Traumeel
Traumeel is an effective medication for acute injuries and inflammation of the musculoskeletal system, avoiding at the same time the notoriously serious side-effects of common anti-inflammatory therapies.
Traumeel has been used to aid recovery from sprains, strains, bruises, nerve pain, swelling, and post-surgical pain.
For several years, Heel, Traumeel’s internationally known manufacturer, has been working with experts and research institutes to conduct studies to confirm the efficacy of its combination preparations.
Positive results have shown that Traumeel is indeed effective and appropriate for use in cases of epicondylitis, tendinitis/tendinosis, etc.
Furthermore, several studies have shown that Traumeel’s inflammation-regulating effects are due to direct impact on immune cells.
The inflammation process is really a complex cascade of different steps. Traumeel does not just stop pain but it acts on the first stages of the inflammation cascade and thus optimizes the whole process towards recovery. Contrarily, NSAIDS block the cascade at one of its essential steps at the end which results masking the injury and pain. The blockade of this central pathway is also the reason for the common side effects of NSAIDs.
As with many other commonly used therapeutic agents, the exact mechanism of action of Traumeel is not fully understood. However, the product’s ingredients appear to modulate various cellular and biochemical pathways.
Placebo-controlled studies, drug monitoring studies, and in vitro experimental models (including the carragenean-induced edema test and the adjuvant arthritis test) have all demonstrated the inflammation regulating, anti-edematous and anti-exudative effects of Traumeel 1 2 3 4 5 6. Various in vitro and in vivo studies offer a possible mechanism for Traumeel’s inflammation regulating effects as observed in clinical practice.
In resting as well as activated immune cells, Traumeel inhibits pro-inflammatory mediators such as IL-1β, TNF-α and IL-8 7.
The ingredients of Traumeel are non-cytotoxic to granulocytes, lymphocytes, platelets, and endothelial cells, indicating that the defensive functions of these cells are preserved during treatment with Traumeel 3. Components of Traumeel raise levels of the anti-inflammatory cytokine TGF-β, indicating that the “immunological bystander reaction†may play a role in the medication’s inflammation regulating effect 8.
Traumeel differs in its mechanism of action from NSAIDs, such as Diclofenac, COX-2 inhibitors and steroids.
References
1 Böhmer D et al. Biological Therapy 1992; X(4): 290-300.
2 Zenner S et al. Biomedical Therapy 1997; XV(1): 22-26.
3 Conforti A et al. Biomedical Therapy 1997; XV(1): 28-31.
4 Zell J et al. Biological Therapy 1989; VII(1): 1-6.
5 Thiel W. Biological Therapy 1994; XII(4): 242-248.
6 Zenner S et al. Biological Therapy 1992; X(4): 301-310.
7 Porozov S et al. Clin Dev Immunol. 2004; 11(2): 143-149.
8 Heine H. Biologische Medizin 1998; 12-14.
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