NAXICAM

Indications

• Osteoarthritis
• Rheumatoid arthritis
• Acute pain
• Postoperative pain
• Musculoskeletal disorders

Dosage

Children: Refer to the BNF for Children for specific dosage recommendations for paediatric patients.

Adults: Refer to the BNF for specific dosage recommendations for adults, considering individual patient needs and clinical circumstances.

Mechanism of action

Lornoxicam's anti-inflammatory and analgesic activity is related to its inhibitory action on prostaglandin and thromboxane synthesis through the inhibition of both COX-1 and COX-2. This inhibition leads to a reduction in inflammation, pain, fever, and swelling, mediated by prostaglandins. However, the precise mechanism of lornoxicam has not been fully elucidated.

Pharmacodynamics

Lornoxicam is a potent inhibitor of the cyclooxygenase enzymes (COX-1 and COX-2), which catalyze the formation of prostaglandins and thromboxanes from arachidonic acid. Unlike some other NSAIDs, lornoxicam does not increase leukotriene formation, thus minimizing the risk of adverse events related to the 5-lipoxygenase pathway. Its pharmacodynamic properties allow for effective pain management and reduction of inflammation without significant increases in certain side effects.

Pharmacokinetics

Lornoxicam is absorbed well following oral administration, with peak plasma concentrations typically reached within 2 hours. It has a half-life of approximately 3 to 5 hours, allowing for dosing flexibility. Lornoxicam is metabolized in the liver primarily through conjugation with glucuronic acid. The drug is excreted mainly via the urine, with both unchanged drug and metabolites present in the excreted material.

Adverse effects

• Gastrointestinal ulceration
• Gastrointestinal bleeding
• Nausea
• Vomiting
• Dizziness
• Headache
• Rash
• Renal impairment

Interactions

• Increased risk of gastrointestinal toxicity when used with other NSAIDs or corticosteroids
• May enhance the effects of anticoagulants
• Potential for increased nephrotoxicity when combined with other renal-affecting drugs

Precautions

• Use with caution in patients with a history of peptic ulcer disease
• Monitor renal function in patients with renal impairment
• Caution in patients with cardiovascular disease due to potential fluid retention

Pregnancy

Lornoxicam should be avoided in pregnancy, especially during the third trimester, as it may affect fetal cardiovascular function and prolong gestation.

Breast-feeding

Limited data suggest that lornoxicam is excreted in breast milk; caution is advised when administering to nursing mothers.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Tablets
• Injection

Indications

• Muscle spasms
• Muscle stiffness
• Spasticity associated with neurological conditions

Dosage

Children: Refer to established clinical guidelines for specific dosing recommendations.

Adults: Refer to established clinical guidelines for specific dosing recommendations.

Mechanism of action

Thiocochicoside acts on the central nervous system, particularly by influencing the GABAergic system. It enhances the inhibitory neurotransmission in the spinal cord, leading to muscle relaxation. The precise pathways involve modulation of GABA receptors which help in reducing motor neuron excitability, thus decreasing muscle tone and spasms.

Pharmacodynamics

Thiocochicoside demonstrates muscle relaxant effects through central mechanisms. Its impact on the GABA receptor system results in decreased muscle tone, inhibition of reflexes, and relief from muscle spasms. The therapeutic effects are typically observed with a rapid onset of action, providing symptomatic relief in conditions characterized by muscle stiffness and spasms.

Pharmacokinetics

Thiocochicoside is well-absorbed following oral administration, with peak plasma concentrations achieved within a few hours. It is extensively metabolized in the liver and has an elimination half-life that varies based on individual patient factors. The drug is primarily excreted via the kidneys, and certain pharmacokinetic parameters may be influenced by hepatic and renal function.

Contra-indications

• Hypersensitivity to thiocochicoside or any of its components
• Severe renal impairment

Adverse effects

• Drowsiness
• Dizziness
• Gastrointestinal disturbances (nausea, vomiting)
• Allergic reactions (skin rash, itching)
• Hypotension

Interactions

• CNS depressants (e.g., alcohol, benzodiazepines) may enhance sedative effects
• Antihypertensive agents may have additive effects leading to increased hypotension

Precautions

• Use with caution in patients with a history of drug abuse
• Caution is advised in patients with hepatic impairment
• Monitor for sedation in patients with respiratory conditions

Pregnancy

There is limited data on the safety of thiocochicoside in pregnancy. It should be used only if clearly needed and prescribed by a healthcare professional.

Breast-feeding

Thiocochicoside is excreted in breast milk. Caution should be exercised when administering to breastfeeding women.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Oral tablets
• Injectable solutions

Mechanism of action

Like other NSAIDS, lornoxicam's anti-inflammatory and analgesic activity is related to its inhibitory action on prostaglandin and thromboxane synthesis through the inhibition of both COX-1 and COX-2. This leads to the reduction of inflammation, pain, fever, and swelling, which are mediated by prostaglandins. However, the exact mechanism of lornoxicam, like that of the other NSAIDs, has not been fully determined.

Pharmacodynamics

Lornoxicam is a non-steroidal anti-inflammatory drug (NSAID) that belongs to the oxicam class. As with other NSAIDS, lornoxicam is a potent inhibitor of the cyclooxgenase enzymes, which are responsible for catalyzing the formation of prostaglandins (act as messenger molecules in the process of inflammation) and thromboxane from arachidonic acid. Unlike some NSAIDS, lornoxicam's inhibition of cyclooxygenase does not lead to an increase in leukotriene formation, meaning that arachidonic acid is not moved to the 5-lipoxygenase cascade, resulting in the minimization of the risk of adverse events.