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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...
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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...
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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...
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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Video Experimental Relacionado

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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
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Cladribina para la esclerosis múltiple

Maria Grazia Celani1, Massimiliano Orso2, Marta Melis3

  • 1Dpt of Neurophysiopathology, Perugia General Hospital, Perugia, Italy.

The Cochrane database of systematic reviews
|January 9, 2026
PubMed
Resumen

La cladribina probablemente reduce las recaídas y puede disminuir las lesiones por resonancia magnética en la esclerosis múltiple (EM), pero su efecto sobre la progresión de la discapacidad es incierto. Se necesita más investigación para confirmar los beneficios y la seguridad.

Conclusiones:

  • La cladribina, un tratamiento oral para la EM, probablemente reduce las recaídas y puede disminuir las lesiones por resonancia magnética, pero muestra efectos inciertos sobre la progresión de la discapacidad.
  • Los datos a largo plazo sugieren un potencial para aumentar la Ausencia de Evidencia de Actividad de la Enfermedad (NEDA) a los cuatro años.
  • Se necesitan más ensayos de alta calidad y registros para fortalecer la base de evidencia de los beneficios y el perfil de seguridad de la cladribina.
Palabras clave:
Esclerosis múltipleCladribinaTratamientoRecaídasLesiones por resonancia magnéticaProgresión de la discapacidadSeguridadRevisión sistemáticaEnsayos controlados aleatoriosAgentes inmunosupresores

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