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PubMed1996

Cytokine imbalance and autoantibody production in T cell receptor-alpha mutant mice with inflammatory bowel disease.

Spontaneous inflammatory bowel disease (IBD) resembling human ulcerative colitis develops in mice mutant for the T cell receptor alpha gene (TCR-alpha-/-). TCR-alpha-/- mice lack TCR-alpha/beta+ cells but contain TCR-gamma/delta+ cells and a small population of a unique CD4+, TCR-alpha-/beta+(low) cells. Since all the immunoglobulin (Ig) classes are present in these mice, help to B cells must be provided by cells other than TCR-alpha/beta+ cells. In the present study, we found serum levels of IgG1 and IgG2 to be markedly increased in TCR-alpha-/- mice with IBD as compared to TCR-alpha-/- mice without IBD or TCR-alpha+/- controls. An increase in IgG1-, IgG2a- and IgA- but not IgM-secreting mesenteric lymph node (MLN) B cells was detected in TCR-alpha-/- mutant mice. There was also a marked increase in MLN B cells secreting autoantibody (IgG) to tropomyosin, a cytoskeletal protein. Examination of the hyperplastic MLN showed a marked increase in the number of B, TCR-delta+, and CD4+ TCR-alpha-/beta+ cells, similar to the cell population observed at the site of colonic inflammation. Analysis of spontaneous cytokine production by MLN cells using an enzyme-linked immunospot assay, immunohistochemistry, and reverse transcription/polymerase chain reaction showed a decrease of interleukin 2 (IL-2) but a marked increase of IL-4 and interferon gamma (IFN-gamma) production in TCR-alpha-/- mice with IBD as compared to TCR-alpha-/- mice without IBD and TCR alpha+/- control mice. Both TCR-alpha-/beta+ and TCR-delta+ cells were found to be capable of producing IL-4; IFN-gamma was produced mostly by non-T cells, many of which were shown to be CD3- NK 1.1+ cells. We propose that the cytokine imbalance present in these mice results in expansion of B cells, production and switching of autoantibodies to IgG2 subclass, and development of IBD. It is possible that the unusual CD4+ TCR-alpha-/beta+ population and expanded TCR-gamma/delta+ population present in TCR-alpha-/- mice plays a central role in this abnormal immune response.

Animals↗
PubMed1998

Multipoint quantitative-trait linkage analysis in general pedigrees.

Multipoint linkage analysis of quantitative-trait loci (QTLs) has previously been restricted to sibships and small pedigrees. In this article, we show how variance-component linkage methods can be used in pedigrees of arbitrary size and complexity, and we develop a general framework for multipoint identity-by-descent (IBD) probability calculations. We extend the sib-pair multipoint mapping approach of Fulker et al. to general relative pairs. This multipoint IBD method uses the proportion of alleles shared identical by descent at genotyped loci to estimate IBD sharing at arbitrary points along a chromosome for each relative pair. We have derived correlations in IBD sharing as a function of chromosomal distance for relative pairs in general pedigrees and provide a simple framework whereby these correlations can be easily obtained for any relative pair related by a single line of descent or by multiple independent lines of descent. Once calculated, the multipoint relative-pair IBDs can be utilized in variance-component linkage analysis, which considers the likelihood of the entire pedigree jointly. Examples are given that use simulated data, demonstrating both the accuracy of QTL localization and the increase in power provided by multipoint analysis with 5-, 10-, and 20-cM marker maps. The general pedigree variance component and IBD estimation methods have been implemented in the SOLAR (Sequential Oligogenic Linkage Analysis Routines) computer package.

Computer Simulation↗
PubMed1998

Linkage and association between inflammatory bowel disease and a locus on chromosome 12.

Genetic epidemiological studies have shown that genetic factors are important in the pathogenesis of the idiopathic inflammatory bowel diseases (IBD), Crohn disease (CD), and ulcerative colitis (UC). A genome screen in the United Kingdom found linkage of IBD to a 41-cM region of chromosome 12, surrounding D12S83. We aimed to replicate this linkage and to narrow the region of interest. Nonparametric linkage analyses at microsatellites surrounding D12S83 were performed in 122 North American Caucasian families containing 208 genotyped IBD-affected relative pairs. Transmission/disequilibrium tests (TDTs) were also performed. We confirmed that IBD is linked to chromosome 12 (peak GENEHUNTER-PLUS LOD* score 2.76 [P = .00016] between D12S1724 and D12S90). The evidence for linkage is contributed by both the group of CD-affected relative pairs (peak GENEHUNTER-PLUS LOD* score 1.79 [P = .0021] between D12S1724 and D12S90) and the group of UC-affected relative pairs (peak GENEHUNTER-PLUS LOD* score 1.82 [P = .0019] at D12S335). The TDT is positive at the D12S83 locus (global chi2 = 16.41, 6 df, P = .012). In conclusion, we have independently confirmed linkage of IBD to the chromosome 12 region that we investigated. A positive TDT at D12S83 suggests that we have greatly narrowed the chromosome 12 region that contains an IBD locus.

Chromosomes, Human, Pair 12↗
PubMed1999

A simulation study of the effects of assignment of prior identity-by-descent probabilities to unselected sib pairs, in covariance-structure modeling of a quantitative-trait locus.

Sib pair-selection strategies, designed to identify the most informative sib pairs in order to detect a quantitative-trait locus (QTL), give rise to a missing-data problem in genetic covariance-structure modeling of QTL effects. After selection, phenotypic data are available for all sibs, but marker data-and, consequently, the identity-by-descent (IBD) probabilities-are available only in selected sib pairs. One possible solution to this missing-data problem is to assign prior IBD probabilities (i.e., expected values) to the unselected sib pairs. The effect of this assignment in genetic covariance-structure modeling is investigated in the present paper. Two maximum-likelihood approaches to estimation are considered, the pi-hat approach and the IBD-mixture approach. In the simulations, sample size, selection criteria, QTL-increaser allele frequency, and gene action are manipulated. The results indicate that the assignment of prior IBD probabilities results in serious estimation bias in the pi-hat approach. Bias is also present in the IBD-mixture approach, although here the bias is generally much smaller. The null distribution of the log-likelihood ratio (i.e., in absence of any QTL effect) does not follow the expected null distribution in the pi-hat approach after selection. In the IBD-mixture approach, the null distribution does agree with expectation.

Alleles↗
PubMed1999

A genomewide analysis provides evidence for novel linkages in inflammatory bowel disease in a large European cohort.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation, typically starting in early adulthood. IBD is subdivided into two subtypes, on the basis of clinical and histologic features: Crohn disease and ulcerative colitis (UC). Previous genomewide searches identified regions harboring susceptibility loci on chromosomes 1, 3, 4, 7, 12, and 16. To expand our understanding of the genetic risk profile, we performed a 9-cM genomewide search for susceptibility loci in 268 families containing 353 affected sibling pairs. Previous linkages on chromosomes 12 and 16 were replicated, and the chromosome 4 linkage was extended in this sample. New suggestive evidence for autosomal linkages was observed on chromosomes 1, 6, 10, and 22, with LOD scores of 2.08, 2.07, 2.30, and 1.52, respectively. A maximum LOD score of 1.76 was observed on the X chromosome, for UC, which is consistent with the clinical association of IBD with Ullrich-Turner syndrome. The linkage finding on chromosome 6p is of interest, given the possible contribution of human leukocyte antigen and tumor necrosis-factor genes in IBD. This genomewide linkage scan, done with a large family cohort, has confirmed three previous IBD linkages and has provided evidence for five additional regions that may harbor IBD predisposition genes.

Cohort Studies↗
PubMed2006

Variance calculations for identity-by-descent estimation.

Nonparametric linkage strategies often involve estimation of identity by descent (IBD) with the use of affected sibling pairs. Methods for IBD estimation are well established and have been successful for mapping complex traits. However, the majority of linkage approaches involving IBD have focused on statistical testing, rather than on the effect estimates themselves. Through a bootstrap procedure developed for linkage-scan data sets, we provide standard errors for the estimated mean IBD that are broadly applicable. Applications that benefit from the availability of standard errors include effect-size estimates and confidence intervals; meta-analyses, including tests for heterogeneity; and discordant-sibling-pair evaluation. We demonstrate the use of estimated mean IBD and its standard errors in the National Institute of Mental Health Human Genetics Initiative linkage samples for bipolar disorder and Alzheimer disease. Mean IBD and its standard errors are valuable tools for the further assessment and evaluation of linkage-scan samples involving complex disease.

Alzheimer Disease↗
PubMed2004

Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system.

Vitamin D is an important immune system regulator. The active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown to inhibit the development of autoimmune diseases, including inflammatory bowel disease (IBD). Paradoxically, other immune system-mediated diseases (experimental asthma) and immunity to infectious organisms were unaffected by 1,25(OH)2D3 treatment. There are similar paradoxical effects of vitamin D deficiency on various immune system functions. Vitamin D and vitamin D receptor (VDR) deficiency resulted in accelerated IBD. Experimental asthma was unaffected by 1,25(OH)2D3 treatment and was less severe among VDR-deficient mice. Vitamin D is a selective regulator of the immune system, and the outcome of 1,25(OH)2D3 treatment, vitamin D deficiency, or VDR deficiency depends on the nature of the immune response (eg, infectious disease, asthma, or autoimmune disease). An additional factor that determines the effect of vitamin D status on immune function is dietary calcium. Dietary calcium has independent effects on IBD severity. Vitamin D-deficient mice on low-calcium diets developed the most severe IBD, and 1,25(OH)2D3 treatment of mice on low-calcium diets improved IBD symptoms. However, the best results for IBD were observed when the calcium concentration was high and 1,25(OH)2D3 was administered. Both the type of immune response and the calcium status of the host determine the effects of vitamin D status and 1,25(OH)2D3 on immunity.

Animals↗
PubMed2006

A population-based ecologic study of inflammatory bowel disease: searching for etiologic clues.

The authors' objective in this study was to determine geographic variations in the incidence of inflammatory bowel disease (IBD), specifically Crohn's disease and ulcerative colitis, in the Canadian province of Manitoba and its association with the sociodemographic, geographic, and disease-related characteristics of the study population. Using the University of Manitoba IBD Epidemiology Database, the authors applied spatial and ecologic techniques to visualize, explore, and model the incidence of Crohn's disease and ulcerative colitis for the period 1990-2001. The study demonstrated marked, statistically significant geographic variability in rates of both Crohn's disease and ulcerative colitis associated with the characteristics of the study population. Incidences of Crohn's disease and ulcerative colitis were observed to be highest among non-Aboriginal persons, persons of high socioeconomic status, persons with the lowest rates of enteric infection, and persons with the highest rates of multiple sclerosis. The observation of an inverse association between IBD incidence and rates of reportable enteric infection at the population level is consistent with the "hygiene hypothesis," which suggests that early exposure to enteric agents affords protection against eventual development of IBD. The positive association between IBD incidence rates and multiple sclerosis suggests that these two chronic, immunologically mediated diseases may have a common environmental etiology. This study underscores the importance of environment in IBD causation.

Climate↗
PubMed2002

Osteoporosis and other complications of inflammatory bowel disease.

Osteoporosis has received increasing attention as a potential complication of inflammatory bowel disease (IBD). The first population-based data on incidence of fractures in an IBD population were published this past year. The incidence of fractures was one per 100 patient years. Compared with the general population, the fracture rate was increased; however, the relative risk was 1.4 and, therefore, not as high as might be expected from the myriad of studies reporting high rates of osteopenia measured by dual energy x-ray absorptiometry (DXA). Another area receiving increasing attention is that of the enhanced risk of venous thrombosis in patients with IBD. The first population-based incidence rates of venous thrombosis in IBD were also published this past year and showed that IBD patients are affected by venous thrombosis at a rate of approximately one per 200 patient years. The relative risk for venous thrombosis compared with the general population was 3.5. Several studies have reported on associated risk markers or genetic clotting abnormalities, but no clear paradigm has emerged to account for those patients who will suffer a clot. Finally, the first North American population-based study was published, quantifying the prevalence rates of extraintestinal manifestations in patients with IBD for at least 10 years. Some gender- and disease-specific findings emerged. This study found that iritis and uveitis were more common in female patients with ulcerative colitis (3.2%), primary sclerosing cholangitis (PSC) was most common in male patients with ulcerative colitis (3%), ankylosing spondylitis was most common in male patients with Crohn disease (2.7%), and erythema nodosum was most likely to occur in female patients with Crohn disease (1.9%).

Journal Article↗
PubMed2000

Prevalence of factor V Leiden and the G20210A prothrombin-gene mutation in inflammatory bowel disease.

A hypercoagulable state has been hypothesized as a contributing factor in the pathogenesis of inflammatory bowel disease (IBD); moreover, such patients have an increased risk of thrombotic complications. The aim of the present paper was to study the prevalence of the two most important causes of inherited thrombophilia: factor V Leiden and the G20210A prothrombin-gene mutation in patients with Crohn's disease (CD) and ulcerative colitis (UC). Fifty-two patients affected by IBD (33 UC and 19 CD, 16 female and 36 male; mean age, 42 years) and 156 healthy controls (48 female and 108 male; mean age, 37 years) were studied. Seven out of 52 patients (13%) had previous thrombotic events. High molecular weight DNA was analysed for the presence of factor V Leiden and the G20210A prothrombin-gene mutation. One out of 52 IBD patients (1.9%) and three out of 156 control subjects (1.9%) were heterozygous for factor V Leiden. One IBD patient (1.9%) and four healthy controls (2.6%) were heterozygous for the prothrombin-gene mutation. The prevalence of the two mutations was similar in patients and controls. In the subgroup of IBD patients with previous thrombotic events, only one patient was heterozygous for the prothrombin-gene mutation. Factor V Leiden and the G20210A prothrombin-gene mutation do not seem to play a major role in the pathogenesis of IBD or be associated with an increased incidence of thrombotic complications, but with limited data.

Adult↗
PubMed1983

Medical and surgical treatment of inflammatory bowel disease in pregnancy.

Inflammatory bowel disease is a relatively common spectrum of disorders of the gastrointestinal tract in women of the reproductive age group. Although Crohn's disease may decrease fertility, female reproductive ability is normal in UC. In general, IBD is not a contraindication to pregnancy or vaginal delivery and is not an indication for therapeutic abortion. Pregnancy will have a variable effect on IBD, and the patient's experience in previous pregnancies is not prognostic of future pregnancies. Whenever possible, pregnancies should be planned when IBD is quiescent and the patient is on a minimal drug regimen. The treatment of IBD is essentially the same regardless of pregnancy. Aggressive medical management with supportive therapy, corticosteroids, and sulfasalazine is effective in the treatment for this disorder. Sulfasalazine is effective in preventing recurrence of UC. Surgical treatment may be necessary in pregnancy. An enlarged uterus may make recognition of acute complications difficult, and fear of radiation may decrease the number of diagnostic x-ray studies performed. A proctocolectomy and ileostomy is curative for UC, but no procedure will cure Crohn's disease. In pregnancy, a limited surgical procedure may be necessary. There is a high incidence of fetal loss if surgery is required in IBD. This fetal loss is probably caused by the fulminant nature of the disease rather than surgery itself. If surgery is indicated, however, it should be performed for maternal indications despite the risk to the fetus. As can be seen, management of IBD in pregnancy is not to be taken lightly and requires extensive collaboration between obstetrician, gastroenterologist, surgeon, and other support personnel.

Adrenocorticotropic Hormone↗
PubMed1982

Inflammatory bowel disease and pregnancy.

Inflammatory bowel disease (IBD) commonly affects women of childbearing age, leading to concerns about the effects of the disease on fertility and pregnancy, the effect of pregnancy on the disease, and the diagnosis and treatment of IBD in the pregnancy women. The literature regarding these issues is reviewed, and a representative case report is discussed. Ulcerative colitis has no effect on fertility. Crohn's disease appears to be associated with an increased risk of infertility. "Subfertility," a temporary inability to conceive associated with chronic disease activity, is perhaps a more suitable description. There have been no studies regarding infertility and males with IBD, although sulfasalazine has recently been reported to cause reversible infertility in men. Ulcerative colitis is not associated with a higher spontaneous abortion rate than the general population, although it is not clear whether certain subgroups of patients have a higher rate of abortion. A similar conclusion has been reached for Crohn's disease, although reported abortion rates of 10-25% are somewhat higher than the general population. Approximately 30-50% of pregnant women with ulcerative colitis have exacerbations during their pregnancy or postpartum, a figure that is applicable to Crohn's disease as well, and which is no different than a control population of nonpregnant women with IBD. Patients with active ulcerative colitis at conception have a higher incidence of disease exacerbation than those with quiescent disease. Postpartum recurrences are more frequent in Crohn's disease, occurring in up to 40% of patients, but respond to standard medical therapy. Women who have had an ileostomy for ulcerative colitis consistently and successfully carry pregnancy to term. There is no data regarding women who have had an ileostomy for Crohn's disease. The approach to the women with abdominal pain during pregnancy is reviewed, including the use of radiographic procedures. No amount of radiation exposure can be considered safe, but the judicious use of standard radiographic tests when considered necessary for the health of the mother appear to be associated with little risk for the fetus. The medial treatment of IBD during pregnancy is the same as that for the nonpregnant patient. Despite animal data to the contrary, the bulk of human data suggests that steroids, when used to treat a variety of conditions including IBD, pose little risk to the human fetus. Similarly, despite the theoretical risk of kernicterus, sulfasalazine appears to be a safe drug even when used during the third trimester of pregnancy.U

Abortion, Spontaneous↗
PubMed2002

Constrictive pericarditis in chronic ulcerative colitis.

Acute pericarditis has been described as an extraintestinal manifestation of inflammatory bowel disease (IBD), as well as a consequence of IBD treatment, specifically sulfasalazine and mesalamine. Until now, there have been no reported cases of constrictive pericarditis associated with IBD or its treatment. A 37-year-old woman with a 24-year history of chronic ulcerative colitis (CUC) presented with a 3-month history of fevers, palpitations, dyspnea, syncope, and retrosternal chest pain. Two weeks before symptoms, she had initiated oral mesalamine for an ongoing CUC flare. Physical examination suggested constrictive pericarditis. An echocardiogram revealed a thickened pericardium with a nearly circumferential fibrinous effusion, with Doppler confirming diastolic compromise. The patient proceeded to radical pericardectomy. Pathological examination showed grossly hemorrhagic acute and chronic pericarditis, with cultures and cytology negative. To date, only 104 cases of IBD with acute pericarditis have been reported, with fewer than 10 cases of mesalamine-induced acute pericarditis reported. This is the first reported case of constrictive pericarditis related to IBD or its treatment. Although our patient may have had IBD-associated constrictive pericarditis, her mesalamine use raises the possibility of a drug-induced constrictive pericarditis.

Adult↗
PubMed2006

Acceptance of telemanagement is high in patients with inflammatory bowel disease.

GOALS: Assess acceptance and attitudes regarding telemanagement (HAT) in patients with inflammatory bowel disease (IBD). BACKGROUND: Noncompliance is a barrier to successful outcomes in patients with IBD. Novel methods for monitoring and assessing compliance are needed. STUDY: HAT consists of a laptop connected to a weight scale. HAT prompts patients to respond to questions about symptoms, medication side effects, and compliance. Ten consecutive adult patients with IBD were trained to use HAT. Attitudinal surveys and structured qualitative interviews were performed at the end of the session. RESULTS: Twenty percent of patients had never used a computer at home. All patients reported that use of the computer and self-testing was not complicated. All patients reported that the symptom diary and questions on side effects were easy to answer. All patients reported that self-testing took little time. Eighty percent said that testing would not interfere with usual activities, that they could comply with testing 3 times/wk, and that they would agree to use the system in the future. CONCLUSIONS: Improved methods of monitoring are needed for patients with IBD. Patients with IBD can be easily trained to use HAT, and patient acceptance is high. Further studies are needed to determine the clinical impact of HAT in IBD.

Adult↗
PubMed1991

Nutritional issues in pediatric inflammatory bowel disease.

Malnutrition, characterized by weight loss, growth failure and micronutrient depletion, are prominent features of inflammatory bowel disease (IBD) in the pediatric age group. Accurate evaluation of the patient's nutritional status and appropriate nutritional support, whether enteral or parenteral, constitute integral parts of the management of the growing child with IBD. Over the past two decades, a number of studies have supported the potential use of nutritional therapy to induce remission and to control disease activity in symptomatic Crohn's disease. More recently, preliminary studies on the use of dietary supplements of marine-oil-derived omega-3 fatty acids have also indicated a beneficial effect in IBD patients. In parallel with these clinical trials, scientific research has recently focused on the concept that specific dietary alterations can modulate the immune response. Components of the diet that may have particular relevance to mucosal immunity and the pathogenesis of IBD include polyunsaturated fatty acids, nucleotides, and amino acids such as glutamine and arginine. Future research in the interactions between specific nutrients and the immune system will likely increase our understanding of the causes of IBD, as well as enhance the development of novel nutritional therapies for IBD patients.

Child↗
PubMed1993

Growth failure in pediatric inflammatory bowel disease.

To assess whether children with inflammatory bowel disease (IBD) develop permanent impairment of linear growth, we analyzed records from 48 young adults who had IBD during childhood or early adolescence (Tanner I-III; 11.8 +/- 2.4 years old at diagnosis). All were fully grown (Tanner V; 21.1 +/- 3.0 years) at last examination. Adult heights were predicted from data obtained at or shortly after the diagnosis of IBD by three methods: height for age percentile, the Bailey-Pinneau (BP), and Roche-Wainer-Thissen (RWT) methods. Predicted adult heights were then compared with the actual ultimate height of each subject. Permanent growth failure occurred in 19-35% of subjects, depending upon the method used to assess growth. Overall, 31% (15 of 48) of the subjects had deficits of adult height identified by two or more methods, including 14 of 38 (37%) of those with Crohn's disease but only one of 10 with ulcerative colitis. Age at diagnosis of IBD, age at last examination, age at cessation of linear growth, and site of IBD did not differ between impaired and normal growth groups. Duration of corticosteroid use was longer (p < 0.05) in growth-impaired subjects. In addition, although 60% of all subjects had periods of poor growth that put them in height-for-age percentiles two or more major growth channels below previous percentiles, only 19% remained at these levels upon achieving their final adult heights. Permanent impairment of linear growth leading to clinically meaningful deficits of ultimate adult height is common in patients with IBD in childhood or early adolescence. New therapeutic approaches are needed to address this problem.

Adolescent↗
PubMed1998

Vitamins A and E serum levels in children and young adults with inflammatory bowel disease: effect of disease activity.

BACKGROUND: Hypovitaminosis and fat-soluble vitamin deficiency have been reported in adults with inflammatory bowel disease (IBD). A prospective study was undertaken to determine the prevalence of low serum levels of vitamins A and E in children and young adults with IBD. METHODS: Clinical information and serum for vitamin levels was gathered prospectively from 61 patients with Crohn's disease, 36 patients with ulcerative colitis, and 23 control subjects. Disease activity and disease location were determined for IBD patients. Serum retinol and alpha-tocopherol levels were determined by high-performance liquid chromatography. RESULTS: The prevalence of hypovitaminosis A (defined as serum vitamin A < 20 micrograms/dl) or hypovitaminosis E (defined as serum vitamin E < 5 mg/l) was 16% in the pediatric IBD population studied. Low vitamin A levels were more common than low vitamin E levels. Serum retinol levels correlated significantly with alpha-tocopherol levels. Hypovitaminosis was significantly more prevalent in the Crohn's disease patients who had active disease, an erythrocyte sedimentation rate of more than 25 mm/hour, or a serum albumin level less than 3 mg/dl. CONCLUSIONS: Children and young adults with active IBD frequently have low serum levels of vitamin A or vitamin E. The severity of disease activity is a better predictor of risk for hypovitaminosis than is nutritional status. Further work is necessary to determine whether the hypovitaminosis seen in children with IBD reflects true deficiency.

Adolescent↗
PubMed2001

Inflammatory bowel disease associated with immune thrombocytopenic purpura in children.

OBJECTIVE: Previous reports suggest an association between inflammatory bowel disease (IBD) and immune thrombocytopenic purpura (ITP) in adults. To date, only five children with both diseases have been described. The aim of the study was to describe the characteristics of children with IBD and ITP. METHODS: Cases were obtained from the pediatric gastroenterology community by means of the pediatric gastroenterology internet bulletin board in June 1999. Eight cases were submitted from seven medical centers. Medical records were reviewed by two pediatric gastroenterologists and a pediatric hematologist. RESULTS: The age range of the patients was 2.1 to 16.5 years, with a mean age of 9.6 +/- 5.2 years. Four children had ulcerative colitis, three had Crohn disease, and one had indeterminate colitis. All had colonic involvement of IBD. Of eight patients, three had IBD first, three had ITP first, and two had both simultaneously. At ITP diagnosis, platelet count was less than 10,000/mL in five children, 17,000/mL in one child, and 50,000 to 60,000/mL in two children. Of the three children diagnosed with ITP first, two initially had rectal bleeding at the time of ITP diagnosis. Bone marrow evaluations, performed in six of eight children, were consistent with ITP. Six of the eight children had chronic ITP, including three children who were 5 years of age or younger. Therapy for ITP included steroids (n = 6), intravenous immunoglobulin (n = 6), Rh o (D) intravenous immunoglobulin (n = 2), and splenectomy (n = 1). CONCLUSIONS: The authors describe the largest pediatric case series of children with IBD and ITP. More than 50% of the children had the chronic form of ITP. Most patients responded to conventional therapy for ITP and IBD.

Adolescent↗