 2 nd. Ed. McGraw-Hill Company, 2003: 108-130.
  2. Scott MM, EkbomA. Epidemiology of inflammatory bowel disease. Current Opinion in Gastroenterology 2002; 18: 416-420.
  3. Sandler RS, Eisen GM. Epidemiology of inflammatuar bowel disease. In: Kırsner JB, Ed. Inflammatory bowel disease. Philadelphia: WB Saunders Company, 2000: 89.
  4. Sands BE, Crohn Disease.Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 7th Ed., Philadelphia: WB Saunders Company, 2002: 2005-2038.
  5. Jewell DP. Ulcerative colitis. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 7th Ed., Philadelphia: WB Saunders Company, 2002:2039-2067.
  6. Tözün N, Hamzaoğlu Över H. İltihabi barsak hastalıklarında etyolojik faktörler. Güncel Gastroenteroloji 1997;1/2:287-294.
  7. Riegler G, Arimoli A, Esposito P. Clinical evolution in an outpatient series with indetermine colitis. Dis Colon Rectum 1997; 40:437-439.
  8. Kirsner JB. Overview of etiology, pathogenesis and epidemiology of inflammatory bowel disease. In:. Haubrich WS, Schaffner F, Berk JE, Eds. Bockus Gastroenterology. Vol:2 5 th Ed., Philedelphia: WB Saunders Company, 1995:1293-317.
  9. Weterman IT, Pena AS. Familial incidence of Crohn disease in the Netherlands and a review of the Literature. Gastroenterology 1984;86:449.
  10. Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B. Ulcerative colitis and Crohn’s disease in an unselected population of monozygotic an dizygotic twins: a study of heritability and the influence of smoking. Gut 1998;29:990-996.
  11. Harvey RG, Bradshaw JM. A simple index of Crohn’s disease. Lancet 1980;1:51
  12. Seo M, Okada M, Tsuneyoshi. An index of disease activity in patients with ulcerative colitis. A J G 1992;87(8):971-5.
  13. Baykal Y, Naharcı Mİ. İnflamatuar barsak hastalığı. Sendrom 2005; 17(4):61-84.
  14. Wakefield AJ, Sawyer AM, Hudson M. Smoking, the oral contraceptive pill, and Crohn’s Dig Dis Sci 1991;36(8):1147-1150.
  15. Cosnes J, Beaugerie L, Carbonnel F. Smoking cessation and the course of Crohn’s disease; an intervention study. Gastroenterology 2001;120:1093-1099.
  16. Odes HS, Fich A, Reif S. Effects of current cigarette smoking on clinical course of Crohn’s disease and ulcerative colitis. Dig Dis Sci 2001;46:1717-1721.
  17. Koutrobakis IE, Ulachonikolis IG. Appendectomy and the development of ulcerative colitis; results of a meta-analysis of published case-control studies. Am J Gastroenterol 2000;95(1):171-176.
  18. Ohkusa T, Sato N. Antibacterial and antimycrobial treatment for inflammatory bowel disease. J Gastroenterol Hepatol 2005;20:340-51.
  19. Guarner F, Schaafsma GJ. Probiotics. Int J Food Microbiol 1998;39:237-8.
  20. Hermon-Tylor J. Mycobacterium avium subspecies paratuberculosis is a cause of Crohn’s disease. Gut 2001;49:755-757.
  21. Chamberlin W, Graham DY, Hulten K. Review article: Mycobacterium avium subspecies paratuberculosis as one cause of Crohn’s disease. Aliment Pharmacol Ther 2001;15:337-346.
  22. Lavy A, Broide E, Reif S. Measles is more prevalent in Crohn’s disease patients. A multicenter Israeli study. Dig Liver Dis 2001;33:472-476.
  23. Duerr H. R. The genetics of inflammatory bowel disease. Gastroeterology Clinics of North America 2002;31:63-76.
  24. Jean-Pierre Hugot, Judy H Cho: Update on genetics of inflammatory bowel disease. Current Opinion in Gastroenterology 2002;18:410-415.
  25. Cuthbert AP, Fisher SA, Mirza MM. The contribution of NOD2 gene mutations to the risk and site of disease in inflammatory bowel disease. Gastroenterology 2002;122:867-874.
  26. Hugot JP, Laurent-Puig P, Gower-Rousseau C. Mapping of susceptibility locus for Crohn’s disease on chromosome 16. Nature 1996;379:821-823.
  27. Ogura Y, Bonen DK, Inohara N. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature 2001;411:603-606.
  28. Grisham MB. Oxidants and free radicals in iflammatory bowel disease. Lancet 1994;344:859-861.
  29. Williams J.G, Hughes LE, Hallet MB. Toxic oxygen metabolyte production by circulating phagocytic cells in inflammatory bowel disease. Gut 1990;31:187-193.
  30. Mullin GE, Lazenby A.J. Increased Interleukin-2 mRNA is in the itestinal mucosal lesions of Crohn’s disease but not of UC. Gastroenterology 1992;102:1620.
  31. Caradonna L, Amati L, Lella P. Phagocytosis, killing, lymphocyte-mediated antibacterial activity, serum autoantibodies, and plasma endotoxins in inflammatory bowel disease. Am J Gastroenterol 2000;95(6):1495-502.
  32. Tözün N, Atuğ Ö. İltihabi Barsak Hastalıkları. In: Memik F, Ed. Klinik Gastroenteroloji. Bursa: Nobel & Güneş Kitabevi, 2004:448-461.
  33. Guslandi M. Probiotics for chronic intestinal disorders. Am J Gastroenterol 2003;98:520-1.
  34. Hamilton SR, Morson BC. Ulcerative Colitis. Pathology. In: Haubrich W, Schafiher F, Berk JE, Eds. Bockus Gastroenterology. Vol:2 5 th Ed., Philedelphia: WB Saunders Company, 1995:1326-37.
  35. Stenson WF. Inflammatory Bowel Disease. In: Yamada T, Ed. Textbook of Gastroenterology. Vol:2 2nd Ed., Philedelphia: JP Lippincott Company, 1995:1748-1806.
  36. Jewel DP. Ulcerative Colitis. In: Feldman M, Scharschmidt B, Sleisenger MH, Eds. Gastrointestinal and Liver Disease. Vol:2 6th Ed., Philedelphia: WB Saunders Company, 1998:1735-61.
  37. Stenson WF. İnflamatuvar Barsak Hastalıkları. In: Goldman Lee, Ausiello D, Eds. Cecil Textbook of Medicine. 22th Ed., Ankara: Güneş Kitabevi, 2006:861-869.
  38. Giaffar MH, Clark KA, Holdsworth CD. ASCA in patients with Crohn’s disease and their possible pathogenetic importance. Gut 1992;33:1071-1075.
  39. Aktan H, İltihabi Barsak Hastalığı. In: Aktan H, Aktan B, Alptuna E, Atmaca NS, Eds. Gastroenteroloji. 1. baskı, Ankara: Makro Yayıncılık, 1988:178-190.
  40. Rachmilewitz D. Coated mesalazine (5 amino salicylic acid) versus sulphasalazine in the treatment of ulcerative colitis; A Randomize Trial. Br Med J 1989;298:82-86.
  41. Muratori P, Muratori L, Guidi M, Maccariello S, Pappas G, Ferrari R, Gionchetti P,Campieri M, Bianchi FB. Anti-Saccharomyces cerevisiae antibodies (ASCA) and autoimmun liver diseases. Clin exp Med 2003;132:473476.

42.Best WR, Becktel JM, Singleton JM, Kern F. Development of a Crohn’s disease activity index. Gastroenterology 1976:70:439-444.

  1. Kaymakoğlu S. İnflamatuar Barsak Hastalıkları. In: Mungan Z, Çakaloğlu Y, Ökten A, Eds. Gastroenteroloji. İstanbul: Nobel Tıp Kitapevleri, 2001:189-211.
  2. Gasche C,Scholmerich J, Brynskov J. A simple classification of Crohn’s disease; report of the Working Party for the World Congresses of Gastroenterology, Vienna. Inflam Bowel Dis 2000;6:11.
  3. Charles N Bernstein: Osteoporosis and other complications of inflammatory bowel disease. Current Opinion in Gastroenterology 2002;18:428-434.
  4. Monsen U, Sorstad J, Hellers G, Johansson C. Extracolonic diagnosis in ulcerative colitis: An epidemiological study. Am J Gastroenterol 1990;85:711-716.
  5. Edward V, Loftus, Jr. William, Sandborn J. Interactions between chronic liver disease and inflammatory bowel disease. Inflammatory Bowel Disease 1997;3(4):288-302.
  6. Wiesner RH, LaRusso NF. Clinicopathologic features of the syndrome of primary sclerosing cholangitis. Gastroenterology 1980;79:200-206.
  7. Greenstein AJ, Janowiz HD, Sachar DB: The extra-intestinal complications of Crohn’s disease and Ulcerative colitis. A study of 700 patients. Medicine 1976;55:401-412.
  8. Kiran M. Das. Relationship of extraintestinal involvements in inflammatory bowel diseae. Dig Dis Sci 1999;14:1-14.
  9. Tözün N, Özdoğan ÖC. İnflamatuar Barsak Hastalıklarında Amip İnfeksiyonu. Aktüel Gastroenteroloji ve Hepatoloji 2003:329-335.
  10. Podolsky DK. Inflammatory bowel disease. N Engl J Med 2002;347:417-429.
  11. Maklansky D, Lidner AE. Ulcerative colitis. Radiologic Features. In: Haubrich W, Schaffner F, Berk JE, Eds. Bockus Gastroenterology. Vol:2 5th,Philedelphia: WB Saunders Company 1995:1342-49.
  12. Halligan S. The Large Bowel. In: Sutton D, Ed. Textbook of Radiology and Imaging, London: Churchill Livingstone, 2003:635-662.
  13. Oktay E. İnflamatuar Barsak Hastalıkları; Etyopatogenez, Semptomatoloji, Tanı ve Komplikasyonlar.

Gastrointestinal Sistem Hastalıkları. İstanbul: Cerrahpaşa Tıp Yayınları. 2001:199-206.

  1. Shannahan F. Crohn’s disease. Lancet 2002;359:62-69.
  2. Çavuşoğlu H. İnflamatuar Barsak Hastalığı. In: İliçin G, Ünal S, Biberoğlu K, Süleymanlar G, Ünal S, Eds.

Temel İç Hastalıkları. 2. baskı, Ankara: Güneş Kitabevi, 2003:1577-1591.

  1. Farrel RJ, Peppercon MA. Ulcerative Colitis. Lancet 2002;359:331-340.
  2. Mamula P, Markowitz JE, Baldassano RN. Inflammatory bowel disease in early childhood and adolescence: special considerations. Gastroenterol Clin North Am 2003;32:967-95.
  3. Aydıntuğ O. Anti-nötrofil Sitoplazmik Anikorlar (ANCA) ile ilişkili Hastalıklar. T Klin Tıp Bilimleri.1992;12:222-230.
  4. Williams CB, Waye ID. Colonoscopy and Flexible Sigmoidoscopy. In: Yamada T, Ed. Textbook of Gastroenterology. Vol:2 2nd Ed., Philedelphia: JP Lippincott Company, 1995:2571-89.
  5. Zholudev A, Zurakowski D, Young Y, Leichtner A, Bousvaros A. Serologic testing with ANCA, ASCA, and anti-OmpC in children and young adults with Crohn’s disease and ulcerative colitis: diagnostic value and correlation with disease phenotype. Am J Gastroenterol 2004;99:2235-2241.
  6. Saibeni S, Folli C, de Franchis R. Diagnostic role and clinical correlates of anti-Saccharomyces cerevisiae antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (p-ANCA) in Italien patients with inflammatory bowel diseases. Dig Liver Dis 2003;35:862-868.
  7. Bansi DS, Chapman RW, Fleming KA. Prevalance and diagnostic role of antineutrophil cytoplasmic antibodies in inflammatory bowel disease. Eur J Gastroenterol Hepatol 1996;8:881-885.
  8. Nugent FW, Haggit RC, Gilbin PA. Cancer surveillance in ulcerative colitis. Gastroenterology 1991;100:1241-1248.
  9. Vermeire S, Peeters M, Vlietnick R. Anti-Saccharomyces cerevisiae antibodies (ASCA), phenotypes of IBD, and intestinal permeability: a study in IBD families. Inflamm Bowel Dis 2001;7(1):8-15.
  10. Peeters M, Jooessens S, Vermeire S. Diagnostic value of anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease. Am J Gastroenterol 2001;96(3):730-734.
  11. Meyers S. Crohn’s Disease. Complications on their management. In: Yamada T, Ed. Textbook of Gastroenterology. Vol:2 2 nd Ed., Philedelphia: JP Lippincott Company, 1995:1588-1645.
  12. Sutherland LR, May GR, Shaffer EA. Sulfosalazine revisited: a meta-analysis of 5-aminosalicylic acid in the treatment of ulcerative colitis. Ann Intern Med 1993;118(7):540-549.
  13. Stein RB, Hanauer SB. Medical therapy for inflammatory bowel disease. Gastroenterol Clin North Am 999;28:297-321.
  14. Panes J, et al. Comparison of heparin and steroids in the treatment of moderate and severe ulcerative colitis. Gastroenterology 2000;119(4):903-908.
  15. Gross V, Andus T, Fischbach W. Comparison between high dose 5-aminosalicylic acid and 6methylprednisolone in active Crohn’s ileocolitis. A multicenter randomized double- blind study. German 5-ASA Study Group. Z Gastroenterol 1995;33:581-584.
  16. Hanauer SB. Inflammatory bowel disease. N Engl J Med 1996;334(13):841-848.
  17. Munkholm P, et al. Frequency of glucocorticoid resistance and dependency in Crohn’s disease. Gut 1994;35(3):360-362.
  18. Summers RW, Switz DM, Sessions JT. National Cooperative Crohn’s Disease Study: results of drug treatment. Gastroenterology 1979;77:847-869.
  19. Tremaine WJ, Hanauer SB, Katz S. Budesonide CIR United States Study Group. Budesonide CIR capsules (once or twice dany divided doses) in active Crohn’s disease: a randomized placebo-controlled study in the United States. Am J Gastroenterol 2002;97:1748-1754.
  20. Sands BE. Therapy of Inflammatory Bowel Disease. Gastroenterology 2000;118:68-82.
  21. Brynskov J, Freund L, Rasmussen SN. A placebo-controlled, double-blind, randomized trial of cyclosporine therapy in active, chronic Crohn’s disease. N Engl J Med 1989;321:845-850.
  22. Tözün N, Tiftikçi A. İnflamatuar barsak hastalıklarında biyolojik tedaviler: İnfliksimab ve diğerleri. Aktüel Tıp Dergisi 2002;7:49-52.
  23. Gomet JM, et al. İnfliximab for refractory ulcerative colitis or indetermine colitis: an open-label multicentre study. Aliment Pharmacol Ther 2003;18(2):175-181.
  24. Lesavre P. ANCA; diversity and clinical applications. Advances 1993;22:237-67.
  25. Jennette JC, Wilkmann AS, Falk RJ. Antineutrophil cytoplasmic autoantibody associated glomerulonephritis and vasculitis. Am J Pathol 1989;135(5):921-30.
  26. Cohen Terveart JW, Huitema MG, Hene RJ. Prevention of relapses in Wegener’s granulomatosis by treatment based on antineutrophil cytoplasmic antibody titre. Lancet 1990;336: 709-11.
  27. Rump JA, Schölmerich J, Gross V, Roth M, Helfesrieder R, Rautmann A, Ludemann J. A new type of perinuclear antineutrophil cytoplasmic antibody (p-ANCA) in active ulserative colitis but not in Crohn’ disease. Immunobiology 1990;181(4-5):406-13.
  28. Gross WF, Schmitt WH, Csernok E. ANCA and associated diseases: Immunodiagnostic and pathogenetic aspects. Clin Exp Immunol. 1993;91(1):1-12.
  29. Gispert JP, Luna M, Legido J, Hermida C, Mate J, Pajares JM. Anti-neutrophil cytoplasmic antibodies in the diagnosis of ulcerative colitis and Crohn’s disease. Med Clin. 2004;122(4):134-5.
  30. Patel R, Stokes R, Brich D. Influence of total colectomy on serum antineutrophil cytoplasmic antibodies in inflammatory bowel disease. Br. J Surg 1994;81:724-726.
  31. Pool M, Ellerbroek PM, Riduvan BU. Serum antineutrophil cytoplasmic antibodies in inflammatory bowel disease are mainly associated with ulcerative colitis. A correlation study between perinuclear antineutrophil cytoplasmic antibodies and clinical parameters medical and surgical treatment. Gut 1993;34:46-50.
  32. Seibold F, Slametschka D, Gregar M. Neutrophil autoantibodies: a genetic marker in primary sclerosing cholangitis and ulcerative colitis. Gastroenterology 1994;107:532-536.
  33. Quinton JF, Sendid B, Reumax D. Anti-Saccharomyces cerevisiae mannan antibodies combined with antineutrophilcytoplasmic autoantibodies in inflammatory bowel disease: prevalence and diagnostic role. Gut 1998; 42: 788-91.
  34. Jooessens S, Reinisch W, Vermeire S. ASCA and pANCA indeteremine colitis: a prospective study. Gut 2000;32:A232.
  35. Rutgeerts P, Vermeire S. Serological diagnosis of inflammatory bowel disease. Lancet 2000;356:2117-18.
  36. Conrad K, et al. Serological differantiation of inflammatory bowel diseases. Eur J Gastroenterol Hepatol 2002;14:129-135.
  37. Damoiseaux JGMC et al. Diagnostic value of anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies for inflammatory bowel disease: high prevalance in patients with celiac disease. J Clin Immunology 2002;22:281-288.
  38. Probert CS, Jayanthi V, Hughes AO, Thompson JR, Wicks AC, Mayberry JF. Prevalance and family risk of Ulcerative colitis and Crohn’s disease: an epidemiological study among Europens and South Asians in Leicestershire. Gut 1993;34:1547-1551.
  39. Satsangi J, Rosenberg WM, Jewell DP. The prevalance of inflammatory bowel disease in relatives of patients with Crohn’s disease. Eur J Gastroenterol Hepatol 1994;6:413-416.
  40. Kuster W, Pascoe L, Purrman J, Funk S, Majewski F. The genetics of Crohn’s disease: complex segregation analysis of a family study with 265 patients with Crohn’s disease and 5387 relatives. Am J Genet 1989;32:105108.
  41. Thompson NP, Driscoll R, Pounder RE, Wakefield AJ. Genetics versus environment in inflammatory bowel disease:results of a British twin study. BMJ 1996;312:95-105.

99.Barnes RMR, Allan S. Serum antibodies reactive with Saccharomyces cerevisiae in IBD: Is IgA antibody a marker for CD? Int Arch Allergy Appl Immunol 1990;92:9-15.

  1. Mc Kenzie H, Main J. Antibody to selected strains of Saccharomyces cerevisiae (baker’s and brewer’s yeast) and Candida albicans in CD. Gut 1990;31:536-8.
  2. Main J, McKenzie H. Antibody to Saccharomyces cerevisiae (baker’s yeast) in CD. BMJ 1988;297:1105-6.
  3. Israeli E,Grotto I, Gilburd B, Balicer RD, Goldin E, Wiik A, Shoenfeld Y. Anti Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease. Gut 2005;54:1232-1236.
  4. Vasiliauskas EA, Plevy SE, Landers CJ. Perinuclear antineutrophil cytoplasmic antibodies in patients with Crohn’s disease define a clinical group. Gastroenterology 1996; 112(1): 316-7.
  5. Targan SR. The utility of ANCA and ASCA in inflammatory bowel disease. Inflammatory Bowel Disease 1999; 5(1):61-3.