Tuberculosis Associated with Infliximab, a Tumor Necrosis Factor –Neutralizing Agent
Joseph Keane, M.D., Sharon Gershon, Pharm.D., Robert P. Wise, M.D., M.P.H., Elizabeth Mirabile-Levens, M.D., John Kasznica, M.D., William D. Schwieterman, M.D., Jeffrey N. Siegel, M.D., and M. Miles Braun, M.D., M.P.H.
Background Infliximab is a humanized antibody against tumornecrosis factor (TNF-) that is used in the treatment of Crohn'sdisease and rheumatoid arthritis. Approximately 147,000 patientsthroughout the world have received infliximab. Excess TNF- inassociation with tuberculosis may cause weight loss and nightsweats, yet in animal models it has a protective role in thehost response to tuberculosis. There is no direct evidence ofa protective role of TNF- in patients with tuberculosis.
Methods We analyzed all reports of tuberculosis after infliximabtherapy that had been received as of May 29, 2001, through theMedWatch spontaneous reporting system of the Food and Drug Administration.
Results There were 70 reported cases of tuberculosis after treatmentwith infliximab for a median of 12 weeks. In 48 patients, tuberculosisdeveloped after three or fewer infusions. Forty of the patientshad extrapulmonary disease (17 had disseminated disease, 11lymph-node disease, 4 peritoneal disease, 2 pleural disease,and 1 each meningeal, enteric, paravertebral, bone, genital,and bladder disease). The diagnosis was confirmed by a biopsyin 33 patients. Of the 70 reports, 64 were from countries witha low incidence of tuberculosis. The reported frequency of tuberculosisin association with infliximab therapy was much higher thanthe reported frequency of other opportunistic infections associatedwith this drug. In addition, the rate of reported cases of tuberculosisamong patients treated with infliximab was higher than the availablebackground rates.
Conclusions Active tuberculosis may develop soon after the initiationof treatment with infliximab. Before prescribing the drug, physiciansshould screen patients for latent tuberculosis infection ordisease.
The role of tumor necrosis factor (TNF-) in the human immuneresponse to tuberculosis remains unclear. This cytokine maybe responsible for some of the clinical manifestations of tuberculousdisease, including weight loss, night sweats, and tissue destruction.1,2Yet in animal models, TNF- plays a central part in the hostresponse against tuberculosis,3,4 including granuloma formationand containment of disease.5,6 Antibodies against TNF- causea reactivation of tuberculosis in a mouse model of latent infection.7Unlike interferon-8 and interleukin-12,9 TNF- has not beenshown to have a protective role in the human immune responseto mycobacteria.
Infliximab (Remicade) is a humanized monoclonal antibody againstTNF- that is approved in the United States and elsewhere forthe treatment of rheumatoid arthritis and Crohn's disease.10,11Infusions of infliximab can be administered in a single dose,a monthly regimen, or on day 0, day 14, day 42, and then every8 weeks. The half-life of infliximab is 10 days,12 and its biologiceffect persists for up to 2 months. The Food and Drug Administration(FDA) approved infliximab in 1998 for use in patients who donot have a response to other antiinflammatory agents.13 Approximately147,000 people throughout the world have received the drug;in the United States, 45,000 patients have received it for rheumatoidarthritis and 76,000 for Crohn's disease (Table 1). One caseof tuberculosis after infliximab therapy was reported in a clinicaltrial.14 We evaluated the clinical pattern of disease and theinterval between the initiation of infliximab therapy and theonset of disease in 70 reported cases of tuberculosis in patientstreated with infliximab. We compared the rate of reported tuberculosisin this group with available data on background incidence rates.The association of this disease in humans with decreased TNF-activity suggests that the cytokine has a key role in the controlof latent tuberculosis.
Table 1. Cumulative Numbers of Patients Treated with Infliximab or Etanercept, According to Location and Indication.
Methods
The FDA monitors the safety of newly licensed products, suchas infliximab. Data from the FDA's Adverse Event Reporting System(AERS) were reviewed for reports of tuberculosis with infliximabfrom its licensure in 1998 through May 29, 2001. AERS receivesspontaneous reports of suspected adverse drug reactions throughthe MedWatch program15 and from pharmaceutical manufacturers.The vast majority of reports are submitted by health care providers,who are sometimes contacted for additional information. Reportsto the AERS may involve any time interval between the administrationof the drug and the suspected reaction. Further details areavailable at http://www.fda.gov/cder/aers/. The current collaborativestudy was undertaken after two of us treated the index patient,in whom tuberculosis developed after treatment with infliximabfor Crohn's disease.
Patients were included in the study if during or after treatmentwith infliximab, they had received a diagnosis of tuberculosison the basis of clinical, radiologic, and laboratory findings.We sought evidence in each case report of preexisting latentinfection with Mycobacterium tuberculosis (i.e., a prior positivetuberculin skin test). Lung-tissue samples from our index patientwere compared with archival lung tissue from a patient withtuberculosis who had not received an anti–TNF- agent.Tissue samples were stained with hematoxylin and eosin, andthe terminal deoxynucleotidyl transferase–uridine triphosphatenicked-end labeling method (Apotag kit, Intergen, New York)was used to identify apoptotic cells according to the manufacturer'sprotocol.
Results
Seventy patients were reported to have tuberculosis during orafter infliximab therapy, including the index patient. Theirages ranged from 18 to 83 years (median, 57) (Table 2). Forty-fiveof the patients were women. Forty-seven patients were takingthe drug for rheumatoid arthritis, 18 for Crohn's disease, and5 for other types of arthritis. The median interval from thestart of treatment with infliximab until the development oftuberculosis was 12 weeks (range, 1 to 52). The distributionof cases according to the interval between the initiation oftreatment and the development of tuberculosis is shown in Figure 1.
Figure 1. Time from the Initiation of Infliximab Therapy to the Diagnosis of Tuberculosis.
Data were available for 57 patients, most of whom had received monthly infusions of infliximab.
Fifty-five patients were reported to have received one or moreother immunosuppressive medications, including corticosteroids(45 patients), methotrexate (35), azathioprine (6), and cyclosporine(1). Five patients were using antiinflammatory agents, suchas mesalamine and indomethacin, before tuberculosis developed.Of 11 corticosteroid-treated patients in the United States forwhom data were available, 9 were taking doses of prednisonethat did not exceed 15 mg per day. The doses of methotrexateranged from 10 to 20 mg per week. More than half of the patients(56 percent) had extrapulmonary tuberculosis, and approximatelyone quarter had disseminated tuberculosis (Table 2). Other manifestationsof extrapulmonary tuberculosis included lymph-node disease (in11 patients), peritoneal disease (in 4), pleural disease (in2), meningeal disease (in 1), enteric disease (in 1), paravertebraldisease (in 1), bone disease (in 1), genital disease (in 1),and bladder disease (in 1). Thirty-three of the 70 patientsunderwent a biopsy to confirm the diagnosis of tuberculosis;biopsy specimens were from a lung (in 12 patients), a lymphnode (in 11), the peritoneum (in 3), enteric tissue (in 2),the pleura (in 1), bone marrow (in 1), the liver (in 1), a paravertebralmass (in 1), and the bladder (in 1).
Two reports noted possible recent exposure to tuberculosis.Eight patients had a history of tuberculosis infection or disease.Most of the 70 reports (91 percent) were from countries witha low incidence of tuberculosis (less than 20 cases per 100,000population per year).16 On the basis of reports to the AERS,the estimated rate of tuberculosis among patients with rheumatoidarthritis in the United States who have received infliximabtherapy within the previous year is 24.4 cases per 100,000.The background rate of tuberculosis in patients with rheumatoidarthritis in the United States was assessed in a recent studywith active follow-up, which found one case of tuberculosisin 10,782 geographically dispersed patients with rheumatoidarthritis who were followed prospectively for approximately18 months.17 On the basis of these data, the background rateof tuberculosis in patients with rheumatoid arthritis in theUnited States is 6.2 cases per 100,000 per year (95 percentconfidence interval, 0.6 to 34.0). Background rates of tuberculosisamong patients with Crohn's disease and among patients withrheumatoid arthritis in Europe are not available for comparisonwith the case rates associated with infliximab therapy. Fiveof the 17 patients in the United States who had tuberculosis(29 percent) were immigrants, but all 5 had lived in the UnitedStates for 10 years or longer. Of the approximately 18,000 casesof tuberculosis reported in the United States in 1999, about44 percent were in foreign-born persons.18
Patients received antituberculosis medication, and infliximabtreatment was stopped after the diagnosis of tuberculosis hadbeen made. Twelve patients subsequently died, and at least fourof these deaths appear to have been directly related to tuberculosis.Other serious opportunistic infections have been reported inpatients treated with infliximab, but the frequency of tuberculosisexceeds that of other infections. Twelve patients treated withinfliximab had listeriosis, nine had Pneumocystis carinii pneumonia,seven had histoplasmosis, six had aspergillosis, and seven hadsevere candida infections. No coinfection with the human immunodeficiencyvirus (HIV) has been reported.
The index patient was a 68-year-old man with Crohn's diseasein whom pulmonary tuberculosis developed seven weeks after hehad received a single dose of infliximab. Shortness of breathwas the first symptom. A thoracic computed tomographic (CT)study suggested the presence of new pulmonary fibrosis (a previousthoracic CT study had shown no abnormalities). Histopathologicalexamination of a specimen from an open-lung biopsy showed idiopathicpulmonary fibrosis with lymphocyte infiltration; no granulomaswere present (Figure 2C). Sputum cultures subsequently grewM. tuberculosis on three separate occasions, although acid-fastbacilli were not seen in the biopsy specimen. TNF-–mediatedapoptosis has been shown to occur after infection with M. tuberculosis,19and extensive macrophage apoptosis is a feature of the normalgranulomatous response to tuberculosis (Figure 2A and Figure 2B).19,20,21,22 There was little apoptosis in the lung specimenfrom the index patient (Figure 2D). Caseating granulomas weredescribed in the biopsy specimens from some of the other patients.
Figure 2. Photomicrographs of Lung Specimens from a Patient with Tuberculosis Who Did Not Receive Infliximab (Panels A and B) and the Index Patient with Tuberculosis Who Did Receive Infliximab (Panels C and D).
The specimen from the patient who did not receive infliximab shows well-formed granulomas with negligible overt necrosis (Panel A; hematoxylin and eosin, x100). A photomicrograph of a granuloma at a higher magnification shows moderate-to-marked apoptosis, as demonstrated by the terminal deoxynucleotidyl transferase–uridine triphosphate nicked-end labeling (TUNEL) reaction. Cells stained brown are positive for apoptosis, and cells with blue nuclei, which are stained with the methyl-green counterstain, are normal (Panel B, x400). The specimen of lung parenchyma from the patient who received infliximab shows prominent interstitial fibrosis and lymphoid inflammation, without granulomas (Panel C, hematoxylin and eosin, x100). TUNEL analysis shows minimal apoptosis (Panel D, x400).
Discussion
Our data suggest an association between treatment with infliximaband the development of tuberculosis. Although passive surveillancedata are often insufficient to prove a causal relation betweenan adverse event and a drug, we believe this association isnot coincidental, because of the large number of reports oftuberculosis in close temporal association with the initiationof treatment and the increased rate of tuberculosis among patientstreated with infliximab, as compared with available data onbackground rates. In addition, data from in vitro investigations,23,24as well as a mouse tuberculosis model,3,4,5,7,25 link susceptibilityto tuberculosis with decreased TNF- activity.
We reviewed the clinical and laboratory findings in 70 casesof tuberculosis that developed after the initiation of treatmentwith infliximab. The pattern of tuberculous disease was unusual.The majority of the patients (56 percent) had extrapulmonarytuberculosis, and 24 percent had disseminated disease —forms of tuberculosis that are associated with marked immunosuppression.In contrast, among cases of tuberculosis that are not associatedwith HIV infection, approximately 18 percent are manifestedas extrapulmonary disease, and disseminated disease accountsfor less than 2 percent.26 The unusual manifestations of tuberculosisin this group of 70 cases may have made the diagnosis uncertain(as reflected by the large number of biopsies performed to establishthe diagnosis); delays in the diagnosis may have contributedto morbidity and mortality. The available data suggest thatthe patients who survived recovered from their infections afterthe withdrawal of infliximab and the administration of appropriatechemotherapy for tuberculosis.
We do not have complete information about the status of thesepatients with respect to tuberculous infection before they receivedinfliximab, but it is likely that most patients had reactivationdisease, in view of their age (median, 57 years), the smallnumber with reported recent exposure to tuberculosis, and thelow incidence of tuberculosis in the countries from which thereports were received.27,28 That only eight reports noted ahistory of tuberculosis infection or disease is not surprising,since medical information from the remote past is frequentlylacking, particularly in passive surveillance reports. Giventhe key role of TNF- in the innate immune response to tuberculosis,patients receiving treatment with infliximab are probably alsosusceptible to disease after primary infection and exogenousreinfection with M. tuberculosis.
Foreign-born persons were not overrepresented in the U.S. reports,and all such persons had been living in the United States formore than 10 years. Persons who move to the United States havea high incidence of tuberculosis for the first five years.29With time, however, the incidence declines and approaches thatin the general population. It is also not surprising that mostof the reports came from countries with a low incidence of tuberculosis,because infliximab is an expensive treatment12 that is rarelyavailable in poor countries, where tuberculosis is most prevalent.
The recent use of other immunosuppressive drugs and systemicillness in infliximab-treated patients may increase the riskof a variety of opportunistic infections, including fungal infection,30but tuberculosis was reported much more frequently than otheropportunistic infections. Tuberculosis is not associated withthe use of prednisone at doses of 15 mg or less,29 and the cytotoxicagents and low doses of corticosteroids used in this group ofpatients have not been associated with tuberculosis in patientswith rheumatic diseases31 or asthma.32,33
Another agent that neutralizes TNF- is etanercept, which hasbeen used, often along with other immunosuppressive medications,in the treatment of approximately 102,000 patients with rheumatoidarthritis throughout the world (Table 1). Etanercept is a fusionprotein that binds free TNF- using the extracellular or solubleportion of tumor necrosis factor receptor 2 (TNFR2) coupledwith an Fc moiety.34 Studies in animals have demonstrated increasedsusceptibility to tuberculosis in association with transgenicexpression of the soluble portion of tumor necrosis factor receptor1 (TNFR1).35 Although the numbers of patients who have beenexposed to etanercept and infliximab are similar, only 9 casesof tuberculosis in patients treated with etanercept have beenreported to the FDA, as compared with 70 cases in patients treatedwith infliximab. This difference may reflect the different waysin which the two agents neutralize TNF-.25 The proportion ofpatients treated with infliximab rather than etanercept is largerin Europe than in other countries (Table 1), and the majorityof the reports are from Europe. These and other factors mayalso explain the difference in the number of reported casesof tuberculosis associated with the two agents.
Since there is underreporting with all passive surveillancesystems, the AERS reports probably represent only a subgroupof incident cases.36 Nonetheless, the rate of reported casesin the United States among infliximab-treated patients withrheumatoid arthritis is substantially higher than the estimatedbackground rate for patients with rheumatoid arthritis in theUnited States. In a randomized, double-blind, placebo-controlledtrial of infliximab treatment in patients with rheumatoid arthritisin Europe, there were no cases of tuberculosis among the 88patients who received placebo and methotrexate.14 Among the340 patients treated with infliximab and methotrexate, disseminatedtuberculosis was diagnosed in 1 patient after a protracted illness;the patient was treated for tuberculosis but died. Adalimumab,an investigational antibody against TNF- that is similar toinfliximab, has been associated with tuberculosis in clinicaltrials involving patients with rheumatoid arthritis.37 The associationwas seen with high doses of adalimumab but not with lower doses,suggesting that there is a dose–response effect. Takentogether, these data suggest that the risk of tuberculosis ishigher among infliximab-treated patients with rheumatoid arthritisthan among patients with rheumatoid arthritis who do not receivethis agent. Infliximab currently leads all other drugs and biologicproducts with respect to the number of cases of tuberculosisreported to the AERS. The association between the use of infliximaband reactivation tuberculosis is strong but not proven. Themanufacturer of the drug has recognized the concern about thisassociation, and the product's package insert now includes awarning about the risk of tuberculosis and the need to screenpatients for tuberculosis before treatment with infliximab isinitiated.
The pattern of tuberculosis observed after anti–TNF- treatmentmay be due to the failure of granulomas to compartmentalizeviable M. tuberculosis bacilli, but the underlying mechanismis unclear. TNF- is an inflammatory cytokine that can inducea broad spectrum of biologic effects mediated by TNFR1 and TNFR2.38Signals from these receptors mediate apoptosis and the activationof nuclear factor-B, which can influence the production of cytokinesand the expression of adhesion molecules.39 Mohan et al. notedthat in a mouse model of latent tuberculosis, reactivation ofdisease followed the neutralization of TNF- with TNF- antibodies.7They also reported markedly increased infiltration of the lungwith immune cells — an increase that was disproportionateto the bacillary load. This finding is consistent with the extensiveinfiltration in the lung specimen from our index patient, althoughacid-fast bacilli were not seen in the specimen. One mechanismby which TNF- is thought to mediate a successful host responseto mycobacteria is the orderly induction of macrophage apoptosisafter bacillary infection.24,40 Macrophage apoptosis is a prominentfeature of tuberculosis-associated granulomas19,20,21,22 (Figure 2B)and may help maintain their integrity. Yet apoptosis wasrare in the pathological specimen from our index patient (Figure 2D).There probably are many mechanisms that lead to apoptosisin tuberculosis, and infliximab may affect one or more of thesemechanisms. Taken together, these observations suggest thatan interruption of TNF- activity may allow an aberrant immuneresponse to a small number of tubercle bacilli. This abnormalresponse may have important pathologic effects.
Our findings have important clinical implications. Infliximabis an effective treatment for two debilitating diseases forwhich other treatments are frequently inadequate.10,11 Physiciansshould be aware of the increased risk of reactivation of tuberculosisamong patients who are receiving infliximab and other immunosuppressiveagents and, in particular, of the unusual clinical manifestationsof the disease. When active tuberculosis is suspected, treatmentwith infliximab should be stopped until the diagnosis has beenruled out or the infection has been treated with antituberculosisagents. Before treatment with infliximab is initiated, everyeffort should be made to determine whether the patient has latenttuberculosis infection. Since tuberculin tests may have falsenegative results in systemically ill or immunosuppressed patients,a detailed assessment of the risk of tuberculosis should beperformed in every case. In our opinion, patients with latentinfection should be given prophylactic treatment to preventactive disease before infliximab is administered. Physiciansprescribing infliximab should advise patients to seek medicalattention if they have symptoms suggestive of tuberculosis whiletaking the drug.
Supported by grants to Dr. Keane from the National Heart, Lung,and Blood Institute (HL-03964), the Massachusetts Thoracic Society,and the American Lung Association of Massachusetts.
We are indebted to Drs. Hardy Kornfeld, John Bernardo, SusanEllenberg, Jay Siegel, and Robert Ball for their careful reviewof the manuscript and constructive comments; and to Dr. ManetteNiu for her review of the early reports of tuberculosis andher review of the manuscript.
Source Information
From the Pulmonary Center, Department of Medicine (J. Keane, E.M.-L.), and the Pathology Department (J. Kasznica), Boston University School of Medicine, Boston; and the Center for Biologics Evaluation and Research, Office of Biostatistics and Epidemiology, Division of Epidemiology (S.G., R.P.W., M.M.B.), and Office of Therapeutics Research and Review (W.D.S., J.N.S.), Food and Drug Administration, Rockville, Md.
Address reprint requests to Dr. Keane at the Boston University School of Medicine, Pulmonary Ctr., 80 E. Concord St., R-304, Boston, MA 02118, or at jkeane{at}lung.bumc.bu.edu.
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–Neutralizing Agent
8 and interleukin-12,9 TNF-
B, which can influence the production of cytokines and the expression of adhesion molecules.39 Mohan et al. noted that in a mouse model of latent tuberculosis, reactivation of disease followed the neutralization of TNF-
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