Description

Diclofenac Potassium is a synthetic nonsteroidal anti-inflammatory drug (NSAID) and a derivative of phenylacetic acid. It is the potassium salt form of diclofenac. The key difference between diclofenac potassium and diclofenac sodium lies in the salt form’s effect on absorption. The potassium salt is more soluble in water, which allows for faster absorption from the gastrointestinal tract and a quicker onset of action.

Indications

Due to its rapid absorption, diclofenac potassium is primarily indicated for the management of acute and painful conditions where a fast onset of pain relief is desired. Its key indications include:

• Mild to Moderate Acute Pain: Such as that following minor surgeries or dental procedures.

• Primary Dysmenorrhea: For the relief of menstrual cramps and pain.

• Migraine Headaches: For the acute treatment of migraine attacks.

• Fever: It can be used as an antipyretic (fever reducer).

Mechanism of Action

The mechanism of action of diclofenac potassium is based on its ability to inhibit the synthesis of prostaglandins, which are key mediators of inflammation, pain, and fever. This mechanism is identical to that of diclofenac sodium.

1. Inhibition of Cyclooxygenase (COX) Enzymes: Diclofenac works by inhibiting the activity of two key enzymes: cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). These enzymes are responsible for converting arachidonic acid into prostaglandins.

2. Blocking Prostaglandin Synthesis:
   • The inhibition of COX-2 reduces the production of prostaglandins that are responsible for inflammation, pain, and fever. This is the source of the drug’s therapeutic effects.
   • The inhibition of COX-1 reduces the production of prostaglandins involved in normal physiological functions, such as protecting the stomach lining and promoting platelet aggregation. This inhibition is the cause of some of the drug’s side effects, such as gastrointestinal irritation.

In summary, diclofenac potassium is a non-selective NSAID that provides its therapeutic effects by blocking the COX-1 and COX-2 enzymes. Its primary clinical advantage over the sodium salt is its faster absorption and quicker onset of action, making it particularly suitable for the management of acute pain.