Tag: Rituximab

Up to 85% of the general adult population carries the John Cunningham (JC) virus, which is typically harmless. However, for those on specific immunomodulating drugs, understanding 'What medication can cause PML?' is vital, as these drugs can reactivate the virus, leading to this serious brain disease.

Progressive Multifocal Leukoencephalopathy (PML) is a rare but serious brain infection caused by the reactivation of the John Cunningham (JC) virus [1.10.2]. This article explores a critical question for many patients: **what drugs increase the risk of PML?**

Originally approved for non-Hodgkin's lymphoma, rituximab is increasingly used for autoimmune diseases, but is rituximab considered an immunosuppressant? The answer lies in its targeted B-cell depletion mechanism, which directly impacts a core component of the immune system.

According to sources like Versus Arthritis and Memorial Sloan Kettering Cancer Center, constipation is a reported side effect of rituximab treatment. While not always the primary cause, this medication can contribute to bowel irregularity, sometimes in combination with other concurrent therapies like chemotherapy.

Progressive multifocal leukoencephalopathy (PML) is a devastating and rare viral brain infection that occurs almost exclusively in severely immunosuppressed individuals. Certain biologic medications can significantly increase the risk of this condition by altering immune function, making it crucial for patients and providers to understand **which biologics cause PML** and the associated risk factors.

For some pediatric patients with new-onset nephrotic syndrome, complete remission has been observed within a median time of 24 days following rituximab therapy. The question, 'how long does rituximab take to work for nephrotic syndrome?' has a variable answer that depends on many factors, including the patient's specific condition and disease severity.

While the detectable concentration of a **rituximab infusion stay in your system** for a limited time, its therapeutic effect of B-cell depletion can last for many months after the drug is no longer in the bloodstream. Understanding the half-life and B-cell recovery timeline is crucial for managing treatment expectations and monitoring long-term effects.

The FDA has issued multiple serious, or 'boxed', warnings for rituximab due to significant adverse event reports. The most important safety information includes risks of fatal infusion reactions, progressive multifocal leukoencephalopathy (PML), and hepatitis B virus (HBV) reactivation.

According to the National Institute for Occupational Safety and Health (NIOSH), the monoclonal antibody rituximab does not meet the criteria for a hazardous drug, and it is explicitly not a biohazard because it contains no microorganisms. This distinction is crucial for understanding the appropriate handling and safety protocols for this potent medication.

In clinical studies, rituximab treatment has been shown to cause a rapid and profound depletion of peripheral B-cells within 72 hours. This monoclonal antibody, therefore, is primarily known for its ability to deplete B-cells by targeting a specific protein on their surface.