Infections Common in IBD, Rates Vary by Treatment
Patients with inflammatory bowel disease (IBD) experienced higher rates of mild and moderate infections. Women, smokers, those with multiple comorbidities, and those with exposure to certain IBD medications showed significantly higher rates of infections.
METHODOLOGY:
Researchers conducted a prospective observational study (June 2020 to July 2021) to evaluate the incidence of and risk factors for mild, moderate, and severe infections in 629 patients (mean age, 48.3 years; 58.2% women) with IBD who used an established remote monitoring platform for IBD management.
They used the Patient-Reported Infections Questionnaire, a validated seven-item tool with a 3-month recall period, to collect data on 15 infection categories, including respiratory tract, urinary tract, and skin conditions and COVID-19.
The presence or absence of disease activity was confirmed using a combination of monitoring questionnaire scores for patient-reported disease activity and faecal calprotectin levels.
The severity of infection was categorised on the basis of the type and route of treatment as mild (self-limiting or requiring topical treatment), moderate (requiring oral treatment), or severe (requiring hospitalisation and/or intravenous treatment).
Exposure to different medications, alone or in combination, was also assessed.
TAKEAWAY:
Overall, 991 infections were reported during 573.8 person-years of follow-up, with an overall incidence rate (IR) of 172.7 per 100 person-years, predominantly comprising mild (68%; IR, 117.5 per 100 person-years) and moderate (29.5%; IR, 50.9 per 100 person-years) infections.
Women demonstrated significantly higher rates of infections than men (IR ratio [IRR], 1.70; P < .001), with increased rates of infections among current smokers vs non-smokers (IRR, 1.43; P = .004).
Patients with a Charlson Comorbidity Index score > 2 had significantly higher rates of infections than those with lower scores (IRR for all infections, 1.69; P = .031).
Glucocorticoid use more than doubled the rates of infections (IRR, 2.02; P = .033), and compared with no treatment, the use of JAK inhibitors, immunomodulator monotherapy, anti-TNF monotherapy, and combination therapy with anti-TNF and immunomodulators were associated with increased rates of infections.
IN PRACTICE:
"Clinicians should adopt a holistic approach that includes vigilant monitoring, preferably using validated tools, such as the PRIQ [Patient-Reported Infections Questionnaire], to identify patients with frequent mild or moderate infections. In addition, proactive application of preventive strategies, like vaccination, optimizing nutritional status, counselling for lifestyle modifications, and careful selection of therapies, should be used to reduce infection risk," the authors of the study wrote.
SOURCE:
This study was led by Ashkan Rezazadeh Ardabili, MD, Department of Gastroenterology and Hepatology, Maastricht University Medical Centre+, Maastricht, the Netherlands. It was published online on July 09, 2025, in the Journal of Crohn's and Colitis.
LIMITATIONS:
The study's 1‐year follow‐up coincided with COVID‐19 public health measures, likely underestimating overall rates of infections. This study was underpowered to precisely assess rare outcomes, and its real‐world design limited the control over the distribution of medication groups, especially when stratifying the analysis by IBD subtype.
DISCLOSURES:
This study was supported in part by an investigator-initiated research grant from Takeda. Some authors reported receiving grants, non-financial support, and research prizes and serving as speaker, advisor, and/or principal investigator for various institutions and pharmaceutical companies, including Takeda.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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A cardiovascular examination reveals normal peripheral pulses and normal heart findings. A chest examination reveals normal auscultation and expansion. His abdomen is soft. Head, eyes, ears, nose, and throat (HEENT) examination findings are unremarkable. He does not have a skin rash. A visual examination reveals normal acuity, field, and fundi. His affect is flat. A neurologic examination of the higher mental functions reveals that the patient is awake and alert, with normal orientation, attention, concentration, fund of knowledge, and language function. His memory is impaired, with recall one-third at 3 minutes. He has a normal past memory. His speech is normal. A cranial nerve examination reveals normal extraocular movements, increased blink rate, normal facial sensation, a symmetric face with abnormal fidgety movement, normal hearing, and normal palate movement. He has abnormal tongue movement and cannot protrude his tongue more than 20 seconds (darting tongue movement). He has normal shoulder shrug. No Kayser-Fleischer ring is noted during slit-lamp examination. An examination of the motor system reveals decreased muscle tone, normal bulk, and 5/5 strength in both upper and lower extremities. No atrophy or fasciculation is noted. Deep tendon reflexes are normal (2+ with flexor planters). Sensory examination findings are normal. Finger-nose test findings are normal. An examination of the extrapyramidal system reveals reduced tone and involuntary choreoathetoid movements that affect both upper and lower extremities as well as his face. He has a dancing gait. Diagnostic tests reveal normal complete blood cell count (CBC) and comprehensive metabolic panel findings. He has normal serum findings and urine copper levels. His erythrocyte sedimentation rate (ESR) is 22 mm/hr (reference range, 0-22 mm/hr). He has normal ECG findings, a normal thyroid-stimulating hormone (TSH) level, a normal transthoracic echo (with ejection fraction 65%), and normal chest radiography findings. Brain MRI can be used to evaluate for selective atrophy of deep gray structures, to document disease burden, and to provide a baseline for future comparison. Whole-body 18-FDG PET/CT may be used to screen for occult neoplasm and paraneoplastic chorea, but this is exceedingly rare and typically subacute. NMDA receptor antibody panel may be used to investigate for autoimmune encephalitic chorea, but the features of this (ie, seizures, psychosis, and autonomic instability) are absent in this case. RPR and FTA-ABS may be used to evaluate for neurosyphilitic chorea, but this is also very uncommon and unnecessary without risk factors or acute symptoms. In this patient, brain MRI reveals evidence of bilateral caudate atrophy, with increased intercaudate distance (Figure). Figure. Cerebrospinal fluid (CSF) examination findings are normal. Discussion This 35-year-old man has Huntington disease. He has insidious-onset, slowly progressive movement disorder, and movements are absent during sleep. His movements are described as choreoathetoid. He has family history that suggests autosomal dominant transmission. Apart from the movement disorder, he also has neuropsychiatric manifestations, with death at an early age in the family. A CT scan of the head revealed evidence of caudate nucleus atrophy. Brain MRI revealed evidence of caudate atrophy (Figure). Figure. In evaluating the differential diagnoses, the patient has no history of antipsychotic medication use to suggest tardive dyskinesia. He has no clinical or diagnostic evidence of infection or heart involvement, which makes Sydenham chorea unlikely. No acanthocytes were observed, helping to exclude neuroacanthocytosis. The strong family history of progressive abnormal movements and neuropsychiatric symptoms across generations supports a genetic etiology, specifically autosomal-dominant Huntington disease. Huntington disease is a rare neurodegenerative disorder of the central nervous system (CNS) characterized by choreiform movements, behavioral and psychiatric disturbances, and dementia.[1] Huntington disease is caused by an autosomal-dominantly inherited expansion of CAG trinucleotide repeats in the huntingtin ( HTT ) gene on chromosome 4; this leads to production of a mutant huntingtin (mHTT) protein, with an abnormally long polyglutamine repeat.[2] Individuals with more than 39 CAG repeats develop the disease, whereas reduced penetrance is seen in those with 36-39 CAG repeats. The disease can be anticipated when the gene is passed down the paternal line, as in this case; a father with a CAG repeat length in the intermediate range may have a child with an expanded pathogenic repeat length. This is because sperm from males shows greater repeat variability and larger repeat sizes than somatic tissues. Mutant huntingtin protein leads to death and neuronal dysfunction through various mechanisms. Postmortem studies reveal diffuse atrophy of the caudate and putamen. The progressive worsening of Huntington disease leads to a bedridden state with cognitive deterioration, and death typically occurs about 20 years after the onset of symptoms.[3] Prevalence in the white population is estimated at 1 in 10,000 to 1 in 20,000. The mean age at symptom onset is 30-50 years. In some cases, symptoms begin before age 20 years, with behavior disturbances and learning difficulties at school; this is termed juvenile Huntington disease (Westphal disease).[4] The first description, by Waters, dates to 1842. However, after a description in 1872 by George Huntington, it became known as Huntington chorea. In 1983, a linkage on chromosome 4 was established, and in 1993 the gene for Huntington disease was found.[1] Diagnosis of Huntington disease is confirmed by demonstration of autosomal dominant transmission or gene testing in the presence of clinical features.[5] The clinical features of Huntington disease consist of motor, cognitive, and neuropsychiatric manifestations. Huntington disease has a biphasic course of hyperkinetic phase with chorea in the early stages of disease that then plateaus into a hypokinetic phase, consisting of bradykinesia dystonia, balance issues, and gait disturbance. The younger-onset variant is associated with predominant bradykinesia.[6] Cognitive disturbance can be seen many years before other symptom onset and is characterized by impaired emotion recognition, processing speed, and executive function abnormality. Neuropsychiatric symptoms widely vary, including apathy, anxiety, irritability, depression, obsessive-compulsive behavior, and psychosis. A lack of awareness of early and progressing behavioral, cognitive, and motor symptoms is a hallmark of Huntington disease. This unawareness is caused by the disease itself (specifically, impaired insight or anosognosia) and is not the result of intentional denial, avoidance, or suppression of symptoms.[7] Therefore, a comprehensive history, including information from a knowledgeable family member/caregiver, is advisable.[7] Numerous conditions can mimic Huntington disease, including a spinal cerebellar ataxia 17, spinocerebellar ataxia 1-3, and Friedreich ataxia, which involve neuropathy. If seizures are also present, dentatorubropallidoluysian atrophy should be considered. Acanthocytes are seen in patients with neuroacanthocytosis.[8-10] Isolated chorea can be seen in acquired conditions, including chorea gravidarum, systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, postinfectious syndromes, polycythemia vera, and some drug use. Genetic testing for the mHTT mutation can be either diagnostic or predictive.[6] A diagnostic test may be performed when a patient presents with typical motor features of Huntington disease. Prior to testing, the patient should be informed about Huntington disease and its hereditary nature, as a positive test result has implications for the patient and family. Predictive testing is performed in asymptomatic patients, mostly for reproductive reasons. Treatment of Huntington Disease The optimal management of Huntington disease involves a multidisciplinary approach that includes neurology, nurses, physical therapy, speech-language pathology, and dietitians and other healthcare professionals. The goal is to optimize the quality of life based on the changing need of the patient. These consist of combined pharmacologic and lifestyle changes, including behavioral therapy. Symptoms may be worsened by stress, fatigue, and intercurrent disorders (eg, anxiety, digestive disorders, infectious or painful conditions), so these aspects must be assessed and treated alongside the primary symptoms of Huntington disease.[3] In clinical practice, information about symptoms should be obtained from both the patient and caregivers, since patients may have impaired awareness of their condition.[11] Identifying coexisting psychiatric symptoms, comorbid medical conditions, and environmental factors is crucial.[11] Educating caregivers about the nature and presentation of symptoms and methods to modify triggers is also vital.[11] Medication choices should be guided by coexisting symptoms and disease stage, and regular reassessment of drug need and potential for dose reduction is important because of adverse effects that can mimic disease progression.[11] Nonpharmacologic interventions, including behavioral therapies and environmental modifications, should be prioritized for neuropsychiatric symptoms in Huntington disease. Pharmacologic agents may be considered if these measures are insufficient, and consultation with a psychiatrist knowledgeable in Huntington disease is recommended for individuals whose symptoms are resistant to standard pharmacologic therapy.[11] Tetrabenazine and its modified version, deutetrabenazine, are commonly used to treat choreiform movements. Side effects of tetrabenazine can include depression, anxiety, sedation, sleep problems, restlessness, and parkinsonism.[7] Citalopram is a selective serotonin reuptake inhibitor used to manage depression. Modafinil and atomoxetine are used to manage apathy. Tiapride, although unavailable in the United States, is considered a first-line treatment option for chorea outside the United States.[7] Other antipsychotics such as olanzapine, risperidone, and quetiapine are also used to manage chorea. Risperidone may also help with psychomotor restlessness, and olanzapine and quetiapine can have additional benefits like weight gain (which can be desirable in Huntington disease) and mood stabilization. Haloperidol has also shown effectiveness.[7] Medications used to suppress chorea (eg, tetrabenazine and deutetrabenazine and certain antipsychotics) should be used sparingly and mainly for subjectively disabling hyperkinesias, starting at low doses and titrating gradually. They make take 4-6 weeks to show results.[7] The choice of medication depends on the individual patient's symptoms, tolerability, and co-existing conditions.[7] Evidence regarding the treatment of psychiatric symptoms in Huntington disease is limited, with recommendations often based on expert opinion owing to a lack of robust controlled studies.[7,11] Nonpharmacologic interventions such as cognitive-behavioral therapy and psychodynamic therapy are recommended, especially for depression, anxiety, obsessive-compulsive behaviors, and irritability. Behavioral strategies (eg, structured routines and distraction) are important for managing irritability and agitation.[3,11] Depression: Selective serotonin reuptake inhibitors (SSRIs) such as citalopram, fluoxetine, paroxetine, sertraline, and venlafaxine are recommended as pharmacologic options. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. [3,7,11] Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. Anxiety: SSRIs or serotonin-noradrenaline reuptake inhibitors (SNRIs) are first-line treatments, especially when anxiety coexists with depression. [3,11] Mirtazapine is an option in patients with sleep disorders. [11] Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. [3,11] Mirtazapine is an option in patients with sleep disorders. Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. Obsessive-compulsive behaviors/perseverations: For true obsessive-compulsive phenomena, SSRIs are considered first-line treatment. [3] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. [3] Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. [11] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. Irritability and aggression: SSRIs are a first-line treatment. [3] For aggressive behavior, neuroleptics are recommended. [3,7] Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. [3,7] For aggressive behavior, neuroleptics are recommended. Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. Psychosis (hallucinations/delusions): Second-generation neuroleptics (antipsychotics) are the first-line pharmacologic treatment. [3,7,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. [7] Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. [3,7,11] Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. [3,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. Apathy: Personalized cognitive stimulation and structured routines and activities are recommended.[3,7,11] If depression is suspected as a contributor, an SSRI should be tried.[3,11] In patients without depression, activating antidepressants or stimulant drugs (eg, methylphenidate, atomoxetine, modafinil) may be considered.[11] Sedative medications may increase apathy, so their dosage should be monitored or reduced.[3,11] Currently, no pharmacological treatment is specifically recommended for cognitive symptoms in Huntington disease.[3,7] Rehabilitation strategies, including speech therapy, occupational therapy, cognitive and psychomotor therapy, may help transiently improve or stabilize cognitive functions.[3,7] Coping strategies can be useful as an alternative to medication. Certain medications, such as sedative drugs, neuroleptics, and tetrabenazine, can negatively affect memory, executive functions, and attention.[3] Apart from symptomatic treatment, pharmacologic agents have failed to show benefit in clinical trials as disease-modifying agents. The most promising approaches in regard to disease modification are emerging therapies aimed at lowering levels of mHTT by targeting either the DNA or RNA of the mHTT gene.[12] RNA-targeting using antisense oligonucleotides (ASOs) have shown disappointing results in clinical trials. This has shifted significant research focus and toward orally available small molecules that modify HTT mRNA splicing, thereby reducing mHTT protein production. DNA-targeting approaches using gene editing tools like CRISPR/Cas9, while demonstrating success in preclinical models, remain in the early stages of development.[13,14] The patient in this case was diagnosed with Huntington disease with CAG repeat 78. He was started on tetrabenazine for abnormal movements and citalopram for depression. He opted to apply for federal disability. His children are asymptomatic, and the family decided not to investigate until symptoms develop or they are age 18 years.
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a day ago
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