Month: October 2024

Can allopurinol be taken during acute gouty attacks?

Is it safe to continue allopurinol therapy during an acute gout attack, or does it risk worsening the flare?

Acute gout attacks are characterized by painful joint inflammation caused by immune cells attacking urate crystals. While chronic management to lower blood urate levels is crucial for preventing flare-ups, the approach to using urate-lowering therapies such as allopurinol during an acute gout attack continues to evolve. This blog will clarify some of the clinical considerations and evidence surrounding the use of allopurinol during acute gout episodes.

The Dilemma: Traditional Teaching vs. Emerging Evidence. Traditionally, initiating or adjusting allopurinol during an acute attack was discouraged, as altering uric acid levels can exacerbate symptoms. This concept led to a common recommendation of holding off allopurinol until the acute phase subsides. However, recent evidence has challenged this approach, suggesting that allopurinol, if already in use, should be continued during acute attacks to maintain steady uric acid levels and prevent rebound hyperuricaemia.

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Why does fingolimod have cardiac effects?

Fingolimod is prescribed as an immunosuppressant for managing multiple sclerosis, but why should clinicians be particularly cautious about its cardiovascular effects during initial dosing?

Fingolimod, an oral immunomodulatory drug approved for the treatment of multiple sclerosis (MS), has a unique mechanism of action that makes it highly effective in reducing MS relapses. However, like many medications, it comes with a specific set of adverse effects that need careful consideration, particularly its impact on the cardiovascular system. Here’s what you need to know.

How Does Fingolimod Work?
Fingolimod functions as a sphingosine-1-phosphate (S1P) receptor modulator. It sequesters lymphocytes in the lymph nodes, reducing their migration out, and preventing them from crossing into the central nervous system (CNS) where they would normally contribute to the inflammatory damage seen in MS. This modulation of S1P receptors is crucial to its therapeutic effect, but it also leads to unintended cardiovascular effects.

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The Difference Between Mycophenolate Mofetil (MMF) and Mycophenolate Sodium (MPS)

What is the difference between mycophenolate mofetil (MMF) and mycophenolate sodium (MPS)

Understanding the nuances between different formulations of a drug is crucial to ensuring optimal patient care. Mycophenolate mofetil (MMF) and mycophenolate sodium (MPS) are two formulations of the immunosuppressant mycophenolic acid, commonly used to prevent organ rejection in transplant recipients and to manage autoimmune conditions. Despite their similar purposes, there are important differences between them that influence their clinical use.

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The Discovery of Fingolimod: From Nature to the Clinic

Fingolimod is prescribed as an immunosuppressant for managing multiple sclerosis, but is it true that it originates from a parasitic fungus like Cordyceps

Fingolimod was originally derived from myriocin, a compound isolated from a curious source: Isaria sinclairii, a type of parasitic fungus that is related to the well-known Cordyceps species. This fungus, which is prominent in traditional Chinese medicine for its rejuvenating properties, offered a glimpse into something incredible—its bioactive compounds showed a profound impact on immune modulation. Researchers began to understand that these molecules could interact with immune cells, leading to potential therapeutic effects.

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