KRF Clinical Practice Guidelines in Keloid Disorder (KRF Guidelines®) Treatment Strategy Version 1.2019


This Guideline reviews the overall strategy for treating keloid patients. Readers are advised to consult with site-specific KRF Guidelines that focus on the treatment of particular types of keloids.

It has long been known that successful treatment of a disease is possible only when we understand the underlying pathophysiology. Our current understanding of keloid disorder (KD) is that of a genetic disorder of the wound healing mechanism(s) of the skin, with a highly variable genotype and a very diverse phenotype.

The wound healing defect that leads to the formation of keloid lesions, although not fully understood, perhaps involves the negative feedback loops and signaling pathways that exert control over the wound healing response. Under normal circumstances, once a wound is adequately healed, the inflammatory response, fibroblast proliferation, and collagen production will all regress to their baseline, preinjury status. It is hypothesized that the regression of all normal wound healing responses is under the control of several negative cytokine signaling and feedback mechanisms. Defects in these signaling processes will result in the continuation of the wound healing reaction, excess fibroblast proliferation, and excess collagen deposition, all of which are seen in keloid tissue. This concept is of utmost importance as it can provide the direction for the proper management of keloid patients.

Some de-novo skin pathologies, for instance basal cell carcinoma, can be successfully treated with surgery. However, post-operative recurrence is observed in almost 100% of patients undergoing keloid removal surgery, hence adjuvant ILT or radiation therapy are incorporated to reduce the risk of recurrence.

The core question to ask here is, “Why is there such a high rate of recurrences after keloid removal surgery?” The answer is that keloid removal surgery starts with, and imposes, a totally new wound and a new injury to the skin, thereby triggering the same keloidal wound healing response that produced the original keloid. Perhaps, this is the only medical condition that is triggered, and even made worse, by surgical treatment. It is in this setting that the millennia-old concept of “Primum non nocere – first, do no harm” applies most.

Furthermore, in a situation in which the peak age of onset is in the late teens, one must be mindful of potential harms and side effects of treatment. Therefore, before we expose a large number of young and otherwise healthy individuals to treatments that can be potentially harmful, we need to better understand and to be fully cognizant of all potential short- and long-term side effects of the treatments we are recommending and using.

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