Collagenous colitis is an uncommon condition charaeterized clinically by diarrhea and weight loss and histologically by thickening of the subepithelial collagen band with chromic inflammation. Laboratory tests of blood, urine and stool, and colonscopic findings are usually normal. The etiology of collagenous colitis is unknown. We report a case of collagenous colitis improved after treatment with sulfasalazine with review of literatures.
Colitis, Collagenous* ; Collagen* ; Diarrhea ; Inflammation ; Sulfasalazine ; Weight Loss

OBJECTIVE: To investigate the frequency of gut inflammation in the ankylosing spondylitis and the role of gut lesion in the pathogenesis of the ankylosing spondylitis. METHODS: Ileocolonoscopy and biopsy were performed in 24 patients with. ankylosing spondylitis. RESULTS: 1) Endoscopic lesions were observed in 7 patients(29.2%) of 24 patients and more often in the terminal ileum(6/7) than in the colon(I/7). Among 7 patients with endoscopic lesions, 5 patients were presented as juvenile chronic arthritis. 2) Histologic signs of gut inflammation were detected in 14 patients(58. 3%). Actue lesions were seen in 2 patients (8. 3%) and chronic lesions were seen in 12 patients (50%). 3) In 12 patients without the involvement of peripheral joints, acute lesion was not seen(0%), and chronic lesions were seen in 6 patients(50%). In 12 patients with the involvement of peripheral joints, acute lesions were seen in 2 patients (16.7%), and chronic lesions were seen in 6 patients(50%). Gut inflammations were more frequent in patients with the involvement of peripheral joints than in those without the involvement of peripheral joints. 4) In 12 patients without the administration of sulfasalazine, acute lesion was not seen(0%), and chronic lesions were seen in 7 patients(58.7%) In 12 patients with the administration of sulfasalazine, acute lesions were seen in 2 patients (16.7%), and chronic lesions were seen in 5 patients(41.6%). The frequency of gut lesions in patients without the administration of sulfasalazine was not different from that in patients with the administration. of sulfasalazine (p<0.05). CONCLUSION: Gut inflammation was frequently found in patients with ankylosing spondylitis. Chronic gut inflammation could play a role in the pathogenesis of the ankylosing spondylitis.
Arthritis, Juvenile ; Biopsy ; Humans ; Inflammation ; Joints ; Spondylitis, Ankylosing* ; Sulfasalazine

Ulcerative colitis is chronic inflammatory disease of bowel without definite cause. Standard therapy of ulcerative colitis consists of aminosalicylates and glucocorticoid. In recent years, the effectiveness of cyclosporine in inflammatory bowel disease has been reported. Cyclosporine is useful in inducing remission in patients with acute exacervation phase who do not achieve remission with an intensive intravenous steroid therapy. We report a case of steroid-resistnat ulcerative colitis, treated with cyclosporine in 45-year-old man. Remission was not achieved with treatment of sulfasalazine and intensive intravenous glucocorticoid therapy for 10 days. We administered cyclosporine parenterally in dose of 4 mg/kg/day for 10 days. He improved dramatically without significant side effects of drug and avoided colectomy. He was discharged with oral cyclosporine and azathioprine and has been followed up outpatients department remained in clinically remission. Cyclosporine seems to be an effective treatment for patients with steroid-resistnat severe ulcerative colitis in whom colectomy seems inevitable.
Azathioprine* ; Colectomy ; Colitis, Ulcerative* ; Cyclosporine* ; Humans ; Inflammatory Bowel Diseases ; Middle Aged ; Outpatients ; Sulfasalazine ; Ulcer*

The goals of treatment in Spondyloarthropathy are to reduce pain and stiffness, and to maintain good quality of life. Regular exercise with stretching of axial skeleton is most important. No drugs have been prevented ankylosis, but non steroidal anti inflammatory drugs (NSAIDs) are the first line drugs and these are very effective in most of patients who have inflammatory back pain. In recent years, reports that long-term use of NSAIDs may reduce the ankylosis are coming out and expect NSAIDs as anti ankylosis drugs. If NSAIDs is not effective, anti TNF agents can be used in severe inflammatory back pain. In peripheral arthritis, sulfasalazine or steoids can be used, and If these are failed, anti TNF agents can be used.
Ankylosis ; Anti-Inflammatory Agents, Non-Steroidal ; Arthritis ; Back Pain ; Humans ; Quality of Life ; Skeleton ; Spondylarthropathies ; Steroids ; Sulfasalazine

PURPOSE: To seek the role of nuclear factor kappa B (NF-kB) on the corneal epithelial cell death after ultraviolet (UV) irradiation. METHODS: Human corneal epithelial cells transfected by Simian Virus 40 were used in this study. UVB(312 nm) located at 10cm distance from bottom (0.6 mW/cm2 ) was irradiated for 10, 20, 30, and 40 seconds. To measure the cytotoxicity, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method was used. Translocation of NF-KB was examined by immunocytochemistry with anti NF-K B p65 antibody and Electrophoretic Mobility Shift Assay (EMSA). To confirm the role of NF-KB , sulfasalazine, a specific inhibitor of NF-KB (0.5 mmole), was pretreated for 30 minutes before irradiatrion, and cytotoxicity and translocation of NF-KB was evaluated. RESULTS: UV irradiation resulted in a significant decrease in viability of cultured human corneal epithelial cells, especially after 20 second duration. When HCECs were irradiated with UVB, the translocation of N F -KB was observed in immunocytochemistry. These translocation was peaked 2 hours after UV irradiation in EMSA. In HCECs pretreated with sulfasalazine, either the cellular death or the translocation of NF-KB was blocked. CONCLUSION: UV irradiation can translocate NF-KB on the cultured human corneal epithelial cells. The cellular death after UV irradiation was blocked by sulfasalazine, a potent inhibitor of translocation of NF-KB. These findings suggest that NF-KB plays an important role in cellular death after UV irradiation.
Electrophoretic Mobility Shift Assay ; Epithelial Cells* ; Humans ; Immunohistochemistry ; NF-kappa B ; Simian virus 40 ; Sulfasalazine

Sulfasalazine produces a varied spectrum of adverse reactions on the hematopoietic system. Sulfasalazine-induced megaloblastic anemia is very rare and a few cases have been reported in patients with inflammatory bowel disease. Most of them show a low serum folate level. The pathogenesis is known as folate deficiency by intestinal folate malabsorption, inhibition of folate enzyme, or hemolysis. We experienced a 43-year old female with Behcet's disease, who presented with megaloblastic anemia having normal serum folate level after treatement of sulfasalazine (2 g/day for 3 months). Megaloblastic anemia recovered after withdrawal of the drug only.
Adult ; Anemia, Megaloblastic* ; Female ; Folic Acid* ; Hematopoietic System ; Hemolysis ; Humans ; Inflammatory Bowel Diseases ; Megaloblasts* ; Sulfasalazine

Human immunodeficiency virus (HIV) infection is a global pandemic affecting more than 2.9 million people. Aside from opportunistic infections and malignancies, it involves multiple organs, resulting in many complications, and frequently shows various rheumatic manifestations. With improving survival of patients due to the development of highly active anti-retroviral therapy, the number of HIV-infected patients with rheumatic complications is certain to increase. However, reports on HIV induced rheumatic manifestations in Korean patients are limited. On the other hand, spondyloarthropathy is the most common form of inflammatory arthropathy in HIV associated rheumatic manifestations and is frequently accompanied by peripheral arthritis and enthesitis, while axial skeletal involvement is a rare presentation. Herein we report on a 46-year-old man with HIV infection presenting with an axial spondyloarthropathy who was treated successfully with nonsteroidal anti-inflammatory drug, sulfasalazine, and low dose steroid.
Arthritis ; Hand ; HIV Infections ; HIV* ; Humans ; Humans* ; Middle Aged ; Opportunistic Infections ; Pandemics ; Rheumatic Diseases ; Spondylarthropathies* ; Sulfasalazine

Leflunomide is a novel, isoxazol based disease-modifying anti-rheumatic drug (DMARD) for the treatment of rheumatoid arthritis (RA). Its mechanism differs from other DMARDs in that it inhibits de novo pyrimidine synthesis by inhibiting the enzyme dihydroorotate dehydrogenase (DHODH). It is a pro-drug and undergoes rapid conversion to its active form in vivo, A77-1726. A77-1726 inhibits the mitochondrial enzyme DHODH, which plays a key role in the de novo synthesis of pyrimidine ribonucleotide uridine monophosphate (rUMP). Leflunomide prevents clonal expansion of activated lymphocytes by interfering with the cell cycle progression due to inadequate production of rUMP and utilizing mechanisms involving p53. The relative lack of toxicity of A77-1726 on non-lymphoid cells may be due to the ability of these cells to fulfill their ribonucleotide requirements by use of salvage pyrimidine pathway, which makes them less dependent on de novo synthesis. Several phase II clinical trials of patients with RA revealed that leflunomide was effective and well tolerated. Large-scale phase III clinical trials have shown that leflunomide (20mg/day) provided a statistically significant clinical benefit and prevention of radiographic progression in comparison to placebo. The clinical benefits of leflunomide were similar to or greater than methotrexate and sulfasalazine. Now, many multi-national studies are in progress and planning, including combination therapy with other DMARD. In future, those studies will provide us more information about the effectiveness and potential adverse effect of leflunomide.
Antirheumatic Agents ; Arthritis, Rheumatoid ; Cell Cycle ; Humans ; Lymphocytes ; Methotrexate ; Oxidoreductases ; Sulfasalazine ; Uridine Monophosphate

Leflunomide is a novel, isoxazol based disease-modifying anti-rheumatic drug (DMARD) for the treatment of rheumatoid arthritis (RA). Its mechanism differs from other DMARDs in that it inhibits de novo pyrimidine synthesis by inhibiting the enzyme dihydroorotate dehydrogenase (DHODH). It is a pro-drug and undergoes rapid conversion to its active form in vivo, A77-1726. A77-1726 inhibits the mitochondrial enzyme DHODH, which plays a key role in the de novo synthesis of pyrimidine ribonucleotide uridine monophosphate (rUMP). Leflunomide prevents clonal expansion of activated lymphocytes by interfering with the cell cycle progression due to inadequate production of rUMP and utilizing mechanisms involving p53. The relative lack of toxicity of A77-1726 on non-lymphoid cells may be due to the ability of these cells to fulfill their ribonucleotide requirements by use of salvage pyrimidine pathway, which makes them less dependent on de novo synthesis. Several phase II clinical trials of patients with RA revealed that leflunomide was effective and well tolerated. Large-scale phase III clinical trials have shown that leflunomide (20mg/day) provided a statistically significant clinical benefit and prevention of radiographic progression in comparison to placebo. The clinical benefits of leflunomide were similar to or greater than methotrexate and sulfasalazine. Now, many multi-national studies are in progress and planning, including combination therapy with other DMARD. In future, those studies will provide us more information about the effectiveness and potential adverse effect of leflunomide.
Antirheumatic Agents ; Arthritis, Rheumatoid ; Cell Cycle ; Humans ; Lymphocytes ; Methotrexate ; Oxidoreductases ; Sulfasalazine ; Uridine Monophosphate

Behcet's disease is a chronic polysymptomatic disease of recurrent systemic vasculitis. The etiology remains unclear. This disease affects several organs of the body concurrently or consecutively and sometimes has a serious outcome, depending upon the system involved. Though gastrointestinal symptoms are relatively common in Behcet's disease, ulcerative change of the intestine is infrequent. The most common sites for the intestinal Behcet's disease are terminal ileum and cecum. Only a few literatures report the esophageal ulcers in Behcet's disease. We describe 2 cases of Behcet's disease who have multiple ulcers in esophagus and terminal ileum. Esophageal ulcers have improved with low-dose prednisolone, colchicine and sulfasalazine in these patients.
Cecum ; Colchicine ; Esophagus* ; Humans ; Ileum* ; Intestines ; Prednisolone ; Sulfasalazine ; Systemic Vasculitis ; Ulcer*