[Lymphocytic colitis induced by carbamazepine].
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The morphologic findings in mildly active colonic Crohn's disease (CD) include crypt disarray, patchy edema, and small lymphoid aggregates with neutrophils, sometimes associated with aphthous ulcers. We describe four patients with CD whose colonic biopsies focally showed a lymphocytic colitis morphology, and one patient with CD whose biopsies showed a collagenous colitis morphology. The lymphocytic and collagenous colitis patterns of injury preceded the eventual clinical pathologic diagnosis of CD in four patients. Colonoscopic abnormalities were found in four patients. The lymphocytic colitis pattern was focal, involving some biopsy fragments, whereas other biopsy fragments were normal or had minimal nonspecific inflammation. In one patient, moderate numbers of neutrophils were admixed with the lymphoplasmacytic infiltrates. The presence of colonoscopic abnormalities, focal changes, and moderate admixed neutrophils could assist in the distinction from lymphocytic or collagenous colitis, both of which are colonoscopically normal, usually diffuse, and devoid of, or contain only a sparse number of, neutrophils. A limited number of biopsy fragments may be incorrectly interpreted as lymphocytic or collagenous colitis. The temporal relationships suggest that these morphologic patterns precede typical active CD.
OBJECTIVE: To review the published studies on collagenous and lymphocytic (microscopic) colitis with specific emphasis on clinical features, investigational studies, characteristic histology, possible pathogenesis, disease course, and empirical treatment. DESIGN: Comprehensive synopsis of the stated objective, prepared for the physician treating patients with collagenous or lymphocytic colitis. MATERIALS AND METHODS: The medical literature on collagenous and lymphocytic colitis. RESULTS: Collagenous and lymphocytic colitis are chronic diarrheal illnesses of indeterminate etiology that typically present in the late sixth or early seventh decade of life. These disorders may be distinct entities, although some data support the idea that they are only different manifestations of the same disease. The pathogenesis is unknown but may be on an inflammatory, possibly autoimmune, basis. Physical examination and investigational studies are normal or nonspecific, with fecal leukocytosis the only abnormality found in the majority of patients tested. Association with various gastrointestinal, autoimmune, and rheumatologic conditions has been observed in some patients. Clinical and occasional histologic response has been observed after treatment with anti-inflammatory agents such as 5-aminosalicylate and corticosteroids, and should be used when there is no response to symptomatic therapy. CONCLUSIONS: Collagenous and lymphocytic colitis are uncommon but important causes of chronic diarrhea which are important to diagnose and treat.
PURPOSE: We present a case of severe diarrhea caused by lymphocytic colitis and concurrent celiac sprue in a patient who did not respond to maximal medical therapy and required surgery. METHODS: The patient was initially treated with fecal diversion via an end ileostomy. Six months later, she underwent colectomy and one-stage ileal J-pouch-anal anastomosis. RESULTS: Notably, the characteristic microscopic changes of lymphocytic colitis were still present at the time of colectomy despite diversion. CONCLUSION: Colectomy with continent reconstruction is an option for treatment of patients with lymphocytic colitis refractory to medical therapy.
INTRODUCTION: Microscopic colitis describes a subset of patients with chronic watery diarrhea of unknown origin, and normal endoscopic findings and microscopic evidence of an inflammatory infiltrate in the colonic mucosa. We report two cases associated with sicca syndrome. EXEGESIS: A 56-year-old woman and a 76-year-old man presented with a history of lymphocytic colitis associated with sicca syndrome. Drugs or infectious agents were not implicated in the cause of lymphocytic colitis, suggesting that sicca syndrome may be involved in the pathogenesis of microscopic colitis. CONCLUSION: These cases suggest that sicca syndrome should be detected in patients with lymphocytic colitis.
The results of a histological and immunohistochemical study of endoscopic colon biopsies of dogs with plasmacytic-lymphocytic colitis are reported. The histological study revealed that a characteristic infiltrate rich in lymphocytes and plasma cells was seen within the lamina propria in all the biopsies. The immunohistochemical investigation suggests that IgG is the major antibody in the immune response of dogs with plasmacytic-lymphocytic colitis.
We report two cases of lymphocytic colitis with severe diarrhea in patients treated by lansoprazole for six weeks. Complete remission occurred rapidly after lansoprazole withdrawal.
We present a 19-year-old patient who was admitted for evaluation of prolonged watery diarrhea. Previous study showed one stool culture positive for Campylobacter jejuni, which was treated with appropriate antibiotics with no response. She underwent colonoscopy with multiple biopsies, which led to a diagnosis of lymphocytic colitis. We believe that the patient's disease was due to the infectious process, which triggered an autoimmune response and caused the lymphocytic colitis.
A 66-year-old woman presented with a bullous skin eruption and chronic diarrhoea. Lesional skin showed subepidermal blistering, and direct immunofluorescence of perilesional skin revealed linear deposits of IgA at the dermoepidermal junction, establishing a diagnosis of linear IgA disease (LAD). Chronic watery diarrhoea complicated by substantial loss of body weight preceded the skin eruption for several months. On endoscopy, the colon appeared macroscopically normal. On histology, the colon mucosa showed increased numbers of intraepithelial lymphocytes and infiltrates of mononuclear cells in the lamina propria, indicative of lymphocytic colitis. Treatment with methylprednisolone and dapsone led to complete clearing of the bullous skin eruption and marked improvement of the patient's diarrhoea. Gastrointestinal disorders such as lymphocytic colitis have rarely been reported in patients with LAD. Whether the simultaneous occurrence of these two diseases is coincidental or due to related pathogenetic mechanisms remains to be seen.
The case of a 66-year-old female patient is presented, who suffered from chronic watery diarrhea. In addition, she developed linear IgA dermatosis after oral treatment of a presumed yeast infection with nystatin. To evaluate the reason for her diarrhea, colonoscopy was performed. The macroscopic aspect of the colon mucosa was described as normal with no specific alterations for chronic inflammatory bowel disease or for bacterial infections. In contrast, the histologic examination revealed the typical characteristics of lymphocytic colitis. This disease is thought to be caused by immunological reactions against as yet unknown luminal antigens. After treatment with steroids and dapsone the diarrhea as well as the skin disease disappeared. To our knowledge, the present report describes for the first time the association of linear IgA dermatosis with lymphocytic colitis after oral treatment with nystatin. A possible causative link between these two disease entities is discussed.
We conducted this retrospective study to evaluate the relationship between symptoms, histological findings, and treatment of collagenous (CC) and lymphocytic colitis (LC). We identified 19 CC and 12 LC patients having multiple colonoscopic procedures with colonic biopsies during their course of illness. A detailed histological review of all biopsies was performed. Clinical history, including symptoms and medications, was obtained in 25 of the 31 patients and was correlated with their histological findings. In all, 25% of the CC patients and 50% of the LC patients who had biopsies prior to their definitive diagnosis had the pathognomonic histological features on their prior biopsies to some extent (but were not recognized by the pathologists); however, these features were more pronounced on the biopsies from the procedure that established the diagnosis. Nonetheless, 10 of 12 such patients with clinical data available had symptoms and were being treated at the time of prior biopsies. Assessment of the relationship among histological, clinical and therapeutic data showed no association between symptoms or histological findings and treatment with any medication. In summary, in this sample of CC and LC patients, symptoms often precede fully developed histological features. No change in symptoms or histological findings was found to be associated with medication.
A baboon died of chronic, intractable diarrhoea. At autopsy gross examination revealed oedema, and signs of chronic inflammation in the entire colon. At histology, marked lymphocytic infiltration within the colonic epithelium covering the crypts was found. The term cryptal lymphocytic colitis is proposed for this previously unreported disease in baboons.
A 69 year old woman developed chronic diarrhoea while being treated with ranitidine. Sigmoidoscopy was performed after six weeks and showed typical histological features of lymphocytic colitis. Ranitidine was withdrawn and the diarrhoea resolved. Eight months later, a 72 hour oral rechallenge period of ranitidine, was performed immediately preceded (period 1) and followed (period 2) by sigmoidoscopy and biopsy. Diarrhoea recurred during the rechallenge period and resolved again within one day after drug withdrawal. The mean (SEM) intraepithelial lymphocyte count was not significantly different between periods 1 and 2 (11.9 (0.6) and 13.1 (0.4) per 100, respectively). An immunopathological study of 30 serial sections of biopsy specimens was performed for both periods 1 and 2. The expression of HLA-DR by the rectal epithelium was mild or absent in all sections from period 1, and was considerable in 25 of 30 sections from period 2 (p < 10(-9)). It is suggested that the oral intake of ranitidine was responsible for the diarrhoea and induced the immunopathological signs of activation of the rectal mucosal immune system during the rechallenge period.
A 66-year-old woman was seen repeatedly over a decade to remove recurrent colonic adenomas and investigate episodes of watery diarrhea. Although the diarrhea was believed to be due to lymphocytic colitis, she developed weight loss, hypoproteinemia and hyposplenism that resulted in further studies, specifically to exclude celiac disease. Small intestinal biopsies, however, showed severely 'flattened' villous architecture with trichrome-positive subepithelial collagenous deposits, characteristic of collagenous sprue. Antiendomysial antibodies, known serological markers of celiac disease, were also detected. While collagenous sprue has been considered a distinct small intestinal disorder, the constellation of clinical and pathological findings in this patient suggests a close link with adult celiac disease.
BACKGROUND: Colonic nitric oxide (NO) production in collagenous colitis (CC) has been studied in a small number of patients and found increased. The cellular source of NO is believed to be the colonic epithelial cells. The aim of this study was to investigate colonic NO levels in patients with CC and lymphocytic colitis (LC), to compare with the histopathological status and with the clinical activity, and to assess the epithelial expression of inducible and endothelial nitric oxide synthase (iNOS and eNOS). METHODS: We included 19 patients with CC, 8 patients with LC and 15 controls. During colonoscopy, luminal gas was sampled and NO levels were measured using the chemiluminescence technique. Mucosal biopsies were obtained for routine histopathologic examination and immunohistochemical studies of iNOS and eNOS. Clinical activity, as measured by the mean frequency of daily bowel movements during the week prior to colonoscopy, was assessed. RESULTS: Luminal NO levels, median (25-75 percentiles), in the patients with CC and LC were greatly increased compared to the controls, 1673 (145-8143) parts per billion (ppb) and 1838 (1065-2694) ppb versus 28 (20-46) ppb (P < 0.005, both). A positive association was seen between NO levels and histopathological status as well as clinical activity. Strong expression of iNOS was seen in the surface epithelium in 5 of 6 patients with CC and in 2 of 5 patients with LC. CONCLUSIONS: The fact that luminal NO levels are related to histopathological status and correlate with clinical activity indicates that NO is involved in the pathophysiology of CC and LC. The epithelial cells are the most likely source of luminal NO.
Lymphocytic and collagenous colitis, uncommon entities that are identifiable by histopathologic examination only, and intestinal spirochetosis may cause chronic diarrhea. Data on incidence, histopathology, and diseases associated with these infrequent forms of colitis are reviewed. Etiology and pathogenesis of lymphocytic and collagenous colitis are still unknown, but immuno-inflammatory factors may be involved in both forms as well as, in collagenous colitis, primary disorders of collagen metabolism or drug-induced toxic effects. The significance of intestinal colonization by spirochetes is disputed; however, recent results indicate that these microorganisms are capable of inducing disease.
Collagenous sprue and collagenous colitis are two well-recognized idiopathic enteritides whose defining histologic attribute is fibrous thickening of the subepithelial basement membrane. Analogous changes in gastric mucosa seem to be quite rare. The term "collagenous gastritis" was recently applied for the first time to an isolated case of refractory gastritis in which distinctive subepithelial gastric fibrosis was noted. We report an additional case of this entity in a 35-year-old woman with refractory dyspepsia. In contrast to the earlier case of collagenous gastritis, our patient also had lymphocytic colitis, a type of colitis associated with watery diarrhea. Collagenous gastritis appears to be a distinct clinicopathologic entity, the histologic changes of which should be sought in patients with unexplained dyspepsia. Increased awareness of this condition and its possible clinical correlates may provide clues to its etiology and pathogenesis.