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PubMed2001

Extraintestinal Complications of Inflammatory Bowel Disease.

Extraintestinal complications of inflammatory bowel disease (IBD) are often secondary to the underlying disease. Therefore, the first priority is to get active IBD into remission with medications, since surgery for IBD is not indicated for the treatment of extraintestinal complications. Symptoms of extraintestinal complications usually can be treated with simple agents; the treatment of patients with refractory symptoms and the use of more complex drug regimens should be done in cooperation with specialists on affected organ systems. Careful consideration of prescribed drugs is necessary because they may negatively influence the course of IBD.

Journal Article↗

PubMed2005

Infliximab: Use in Inflammatory Bowel Disease.

Crohn's disease (CD) and ulcerative colitis (UC) are chronic and often debilitating inflammatory bowel diseases (IBD) without medical cures. Despite the existence of multiple therapies, the medical treatment of these diseases often has proven insufficient and surgery is frequently required. However, as our understanding of the pathogenesis of these disorders and other immune-mediated inflammatory diseases (eg, rheumatoid arthritis and psoriasis) has grown, new and more specific biologic therapies have been developed that are proving more effective than traditional agents. Infliximab is a genetically engineered monoclonal antibody that targets the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and represents the first effective biologic therapy for IBD and has largely revolutionized treatment. Infliximab initially was developed to be used in patients with moderate to severe luminal or fistulizing CD who are refractory to standard medical therapy. More and more practitioners now are using infliximab as first-line therapy because of its superior efficacy. Infliximab rapidly induces remission in CD, but when given chronically, it can provide long-term maintenance of remission. In addition, there are some data to support its use as a steroid-sparing agent and treatment for various extraintestinal manifestations of IBD and, although used predominantly to treat CD, recent data suggest that infliximab also may have a role in the management of UC. Overall, infliximab represents a clinically useful, cost-effective therapy that works well, even though careful patient monitoring is required to avoid rare but significant toxicities. The hope is that infliximab, together with other biologic agents that currently are in development, will allow us to modify the course of IBD, avoid complications such as strictures and abscesses, and reduce the need for surgery.

Journal Article↗

PubMed2005

Treatment of iron deficiency anemia in pediatric inflammatory bowel disease.

Anemia is a frequent extraintestinal manifestation of inflammatory bowel disease (IBD) that is commonly overlooked, despite its significant impact on quality of life. Characteristic symptoms include chronic fatigue, headache, and subtle impairment of cognitive function, although some less common symptoms include dyspnea, dizziness, pica, angular stomatitis, shortened attention span, and esophageal webs. Several types of anemia are associated with IBD, but iron deficiency anemia (IDA) accounts for the majority of cases and others include anemia of chronic disease, anemia associated with vitamin deficiency (vitamin B12 and folate), autoimmune anemia, and anemia caused by medication used to treat IBD. The diagnosis of IDA relies on laboratory blood tests. Therefore, these tests should be obtained on a regular basis because characteristic symptoms may be absent or not readily recognized by patients and their clinicians. Complete blood count may suffice; however, iron studies and serum vitamin levels may be necessary to differentiate between specific types of anemia. During the diagnostic process, it is important to consider coexistence of different types of anemia, especially if no response to therapy is noted. The therapy for anemia is directed towards treatment of the underlying inflammatory process and supplemental therapy, depending on the type of deficiency. Iron deficiency anemia is treated with iron preparations, first orally, and if unresponsive or if associated with untoward adverse events leading to decrease in adherence with the therapeutic regimen, with intravenous preparations. Intramuscular therapy has been abandoned due to high rate of complications. Intravenous therapy may be administered as a multiple-dose regimen (intravenous iron sucrose and gluconate) or as a single intravenous dose (iron dextran), which is associated with a higher risk of allergic infusion reactions and requires obligatory test dose administration. Treatment with erythropoietin is reserved for a select subgroup of patients with anemia of chronic disease. With appropriate treatment, the majority of patients with IBD will have significant improvement or resolution of anemia, which can lead to a better quality of life. However, a high index of suspicion should be maintained in order to identify the precise cause of anemia and to prescribe the appropriate therapy.

Journal Article↗

PubMed1991

Evaluation of a psychological treatment for inflammatory bowel disease.

Inflammatory bowel disease (IBD) encompasses two related gastrointestinal-tract diseases, ulcerative colitis (UC) and Crohn's Disease (CD). This study, a randomized controlled trial, compared the effectiveness of a multi-component behavioral treatment package (n = 11), which included IBD education, progressive muscle relaxation, thermal biofeedback, and training in use of cognitive coping strategies, to the effectiveness of symptom-monitoring (n = 10) as a control condition; 8 controls subsequently completed treatment. At posttreatment, the treatment group showed mean reductions on 5 symptoms, while the symptom monitoring controls showed mean reductions on all 8 symptoms. On a measure of Total Symptomatic change, the controls showed more improvement than the treated group; the treated controls at posttreatment, showed increases on all 8 symptoms. However, treated subjects perceived themselves as coping better with IBD, as feeling less IBD-related stress, and as experiencing less depression and anxiety. It is hypothesized that inherent differences may have existed between CD and UC subjects which could have led to the differences seen in treatment responses.

Adaptation, Psychological↗

PubMed1993

Psychological aspects of irritable bowel syndrome: comparisons with inflammatory bowel disease and nonpatient controls.

Patients with irritable bowel syndrome (IBS) (n = 121) were compared to 46 patients with inflammatory bowel disease (IBD), and to 45 nonpatient controls on a variety of psychological tests and on symptomatology. The most consistent finding was the ordering of group psychological test means such that, on 11 of 14 measures, IBS patients scored higher than IBD patients, who in turn scored higher than the nonpatient controls. The two patient groups differed significantly only on measures of anxiety with the IBS patients scoring significantly higher on all three measures. IBS patients also reported significantly more severity of abdominal pain than the IBD patients; while IBD patients reported more episodes of diarrhea, they did not rate them as significantly more severe than did the IBS patients. Various other parameters of the IBS population are also explored and implications for treatment and future study are discussed.

Adaptation, Psychological↗

PubMed1992

Corticosteroid treatment for inflammatory bowel disease in pediatric patients increases intraocular pressure.

Intraocular pressure (IOP) was measured in 54 pediatric patients (aged 7-21 years) with inflammatory bowel disease (IBD) who were treated with oral prednisone for 1-104 months. The difference in mean IOP between the treated patients (mean +/- SD, 15.62 +/- 4.11 mm Hg) and 55 age-matched controls (13.83 +/- 2.42 mm Hg) was statistically significant (P = 0.007). The IBD patients were classified as group I, IOP less than or equal to 19 mm Hg in both eyes, and group II, IOP greater than or equal to 20 mm Hg in either eye. Twelve of the 54 patients (22.2%) and none of the controls had IOP greater than or equal to 20 mm Hg (P less than 0.001). Seventeen of the 54 patients (31.5%) were characterized as "steroid responders" (IOP of greater than or equal to 20 mm Hg, change in IOP of greater than or equal to 6 mm Hg between visits, or difference in IOP of greater than or equal to 6 mm Hg between the two eyes). When the dose of prednisone was reduced to 0-10 mg/day 30 days or more before measurement, 9 steroid responders showed a decrease in IOP to within 2 SD of the mean control IOP; 7 of the 9 showed a decrease in IOP of greater than or equal to 6 mm Hg. These observations indicate that while prednisone is a causative factor in increasing the IOP, susceptibility to average doses of prednisone is highly variable, and patients need to be monitored on an individual basis. Because IBD is a chronic disorder that requires prolonged corticosteroid treatment, these children are at risk of developing steroid-induced glaucoma. Careful ophthalmologic monitoring of pediatric IBD patients, as well as of other pediatric patients who receive corticosteroid therapy, is recommended.

Adolescent↗

PubMed1993

Gut lavage fluid protein concentrations: objective measures of disease activity in inflammatory bowel disease.

BACKGROUND: Fluid obtained by whole gut lavage normally contains traces of immunoglobulin (Ig) G, albumin, and alpha-1-antitrypsin; higher concentrations have been found in patients with inflammatory bowel disease (IBD). METHODS: In a prospective study, 53 lavages were performed in 45 IBD patients (27 Crohn's disease, 18 ulcerative colitis), in whom disease activity was simultaneously assessed by Crohn's Disease Activity Index or Powell Tuck index. Concentration of IgG in lavage fluid was measured by enzyme-linked immunosorbent assay, and of albumin and alpha-1-antitrypsin by immunoturbidimetry. RESULTS: For IgG, concentrations in lavage fluid correlated closely with activity indices: in Crohn's disease, r = 0.723 (P < 0.0001), in ulcerative colitis, r = 0.714 (P < 0.0001). Results for albumin and alpha-1-antitrypsin concentrations were similar to those for IgG, but they were less sensitive in detecting active disease. However, this method cannot be used as a diagnostic test for IBD; normal results were obtained for IgG in 6 (all inactive) of 42 lavages in patients who had unequivocal radiological or endoscopic abnormalities. CONCLUSIONS: Assay of protein concentrations in gut lavage fluid is a simple, objective means of grading disease activity in patients with IBD; its potential uses are likely to be in the evaluation of complex cases and in clinical trials.

Adult↗

PubMed1994

Tumor necrosis factor alpha-producing cells in the intestinal mucosa of children with inflammatory bowel disease.

BACKGROUND/AIMS: Cytokines are thought to be important in mediating tissue damage in inflammatory bowel disease (IBD). Many of the in vivo activities of tumor necrosis factor alpha (TNF-alpha) match the changes found in IBD, but its importance is controversial. METHODS: A sensitive, reverse hemolytic plaque assay was used to determine the frequency of TNF-alpha secreting cells isolated from mucosal biopsy specimens of children with Crohn's disease or ulcerative colitis (UC) and non-IBD controls before and after medical treatment. RESULTS: Frequency of TNF-alpha secreting cells was significantly increased in biopsy specimens from children with mild, nonspecific inflammation compared with those with histologically normal intestine. Frequency did not increase in UC compared with children with nonspecific inflammation but was significantly greater in Crohn's disease than in UC. After treatment, the frequency of TNF-alpha secreting cells was reduced in patients receiving cyclosporin A, not reduced in patients with steroids or enteral nutrition, and not changed with treatment in UC. CONCLUSIONS: TNF-alpha secreting cells are increased in the mucosa of inflamed intestine, regardless of pathogenesis. In patients with IBD, higher levels are seen in Crohn's disease than in UC, probably reflecting the extensive T-cell activation in Crohn's disease. No relation existed between histological healing and the frequency of TNF-alpha-secreting cells.

Adolescent↗

PubMed1995

Production of immunoglobulin G and G1 antibodies to cytoskeletal protein by lamina propria cells in ulcerative colitis.

BACKGROUND & AIMS: Recent studies suggest an autoantigenic role for tropomyosin-related protein(s) in ulcerative colitis (UC). This study examined whether immunoglobulin G and G1 subclass antibodies against tropomyosins are produced spontaneously by the lamina propria mononuclear cells (LPMCs) that infiltrate the inflamed UC tissue. METHODS: LPMCs were isolated from colonic biopsy specimens from 29 patients with UC, 15 with colonic Crohn's disease (CD), and 13 with non-inflammatory bowel disease (IBD). The autologous peripheral blood mononuclear cells (PBMCs) were obtained. Cells were cultured in vitro and unstimulated for 10 days. Spontaneous production of immunoglobulin G and G1 antibodies against tropomyosins was measured by enzyme-linked immunosorbent assays using highly enriched tropomyosins from skeletal muscle and colonic mucosa. RESULTS: The total immunoglobulin G produced by LPMCs from both patients with UC and CD was comparable but higher than from patients with non-IBD (P < 0.05). However, immunoglobulin G antibodies to tropomyosins were higher in patients with UC than in patients with CD (P < 0.04) and non-IBD (P < 0.02). LPMCs from patients with symptomatic UC produced higher immunoglobulin G antibodies to tropomyosins than patients with UC in remission (P < 0.03), symptomatic CD (P < 0.04), and non-IBD (P < 0.02). Immunoglobulin G antibodies to tropomyosins predominantly belonged to immunoglobulin G1 subclass. The autologous PBMCs showed comparable results. CONCLUSIONS: Immunoglobulin G antibodies predominantly belonging to immunoglobulin G1 subclass and reactive against tropomyosin-related protein(s) are spontaneously produced by LPMCs from the colonic mucosa in patients with UC.

Adolescent↗

PubMed1986

Quantitation of natural antibodies to infectious bursal disease in Nigerian indigenous chickens.

Serum samples collected from 687 indigenous chickens located in small scattered groups in four states of Nigeria were examined for antibodies to infectious bursal disease (IBD) virus by the agar-gel precipitation (AGPT) and counterimmunoelectrophoresis (CIEOP) tests. 51 of the positive samples were further titrated by each of the two techniques. CIEOP detected more positive reactors (74.59%) than AGPT (58.95%). CIEOP also detected higher antibody levels among the reactors [geometric mean titre (GMT) of 51 samples was 23.02] when compared to AGPT. GMT of the same 51 samples was 21.8. The prevalence of antibodies to IBD virus in the indigenous chickens ranged from 64.7 to 77.7% CIEOP reactors between states. Since reports of IBD outbreaks among these chickens are rare unlike the situation among commercial poultry flocks, it was concluded that local chickens probably act as carriers of IBD virus.

Animals↗

PubMed1986

Inhibition of cytotoxicity by sulfasalazine. I. Sulfasalazine inhibits spontaneous cell-mediated cytotoxicity by peripheral blood and intestinal mononuclear cells from control and inflammatory bowel disease patients.

We have studied the effects of sulfasalazine and its metabolites on cell-mediated cytotoxicity by peripheral blood and intestinal mononuclear cells from both control and inflammatory bowel disease (IBD) patients. Sulfasalazine and sulfapyridine, as well as hydrocortisone and nordihydroguaiaretic acid inhibited spontaneous cell-mediated cytotoxicity by control and IBD peripheral blood cells. Sulfasalazine and nordihydroguaiaretic acid inhibited spontaneous cell-mediated cytotoxicity by control and IBD intestinal mononuclear cells cultured for 72 h in media alone. In contrast, 5-aminosalicylate, indomethacin and benzylimidazole had no effect on cytotoxicity by any cell population. Lectin-induced, antibody-dependent and interleukin-2-induced cell-mediated cytotoxicity, as well as lymphokine-activated killing were not inhibited by the drugs: inhibitory effects in these assays were primarily upon the underlying spontaneous cell-mediated cytotoxicity. The inhibition induced by sulfasalazine, sulfapyridine and nordihydroguaiaretic acid could not be reversed by adding the lipoxygenase metabolites leukotriene B4 or 12-hydroxyeicosatetraenoic acid. These findings demonstrate that spontaneous cell-mediated cytotoxicity by control and IBD mononuclear cells can be inhibited by sulfasalazine.

Catechols↗

PubMed2004

Inflammatory bowel disease.

Crohn's disease (CD) and ulcerative colitis (UC), collectively known as inflammatory bowel disease (IBD) are idiopathic, life-long, destructive chronic inflammatory conditions of the gastrointestinal tract that typically manifest during late childhood and adolescence. These chronic relapsing diseases may have devastating effects on patients. New medical progress in IBD includes genetics, gut ecology and microflora, immune mechanisms, and targeted biologic therapies. This article reviews the current understanding of the etiopathogenesis of IBD, the emerging epidemiologic data in pediatric IBD, clinical presentations, diagnostic evaluation, distinctions between adult and pediatric-onset disease, and a comprehensive review of both conventional and new therapies, highlighting age-specific issues such as growth, sexual delay, and psychological and behavioral health.

Adolescent↗

PubMed2006

Effects of gastrointestinal inflammation on enteroendocrine cells and enteric neural reflex circuits.

Inflammation of the gastrointestinal (GI) tract has pronounced effects on GI function. Many of the functions of the GI tract are subject to neural regulation by the enteric nervous system (ENS) and its extrinsic connections. Therefore, it is possible that inflammatory effects on the ENS contribute to altered function during GI inflammation. The reflex circuitry of the ENS is comprised of sensory transducers in the mucosa (enteroendocrine cells), afferent neurons, interneurons and motor neurons. This review focuses on recent data that describe inflammation-induced changes to the ENS and mucosal enteroendocrine cells. Studies of tissues from patients with inflammatory bowel disease (IBD) and from animal models of IBD have demonstrated marked changes in mucosal enteroendocrine cell signaling. These changes, which have been studied most intensely in 5-HT-containing enterochromaffin cells, involve changes in the number of cells, their signaling molecule content or their means of signal termination. Morphological evidence of enteric neuropathy during inflammation has been obtained from human samples and animal models of IBD. The neuropathy can reduce the number of enteric neurons in the inflamed region and is often accompanied by a change in the neurochemical coding of enteric neurons, both in the inflamed region and at distant sites. Electrophysiological recordings have been made from enteric neurons in inflamed regions of the colon of animal models of IBD. These studies have consistently found that inflammation increases excitability of intrinsic primary afferent neurons and alters synaptic transmission to interneurons and motor neurons. These data set the stage for a comprehensive examination of the role of altered neuronal and enteroendocrine cell signaling in symptom generation during GI inflammation.

Animals↗

PubMed2026

Transgenerational continuity: Persistence as a dimension of inheritance and evolution.

Transgenerational continuity (TC) describes the persistence of inherited molecular architectures across generations. Progress in identity-by-descent (IBD) detection, recombination dynamics, and epigenetic research highlights the growing need for a more comprehensive model of inheritance. This theoretical framework synthesizes evidence from genomics, population studies, and epigenetics to outline how inherited molecular architectures, which are transmitted through IBD, together with heritable epigenetic modifications, can preserve ancestral information across generations. IBD captures genomic continuity across three nested scales, where recent familial segments link close relatives, population-level haplotypes are shared across cohorts, and archaic fragments from Neanderthal and Denisovan admixture persist as molecular fossils of ancient lineages. Although recombination and selection reshape these regions, their persistence across time scales highlights the evolutionary durability of genomic continuity. Epigenetic memory reflects regulatory persistence, whereby molecular modifications can preserve functional states across cell divisions and sometimes across generations. Together with familial and population-level IBD persistence and the long-term retention of introgressed haplotypes, these findings demonstrate that inherited molecular architectures can persist across multiple timescales. Evolutionary processes shape this persistence. Purifying selection preferentially removes deleterious inherited variants, whereas positive selection can favor the persistence of functionally relevant genomic architectures. From this perspective, evolutionary dynamics arise not only from the generation of variation, but also from the differential persistence of inherited molecular architectures through selection. Transgenerational continuity therefore provides a conceptual framework in which persistence serves as an explanatory dimension of inheritance and evolution that complements variation and explains the persistence of biological identity across generations and evolutionary time.

Biological identity↗

PubMed2006

Inosine triphosphate pyrophosphatase and thiopurine s-methyltransferase genotypes relationship to azathioprine-induced myelosuppression.

BACKGROUND & AIMS: The use of azathioprine (AZA) in inflammatory bowel disease (IBD) patients is limited by toxicity, which occurs in up to 20% of treated patients. Mutations in the thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) genes have been associated with the occurrence of AZA-related toxicity. The aim of our study was to determine the relative contribution of ITPA and TPMT mutations to the development of toxicity induced by AZA treatment in IBD patients. METHODS: ITPA(94C>A, IVS2+21A>C) and TPMT (238G>C, 460G>A, and 719A>G) genotypes were assessed in 262 IBD patients (159 females, 103 males; 67 patients with ulcerative colitis, 195 patients with Crohn's disease) treated with AZA and were correlated with the development of leukopenia and hepatotoxicity. RESULTS: Leukopenia (leukocyte count, <3.0 x 10(9)/L) was observed in 4.6% of treated patients. The frequencies of mutant ITPA 94C>A and TPMT alleles were significantly higher in the leukopenic population compared with patients without leukopenia (16.7% and 5.4%, respectively, for ITPA 94C>A, and 20.8% and 4%, respectively, for TPMT). Moreover, the ITPA 94C>A and TPMT mutations predicted leukopenia: ITPA 94C>A odds ratio, 3.504; 95% confidence interval, 1.119-10.971 (P = .046); TPMT odds ratio, 6.316; 95% confidence interval, 2.141-18.634 (P = .004). Neither TPMT nor ITPA genotype predicted hepatotoxicity. CONCLUSIONS: ITPA 94C>A and TPMT polymorphisms are associated with AZA-related leukopenia in IBD patients.

Adolescent↗

PubMed2006

Incidence and risk factors for herpes zoster among patients with inflammatory bowel disease.

BACKGROUND & AIMS: An increased risk of herpes zoster in patients with inflammatory bowel disease (IBD) is hypothesized based on altered immune function, especially among patients receiving immunosuppressive medications. METHODS: We performed a retrospective cohort study and a retrospective nested case-control study using 1988-1997 data from the General Practice Research Database. In the cohort study, 7823 Crohn's disease (CD) and 11,930 ulcerative colitis (UC) patients were matched on age, sex, and primary care practice to 79,563 randomly selected controls without CD or UC. In the nested case-control study, 185 CD patients with zoster and 266 UC patients with zoster were matched on sex and year of birth to 1787 IBD patients without zoster. RESULTS: In the cohort study, the incidence of zoster was higher in patients with CD and UC compared with their matched controls (UC incidence rate ratio, 1.21; 95% confidence interval [CI], 1.05-1.40; CD incidence rate ratio, 1.61; 95% CI, 1.35-1.92). In the nested case-control study, receipt of a prescription for corticosteroids (adjusted odds ratio, 1.5; 95% CI, 1.1-2.2) or azathioprine/6-mercaptopurine (adjusted odds ratio, 3.1; 95% CI, 1.7-5.6) were both associated with zoster. CONCLUSIONS: Patients with IBD, especially those on immunosuppressive medications, are at higher risk for herpes zoster compared with the general population. Future studies should clarify the relative risk associated with anti-tumor necrosis factor alpha therapies and determine the use of the new zoster vaccine for patients with IBD.

Adolescent↗

PubMed2006

The relationship of inflammatory bowel disease type and activity to psychological functioning and quality of life.

BACKGROUND & AIMS: We aimed to assess the relationship of disease type and disease activity with psychological functioning and quality of life (QOL) in a population-based cohort of patients with recently diagnosed inflammatory bowel disease (IBD). METHODS: A total of 388 individuals diagnosed within 7 years were recruited from a population-based registry of IBD patients for the Manitoba IBD Cohort Study. Participants completed a clinical interview and standardized self-report measures of positive and negative psychological functioning, and QOL. Disease activity was determined by symptom self-report over the prior 6 months; Harvey-Bradshaw or Powell-Tuck disease activity indices also were used. Disease type was determined through chart verification. RESULTS: Seventy-four percent of Crohn's disease and 66% of ulcerative colitis participants had active disease during the previous 6 months. Multivariate regression showed that those with active disease had higher levels of distress, health anxiety, and perceived stress, lower social support, well-being and mastery, and poorer disease-specific QOL, relative to those with inactive disease. Disease type was not contributory to psychological functioning or QOL. Pain anxiety (fear of pain) and pain-specific catastrophizing were not associated with disease activity, after controlling for other psychological variables. Participants with either active or inactive disease had suboptimal general QOL. CONCLUSIONS: Ulcerative colitis and Crohn's disease participants were not differentiated in their psychological profiles. Given the strong association between disease-specific QOL, psychological functioning, and disease activity, it is important to be aware of related difficulties in patients with active IBD. There is a continued impact on QOL by the disease, even when it is inactive.

Adaptation, Psychological↗

PubMed2025

Comparative Safety of Janus Kinase Inhibitors vs Tumor Necrosis Factor Antagonists in Patients With Inflammatory Bowel Diseases.

BACKGROUND & AIMS: We conducted a retrospective cohort study comparing the safety of Janus kinase (JAK) inhibitors vs tumor necrosis factor-a (TNF) antagonists in patients with inflammatory bowel diseases (IBDs). METHODS: Using an administrative claims database, we identified patients with IBD who were new users of either JAK inhibitors or TNF antagonists between 2016 and 2023 and had insurance coverage for at least 1 year before and after treatment initiation. We compared the risk of infections (overall and serious infections requiring hospitalization), venous thromboembolism (VTE), and major adverse cardiovascular events (MACE) through stabilized inverse probability of treatment weighted Cox proportional hazards model accounting for disease characteristics, health care utilization, comorbidities, prior and concomitant medications, and competing risk of mortality. RESULTS: We included 856 patients treated with JAK inhibitors (age, 47 ± 17 years; 82% with ulcerative colitis [UC]) and 9422 patients treated with TNF antagonists (age, 45 ± 18 years; 44% with UC). JAK inhibitors were associated with higher risk of overall infections (incidence rate, 62.4 per 100 person-years [PY] vs 37.4 per 100 PY; hazard ratio [HR], 1.60; 95% confidence interval [CI], 1.33-1.93), but not serious infections (4.9 vs 5.4; HR, 0.97; 95% CI, 0.66-1.44) compared with TNF antagonists. There was no difference in the risk of VTE (1.3 vs 1.2; HR, 0.66; 95% CI, 0.28-1.57) and MACE (0.4 vs 0.7; HR, 0.50; 95% CI, 0.19-1.30). Findings were largely stable on subgroup analyses based on type of IBD, type of JAK inhibitors, age, prior biologic exposure, concomitant use of corticosteroids, and baseline risk of adverse events. CONCLUSIONS: In an observational study of patients with IBD, JAK inhibitors were not associated with an increased risk of serious infections, VTE, or MACE compared with TNF antagonists, although the overall risk of infections was higher.

Humans↗