History Of Ulcerative Colitis Research Articles

Pan-enteritis in Patients with a History of Ulcerative Colitis

Pan-enteritis in Patients with a History of Ulcerative Colitis

Effect of Gender on the Natural History of Ulcerative Colitis in Pediatric Population: A 20 Year Population-based Study

Effect of Gender on the Natural History of Ulcerative Colitis in Pediatric Population: A 20 Year Population-based Study

Refractory Urticarial Vasculitis as a Complication of Ulcerative Colitis Successfully Treated With Rituximab

Ulcerative colitis can be complicated by the development of leukocytoclastic vasculitis, a cutaneous vasculitis with the potential for systemic involvement. We present a man with a history of ulcerative colitis complicated by end-stage liver disease secondary to sclerosing cholangitis requiring a liver transplant. The patient developed new-onset vasculitis and diarrhea refractory to therapy with standard immunosuppression. He was treated with anti-CD20 therapy with a positive response. The basis of the vasculitis was likely one related to an underlying monoclonal paraprotein with cryoprecitable properties. Treatment with anti-B-cell therapy may be a new treatment option for patients with gammopathy-associated leukocytoclastic vasculitis.

Ostomy Literature Review 2010

Ostomy Literature Review 2010

Association between Takayasu arteritis and ulcerative colitis – case report and review of serological HLA analysis

SummaryBackgroundTakayasu arteritis and ulcerative colitis are immune-mediated inflammatory diseases; genetic factors are assumed to play an important role in the pathogenesis of these 2 diseases. However, the coexistence of these 2 diseases has rarely been reported.Case ReportIn this report, we present a rare case of a 29-year-old man with a 4 years history of ulcerative colitis who developed Takayasu arteritis. He was found to carry the following human leukocyte antigens (HLA): A11, A24, B52, B62, DR4, and DR9.ConclusionsWe present a case report and review of the pertinent literature on serological analysis of HLA haplotype of the patients who exhibit both these diseases. In patients with both Takayasu arteritis and ulcerative colitis, high frequency of HLA-A24, B52, and DR 2 is observed. The pathological relevance of HLA-A24, B52, and DR2 to concomitant Takayasu arteritis and ulcerative colitis requires further investigation.

Case of Fulminant Colitis after Docetaxel Therapy for Breast Carcinoma in a Patient with History of Ulcerative Colitis

Case of Fulminant Colitis after Docetaxel Therapy for Breast Carcinoma in a Patient with History of Ulcerative Colitis

An Interesting View

This is a 54-year-old female patient with a history of ulcerative colitis. She underwent proctocolectomy and end ileostomy in the 1970s, and now presented with pain around the end of her stoma. The area was biopsied and the pathology report showed an invasive moderately differentiated adenocarcinoma with mucinous features. Subsequently, a PET-CT was performed for initial treatment strategy examination. PET-CT, including volume rendering, demonstrated increased FDG uptake within the stoma site as well as within a loop of bowel traversing through the ostomy tract (maximal SUV is 5.9 and 6.6, respectively). This case is of particular interest, because (1) a volume-rendered PET (only PET—without CT) of such a lesion has not been shown in the literature, (2) this scenario (primary cancer to the stoma detected by PET) is rarely encountered, and (3) these volume-rendered images are useful tools for demonstration of disease sites to clinicians.

Cerebral Venous Thrombosis Presenting With Cerebellar Ataxia and Cortical Blindness

Venous infarction in the cerebellum has been reported only rarely, probably because of the abundant venous collateral drainage in this region. Bilateral occipital infarction is a rare cause of visual loss in cerebral venous thrombosis. We describea 50-year-old woman with a history of ulcerative colitis who developed acute cerebellar ataxia and cortical blindness. She had bilateral cerebellar and occipital lesions related to sigmoid venous thrombosis and achieved complete recovery with anticoagulation therapy. Cerebral venous thrombosis should be considered in cases of simultaneous cerebellar and occipital vascular lesions.

Cutaneous Lymphoproliferative Disorder Complicating Infectious Mononucleosis in an Immunosuppressed Patient

Infectious mononucleosis is the syndrome produced by primary infection with Epstein-Barr virus during adolescence or early adulthood. In immunosuppressed individuals, depressed T-cell function allows the Epstein-Barr virus-driven B-cell proliferation to continue unabated, potentially leading to a lymphoproliferative disorder. A 15-year-old girl with a history of ulcerative colitis treated with 6-mercaptopurine and mesalamine presented with the acute onset of a rapidly enlarging, ulcerative nodule on her left lower eyelid 4 weeks following recovery from infectious mononucleosis. The biopsy revealed an Epstein-Barr virus-positive lymphoproliferative disorder. Systemic disease was absent. Following discontinuation of 6-mercaptopurine, the patient was treated with two courses of intravenous cyclophosphamide. The lesion resolved completely and she remains disease free at 14 months following diagnosis. We report a solitary cutaneous lesion of an immunosuppression-related lymphoproliferative disorder (IR-LPD) occurring as a complication of infectious mononucleosis, and review the pathogenesis and reported cases of Epstein-Barr virus-related immunosuppression-related lymphoproliferative disorder arising in the setting of inflammatory bowel disease. It is important for dermatologists and dermatopathologists to be aware of the occurrence of IR-LPD in patients being treated for inflammatory conditions, including inflammatory bowel disease. Given the role of primary infection with Epstein-Barr virus in the development of IR-LPD, consideration may be given to assessing Epstein-Barr virus status prior to initiating immunosuppressive therapy in young patients.

Menetrier’s disease: report of three cases and a review of the literature

Introduction Menetrier’s disease (MD) is an uncommon entity characterised by massive foveolar hyperplasia of the gastric mucosa, typically confined to the gastric body and associated with hypoalbuminaemia, and carrying an increased risk of malignancy. Nevertheless, no diagnostic criteria for the disease have been established since Menetrier’s description in 1888, and its aetiology remains unclear. Aims and Methods Gastrectomy specimens from three recent cases of MD with differing clinical presentations were studied and their histopathological and clinical features reviewed. Discussion All three cases showed Menetrier-like features, with florid foveolar hyperplasia, cystic dilation of underlying glands and paucity of inflammation, sometimes including the antrum. No Helicobacter were identified in any of the cases. One patient had intramucosal adenocarcinoma, and another had a long history of ulcerative colitis. Recently, transforming growth factor (TGF) α has been implicated in the genesis of MD. As TGFα shares a receptor with epidermal growth factor, a trial of the EGFR inhibitor cetuximab was attempted in one patient, with limited clinical benefit. Current knowledge of MD will be reviewed, using the three cases to highlight diagnostic and clinical features of this rare disease.

Rash associated with pandemic (H1N1) influenza

A 44-year-old man presented with a two-day history of severe nausea, vomiting and fever with a temperature of 39°C. The patient had a history of ulcerative colitis; however, his symptoms were unlike those of previous flare-ups of the disease. He was experiencing non-bloody diarrhea and had no

Mycosis fungoides and CD30+ cutaneous T-cell lymphoma simulating pyoderma gangrenosum in a patient with ulcerative colitis

Pyoderma gangrenosum is estimated to occur in 5% to 12% of ulcerative colitis patients. Primary CD30+ cutaneous large cell lymphoma is the second most common cutaneous lymphoma. It may coexists with mycosis fungoides. We report a 38-years-old female patient with 12 year history of ulcerative colitis, treated previously with 5-aminosalicylic acid and systemic corticosteroids. The disease has been in remission for the past 1.5 years, with no maintenance treatment. The patient then developed a rapidly progressing ulcerated lesion clinically simulating pyoderma gangrenosum. Physical examination revealed also a small number of hairless hypopigmented patches on the upper and lower limbs which she claimed to have appeared 4 years ago. Surprisingly a histological evaluation of the ulcer revealed a CD30+ primary cutaneous large cell lymphoma, while histology of hypopigmented lesions revealed mycosis fungoides, patch stage. T-cell receptor gene rearrangement from the two lesions didn't reveal the same T Cell clonalitiy and the patients lymphoma was stable. Our case presents the rare coexistence of primary mycosis fungoides and primary CD30+ cutaneous large cell lymphoma, rather than the CD30+ cutaneous large cell lymphoma developing from mycosis fungoides. This case also presents the development of a pyoderma gangrenosum-like lesion of CD30+ cutaneous large cell lymphoma in a patient with ulcerative colitis. An observation that emphasizes the need for a high index of suspicion in cases diagnosed as pyoderma gangrenosum based solely on clinical appearance.

A Case of Refractory Peristomal Variceal Bleeding Post-TIPSS and Review of the Therapeutic Options

Purpose: Results: A 69 year old man has a history of Ulcerative Colitis with total abdominal colectomy with ileostomy performed Febuary 2002 due to treatment refractory disease. He presented four years later with presumed lower GI bleed with bright red blood noted in his ostomy bag. Ileoscopy performed at that time showed normal ileal mucosa, while careful inspection of the ileostomy site showed continued oozing from an external source. Upper endoscopy was performed to assess other signs of portal hypertension showing mild gastropathy and small esophageal varices. Non-selective beta-blocker therapy was initiated at that time with a diagnosis of Laennec's Cirrhosis. A diagnosis of peristomal varices was made after confirmation on review of abdominal imaging. Recurrent bleeding continued to require hospitalization and transfusion on three separate presentations leading to initial TIPSS procedure as well as revision bringing porto-systemic pressure gradient from 15 mmHg to 4 mmHg. He was placed prophylactically on lactulose at that time, but progressive difficulties required the addition of rifaximin. Despite the TIPSS procedure, he continued to have episodes of bleeding from his peristomal varices requiring transfusion. Conservative measures were initially employed in attempts to control bleeding after repeat porto-systemic pressure gradient measurement confirmed a widely patent TIPSS. Application of silver nitrate, oversewing with suture, and injection sclerotherapy were all attempted in addition to direct pressure without durable result. After initial consultation with Colorectal Surgery, his ostomy was taken down and re-sited for definitive therapy of his recurrent peristomal variceal hemorrhage. In the 13 months since revision of his ileostomy, he has had far fewer difficulties with bleeding only requiring transfusion on two occasions. Conclusion: Peristomal variceal bleeding is difficult to control and can be a life-threatening complication of portal hypertension in patients with colonic resection requiring ileostomy. In patients with advanced liver disease as defined by Childs Classification, ectopic variceal bleeding frequently represents a terminal event. Stoma revision with devascularization has been found in previous reports to be temporarily effective in reducing recurrent peristomal variceal bleeding and has reduced the need for transfusion in our patient. Liver transplantation remains the only potential therapy for our patient at this time, but given his age and comorbid medical status it has been determined that he is not a candidate.

Guillain–Barré Syndrome During a Relapse of Ulcerative Colitis: A Case Report

To the Editor: A 59-year-old male patient was admitted to the hospital for bloody diarrhea and fever. He had a 5-year history of ulcerative colitis (UC) but he was in remission during the last 2 years, being treated with 5-aminosalicylate (5-ASA). Clinical examination demonstrated a well-nourished patient with a normal abdomen. He had mild iron deficiency anemia, the erythrocyte sedimentation rate (ESR) was normal, but C-reactive protein (CRP) was raised to 15.2 mg/L. His biochemical profile was within normal limits except for a slight decrease of the albumins. An abdominal ultrasound showed a slightly enlarged liver with mild steatosis and the presence of sludge in the gallbladder. Chest and abdominal x-ray were normal. Tumor markers (CEA, AFP, CA19-9, CA125, PSA) and thyroid hormones were within normal limits. Stool specimens did not reveal any ova or parasite and stool cultures including Clostridium difficile testing were negative. A colonoscopy showed a typical flare-up of UC with a moderately active chronic UC on histology. He was treated with intravenous (IV) prednisolone 25 mg twice daily and 5-ASA 1000 mg 3 times daily and as soon as clinical improvement was achieved he was discharged. Three days later he was readmitted with lower extremity weakness. On neurological examination the patient was fully consciousness. He had no deficit from cranial nerves. No speech or articulation disorders were detected. We observed neither meningial sign nor jaw reflex. There was a mild to moderate decrease in proximal muscle strength with normal tone. Superficial, vibration, and deep sensory modalities were apparently normal. Deep tendon reflexes of upper and lower extremities were reduced bilaterally. The muscle weakness of the lower extremities was more profound proximally than distally. A moderate impairment of deep sensation was observed, while superficial sensation was normal. There was a flexor plantar response. He was unable to stand or walk without aid. Therefore, he underwent neurophysiological and electromyographical studies. Electromyogram did not show any evidence of acute or chronic denervation in several muscles. However, electroneurogram (ENG) demonstrated a motor-sensory symmetrical demyelinating peripheral polyneuropathy. Cerebrospinal fluid was clear and colorless. Examination showed normal glucose up to 52 mg/dL and pathologically increased albumin up to 905 mg/L. As far as cells were concerned, 2/mm 3 lymphocytes were

New serologic findings in a patient with ulcerative colitis and a warm autoantibody

Abstract IgG-RBC sensitization associated with serine proteases is the current prevailing hypothesis used to explain an uncommon phenomenon in which a positive DAT is obtained using the RBCs from a patient’s clotted blood sample but a negative DAT is obtained when testing RBCs from the patient’s unclotted sample. Similarly, the patient’s serum but not plasma will also be reactive by IAT against all RBCs tested. The majority of patients demonstrating this phenomenon have had a history of ulcerative colitis but no signs of hemolytic anemia. A case of IgG-RBC sensitization associated with serine proteases and a warm autoantibody in a 14-year-old Hispanic girl with ulcerative colitis is reported. The patient was admitted for severe anemia (Hb, 6.9 g/dL). On admission, pretransfusion testing of the patient’s serum and RBCs showed an ABO/Rh discrepancy between the forward typing and reverse grouping. The phenomenon of IgG-RBC sensitization associated with serine proteases was considered in the differential evaluation of the serum versus plasma typing discrepancy. To confirm the presence of the phenomenon of IgG-RBC sensitization associated with serine proteases, the plasma was clotted and converted to serum by the addition of thrombin. The initially nonreactive plasma was 2+ reactive when converted to serum. A warm autoantibody was also detected during the course of serologic evaluation. The patient was transfused with 2 units of incompatible RBCs with no adverse reaction observed. Immunohematology 2009;25:160–164.

Effects of a supplementary diet with specially processed cereals in patients with short bowel syndrome

Short bowel syndrome patients frequently experience impaired health-related quality of life. This syndrome is also associated with increased costs for the individuals concerned and the community. Intake of specially processed cereals has been demonstrated to decrease intestinal secretion. This study evaluates the effect of a supplementary diet with specially processed cereals compared with nonprocessed cereals. This investigation is a randomized double-blind, cross-over multicentre prospective study of 26 intestinal resected out patients, considered as short bowel syndrome patients. The patients were divided into groups A or B, in accordance with the first allocated treatment. Subgroup analyses of the underlying diagnoses and type of surgical procedure were performed. The studied parameters were faecal volume, nocturnal stools, abdominal pain/discomfort, health-related quality of life, peripheral blood tests and anthropometric data. In both groups, intake of nonprocessed cereals significantly decreased the faecal volume. The subgroup analyses of patients with a history of ulcerative colitis (compared with Crohn's disease) and nonileostomy-operated procedure (compared with ileostomi-operated procedure) showed significantly decreased faecal volume during nonprocessed cereals intake. Peripheral blood tests, quality of life and anthropometry were not affected. In this study, nonprocessed cereals seemed to be as effective as specially processed cereals in decreasing faecal volume in general and especially in ulcerative colitis patients (mainly operated with nonileostomy techniques). Our results indicate that use of supplementary cereals is safe for this group of patients, but should optimally include evaluation of the underlying diagnosis and the surgical method used.

Case 33-2008

A 63-year-old woman was admitted to the hospital because of a 3-week history of dyspnea on exertion, associated left subscapular burning pain, and a mild dry cough. She had a history of ulcerative colitis, which was most recently treated with azathioprine and infliximab. On examination, there were inspiratory wheezes and rales, without expiratory wheezes. Chest imaging showed ground-glass opacities in both lower lobes. A diagnostic procedure was performed.

Colonic diaphragm disease without significant non-steroidal anti-inflammatory drug use: a case report

IntroductionColonic diaphragm disease is an uncommon condition usually associated with the long-term use of non-steroidal anti-inflammatory drugs.Case presentationA 48-year-old woman presented as an emergency patient with abdominal pain and vomiting. Past medical history included inflammatory bowel disease of ulcerative colitis type for which she was taking azathioprine and prednisolone. On examination, she was shocked with signs of peritonism. Following resuscitation, she was taken for a laparotomy upon which a small amount of turbid fluid was identified but there was no direct evidence of an intra-abdominal perforation. A peritoneal lavage was performed and she was taken to the intensive care unit. A repeat laparotomy was performed on the sixth postoperative day, following a clinical deterioration and again no leak was identified. Given the history of ulcerative colitis, the perforation was presumed to be of colonic origin and a total colectomy and ileostomy was performed. Histopathological examination of the colectomy specimen revealed extensive colonic diaphragm disease with 30 thin-walled diaphragms, one of which reduced the lumen to a pin-hole. No perforation was identified.ConclusionTo the best of the our knowledge, this is the first report of the development of colonic diaphragm disease in the absence of a history of non-steroidal anti-inflammatory drug ingestion. Given the history of ulcerative colitis we believe that the disease may have arisen as a result of the healing of the underlying inflamed colon rather than as a direct effect of non-steroidal anti-inflammatory drugs.

Ulcerative Colitis and Sweet’s Syndrome: A Case Report and Review of the Literature

A 47-year-old man with a history of ulcerative colitis on prednisone and azathioprine was admitted to the hospital with a four-day history of fever, skin rash, arthralgias and leukocytosis. A skin biopsy demonstrated neutrophilic infiltration of the dermis that was consistent with Sweet's syndrome. He improved after several days with an increase in his prednisone and azathioprine. Sweet's syndrome is a rare cutaneous manifestation of inflammatory bowel disease, with approximately 40 cases reported in the literature. In a previously reported case of a patient with ulcerative colitis-associated Sweet's syndrome who was on azathioprine at the time of the skin eruption, the azathioprine was stopped, raising the possibility of drug-induced Sweet's syndrome. In the present case, the azathioprine was actually increased with complete resolution of the skin manifestations. This would support the theory that immunosuppressive therapy is the mainstay of therapy for this condition. In conclusion, Sweet's syndrome is a neutrophilic dermatosis that is rarely associated with ulcerative colitis. It may occur while on immunosuppressive therapy and responds to an intensification of immunosuppression.

Eosinophilic Pneumonia in an Ulcerative Colitis Patient

We present the case of 16-year-old woman with a 2-month history of ulcerative colitis who presented with cough, fever, dyspnea on exertion, and nasal congestion. Computed tomography of the chest demonstrated peripheral alveolar opacities with relative sparing of the central portions of the lungs. The clinical and radiologic findings raised the suspicion of eosinophilic pneumonia, possibly drug-related. The patient had recently been started on a trial of Mesalamine (5-aminosalicylic acid or 5-ASA) for treatment of her ulcerative colitis 2 months ago. The patient's condition improved after discontinuation of mesalamine and treatment with prednisone. The clinical course and radiologic features supported the presumptive diagnosis of Mesalamine-induced eosinophilic pneumonia.