Post-irradiation fibrosis L59.8

Fibrosis is a common adverse effect of radiotherapy. There are currently no effective treatments to prevent or reverse radiation-induced fibrotic diseases of the various organs. See also Radiodermatitis chronica; see also Cutaneous radiation syndrome.

The severity of radiation fibrosis is influenced by several factors and tends to be more pronounced in older patients, with larger tumors, higher radiation doses, treatment volume, and in patients who have undergone other treatment modalities such as surgery and chemotherapy. Even in patients treated with modern techniques such as intensity modulated radiotherapy (IMRT), the incidence is still 30%. The severity of fibrosis is significantly influenced by individual radiosensitivity and the presence of genetic syndromes such as (rare) ataxia telangiectasia and Marfan syndrome.

Radiation fibrosis is most evident in the skin tissue and can be a long-term consequence of radiation dermatitis . In particular, the severity of acute skin reactions at the end of radiotherapy has been shown to be a prognostic factor for the development of radiation fibrosis (Nevens D et al. 2017). Chronic radiation skin fibrosis is not only a cosmetic burden, but also a predisposing factor for complications due to poor wound healing and rarefied vessels. Fibrosis in the skin can lead to xerosis, dyspigmentation, epidermal atrophy and slow healing of painful ulcers (Bray FN et al. 2016).

A correlation with the later occurrence of radiation fibrosis was demonstrated for the genetic enhancer element of the enzyme DGKA (diacyl-glycerol kinase alpha - see DGKA gene below). Patients whose DGKA enhancer was only weakly occupied with methyl groups proved to be particularly sensitive to fibrosis. "If this gene enhancer is only weakly methylated, certain transcription factors can dock there and the DGKA gene is read more frequently, which ultimately leads to activation of the connective tissue cells."

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