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Biomedical subjects

Raymond P Abratt

Publications and source records attributed to Raymond P Abratt.

6 recordsLinked to original sources
PubMed2002

Lung toxicity following chest irradiation in patients with lung cancer.

Classical radiation pneumonitis has been described after single dose whole lung irradiation in experimental animals where above a threshold dose of irradiation, there is a sigmoid dose response curve with increasing morbidity and mortality. After clinical fractionated irradiation, however, acute radiation pneumonitis consisting of cough shortness of breath and patchy radiological changes, occurs in <10% of patients, has dyspnoea out of proportion to the volume of lung irradiated and usually resolves completely without long-term effects. There is increasing evidence that this represents a bilateral lymphocytic alveolitis or hypersensitivity pneumonitis and has been termed sporadic pneumonitis. Late radiation toxicity results in pulmonary fibrosis. This is a consequence of repair, which is initiated by tissue injury within the radiation portal. It follows release of chemotactic factors for fibroblasts including transforming growth factor-beta, fibronectin and platelet derived growth factor. Radiation fibrosis is the clinically more significant syndrome for patients. It may result in progressive dyspnoea and mortality in patients. The most predictable change in laboratory lung function tests is a decrease in transfer factor due to damage at the capillary-alveolar level. It also results in decreased lung compliance, which will affect the total lung capacity and the forced vital capacity. The forced expiratory volume in 1 s is less affected, although this seems to depend on the volume of lung irradiated. There is also a decrease in perfusion in the irradiated lung. Radiation fibrosis seems to depend, amongst other factors, on the volume of lung, which is irradiated above a threshold of 20-30 Gy. The morbidity of radiation fibrosis may therefore be minimized by the use of dose volume histogram to minimize the volume of normal lung irradiated in patients at high risk, e.g., patients with who present with poor lung function. The importance of the baseline perfusion in the irradiated areas continues to be studied.

Dose Fractionation, Radiation↗
PubMed2002

Hypofractionated irradiation for non-small cell lung cancer.

Large radiation fractions are an effective way of killing tumour cells but have generally been avoided in curative treatment of patients because of concerns of a disproportionate increase in late normal tissue toxicity. Radiobiological modelling of the effect of radiation on lung tumours and late-reacting normal tissues, which are more sensitive to large radiation fractions, has been undertaken. The biological effect of radiation on tumours is increased as the overall treatment time is shortened but this is not true for late-reacting normal tissue. Sample data are shown in which the relative increases in radiation effect on the tumour and late-reacting normal tissues are similar after hypofractionation. A favourable therapeutic ratio can be achieved because the bulk of normal tissue will receive a lower dose of radiation at a lower dose per fraction than the tumour, especially with current techniques where the volume of normal tissue irradiated can be sharply reduced. The clinical evidence confirms that lung toxicity is volume-dependent. It is the small Stage I and II tumours which are most likely to benefit from hypofractionated regimens, as the volumes to be treated are smaller and they have a lower incidence of distant metastases. Patients with Stage III tumours with favourable prognostic factors are nowadays treated with combined chemotherapy and radiotherapy and so for this group more conservative hypofractionation regimens are being explored. However, more advanced tumours may be treated with hypofractionation to lower total doses to achieve palliation and a modest degree of survival benefit.

Carcinoma, Non-Small-Cell Lung↗