Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...

Inflammatory Bowel Disease IV: Pharmacological Management

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...

Inflammatory Bowel Disease I: Ulcerative Colitis

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...

Inflammatory Bowel Disease II: Crohn's Disease

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by transmural...

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Clinical standards for the management of adverse effects during treatment for TB.

The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease·2023

Same author

Salt-The Forgotten Renal Risk Factor: Sodium Intake Affects Urinary Albumin Excretion Especially in Overweight Subjects. J Intern Med 256: 324-330, 2004.

Journal of the American Society of Nephrology : JASN·2023

Same author

Clinical standards for the dosing and management of TB drugs.

The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease·2022

Same author

Progressive kidney failure in chronic myelomonocytic leukaemia: don't forget lysozyme damage.

The Netherlands journal of medicine·2018

Same author

Pharmacokinetics of 2,000 Milligram Ertapenem in Tuberculosis Patients.

Antimicrobial agents and chemotherapy·2018

Same author

Pharmacokinetic Modeling and Limited Sampling Strategies Based on Healthy Volunteers for Monitoring of Ertapenem in Patients with Multidrug-Resistant Tuberculosis.

Antimicrobial agents and chemotherapy·2017

Search research articles

Related Experiment Video

Updated: Jul 7, 2026

Fecal Microbiota Transplantation via Colonoscopy for Recurrent C. difficile Infection

Fecal Microbiota Transplantation via Colonoscopy for Recurrent C. difficile Infection

Published on: December 8, 2014

Tuberculous peritonitis during infliximab therapy.

J C Verhave¹, R van Altena, M J H Wijnands

¹Department of Internal Medicine and Rheumatology, TweeSteden Hospital, Tilburg, the Netherlands. j_c_verhave@yahoo.com

The Netherlands Journal of Medicine

|February 23, 2008

Summary

Anti-TNF therapy, like infliximab, can cause tuberculosis reactivation. Tuberculous peritonitis is a difficult-to-diagnose extrapulmonary form requiring prompt treatment and screening before therapy.

Related Experiment Videos

Last Updated: Jul 7, 2026

Fecal Microbiota Transplantation via Colonoscopy for Recurrent C. difficile Infection

Fecal Microbiota Transplantation via Colonoscopy for Recurrent C. difficile Infection

Published on: December 8, 2014

Area of Science:

Immunology
Infectious Diseases
Rheumatology

Background:

Anti-tumor necrosis factor (anti-TNF) therapies, including infliximab, are effective for autoimmune diseases like rheumatoid arthritis.
However, these treatments carry a risk of opportunistic infections, notably tuberculosis (TB).
Extrapulmonary TB, particularly tuberculous peritonitis, presents diagnostic challenges during anti-TNF therapy.

Observation:

Two rheumatoid arthritis patients developed tuberculous peritonitis after infliximab treatment.
Clinical presentation of tuberculous peritonitis was nonspecific, complicating early diagnosis.
Mycobacterium tuberculosis was difficult to detect in ascites fluid samples.

Findings:

Infliximab therapy was associated with the development of tuberculous peritonitis in these cases.
Nonspecific symptoms and low bacterial load in ascites hinder rapid diagnosis of TB peritonitis.
Early initiation of tuberculostatic therapy is crucial upon clinical suspicion.

Implications:

Thorough screening for latent or active tuberculosis is essential before initiating anti-TNF therapy.
Increased vigilance for extrapulmonary TB is required in patients on anti-TNF agents.
Prompt diagnosis and treatment of TB peritonitis are critical to prevent severe outcomes.