Radiation Pathology and the Clinical Response of Lung and Esophagus1

Phillips, T.L.; Margolis, Lawrence W.

doi:10.1159/000392812

Cited by 103 publications

(23 citation statements)

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“…Detailed literature data on oesophageal radiosensitivity are scarce. In mice, acute single LD 50 values for this endpoint of 25-32 Gy and higher have been reported for sparsely ionising radiation [17,18,19]. After irradiation with 10 fractions, the acute LD 50 increased to 57.5-71 Gy [19,20].…”

Section: Discussionmentioning

confidence: 82%

Response of pig lung to irradiation with accelerated 12 C-ions

Dörr

Alheit

Appold

et al. 1999

Radiation and Environmental Biophysics

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The response of pig lungs to irradiation with 12C-ions was assessed in two experiments to validate the procedures for heavy ion therapy planning at the Gesellschaft für Schwerionenforschung (GSI) and to explore their range of applicability. In both experiments, the target volume (spread-out Bragg peak, SOBP) was planned to be a 4 cm long cylinder with a diameter of 4 cm. Doses in the SOBP were prescribed to be equivalent to 5x4 Gy, 5x5.5 Gy and 5x7 Gy of x-rays in the first experiment, and to 5 fractions of 7 Gy and 9 Gy in the second experiment. The lung response in the first experiment was less than expected on the basis of earlier experiments with photons. Pneumonitis reaction and chronic fibrotic changes were observed outside the prescribed high-dose region. In the second experiment, the effects were more pronounced than had been expected on the basis of the first experiment. Changes were most intense in the high-dose region, but were also seen throughout the lung along the beam channel. Moreover, significant skin reactions were observed at the beam entrance site in all animals and - less pronounced - at the beam exit site in 3 of the 6 animals. In conclusion, the complex irradiation geometry of the pig lung, the changes of body weight between the two experiments, and insufficient accounting for a change in the relative biological effectiveness (RBE) computation led to substantial deviations of the observed reactions from expectations, the reasons for which could be identified in a subsequent analysis. The less pronounced lung reaction in the first experiment was due to an overestimation of RBE in a preliminary version of the algorithm for its determination. The extension of the fibrotic reaction resulted from the smear-out of the high-dose region due to density variations in tissue structures, respiratory movement, and limited positioning accuracy. The skin reactions at the entrance port reflect the different treatment geometry in the two experiments. The one unexplained observation is the mild skin reaction that was observed in the second experiment at the beam exit site.

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Section: Discussionmentioning

confidence: 82%

Response of pig lung to irradiation with accelerated 12 C-ions

Dörr

Alheit

Appold

et al. 1999

Radiation and Environmental Biophysics

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“…Denudation and thinning of the epithelium was followed, 1-2 weeks later, by foci of proliferating basal cells and inflammatory infiltrate in the submucosa (Phillips & Ross, 1974). Areas of denudation were seen to coexist with areas of regeneration and these structural changes coincided well with changes in body weight and lethality (Kurohara & Casarett, 1972;Phillips & Margolis, 1972;Phillips & Ross, 1974). Proliferation studies on mouse skin indicate that repopulation of mouse oesophageal epithelium, after fractionated treatments, would start later rather than earlier than the time scale seen with large single doses (Denekamp, 1973;Tsang et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Decreased food intake, body weight loss and lethality after whole thorax irradiation in rodents have all been shown to be caused primarily by acute and subacute oesophageal damage and to be good indicators of oesophageal response (Kurohara & Casarett, 1972;Phillips & Margolis, 1972;Phillips & Ross, 1974). It was shown that lethality due to epithelial denudation occurred over a well denned period of time, with dehydration and starvation as the main cause of death, and no evidence of mediastinitis and/or oesophageal perforation was seen (Phillips & Ross, 1974).…”

Section: Oesophagusmentioning

confidence: 99%

The influence of a seventy-two hour gap on the acute response of mouse skin and oesophagus

Marino

Hirn-Stadler²,

Rojas

1990

The British Journal of Radiology

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The sparing effect of a 72 h gap, inserted after the third, sixth or ninth fraction of a 12 fraction X-ray schedule, was investigated in two early responding normal tissues: mouse skin and oesophagus. Acute skin reactions and body weight loss were used as assays to quantify changes in the radiation tolerance of these tissues. In skin, no evidence of compensatory proliferation was seen if a gap was inserted, whatever its position in the schedule. In oesophagus, a small but significant increase in radioresistance was observed if the gap was positioned 1/4 of the way through treatment compared with the schedule delivered without an interruption (12F/12 days). Although an increase in normal tissue tolerance is not observed by increasing the overall time from 12 to 15 days, provided tumour clonogen proliferation does not occur during the weekend split, the insertion of a gap makes continuous accelerated clinical regimes, currently given without an interruption at weekends, easier to introduce into wider clinical practice.

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“…There is no generally accepted theory of the pathogenesis of radiation pneumonitis . Damage to the capillary endothelial cells has been cited as the major lesion causing interstitial leakage and leakage onto the alveolar surface (Phillips 1966, 1972, Maisin 1970 . Other work suggests the primary damage is the death of type I pneumonocytes which leaves denuded basement membranes and alveolar debris (Adamson et al .…”

Section: Introductionmentioning

confidence: 99%

Proliferation of Type II Pneumonocytes after X-irradiation

Coggle

1987

International Journal of Radiation Biology and Related Studies

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This paper reports preliminary data on the proliferative response of type II cells in the mouse lung over a five-month period after external thoracic doses of 2, 5, 10 and 12 Gy of X-rays. The DNA labelling index (LI) of control (0 Gy) mice was at all times exceedingly low (0.3-0.4 per cent). The LI after 2 and 5 Gy showed a slight though transient fall below controls during the first week post-irradiation, and thereafter the LIs were similar to the controls for the 5 months of the experiment. The LI after 10 and 12 Gy again showed a significant depression during the first week, but this was followed by a significant increase (P = 0.01) in LI which peaked at 4 weeks after irradiation. The LI returned to control values at 3-4 months and again rose significantly (P = 0.05) at 5 months. The first wave of proliferation corresponds to data showing an increase in surfactant in alveolar fluids within 2-6 weeks of 10-15 Gy of X-rays; and the second wave coincides with the pneumonitic phase and is consistent with a delay before the alveolar epithelial continuity is sufficiently compromised by the low rates of type I cell loss to trigger a compensatory wave of type II cell divisions. This relatively chronic radiation response is discussed and contrasted with the dramatic and immediate hyperplastic responses which many toxic irritants produce in type II epithelial cells.

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Radiation Pathology and the Clinical Response of Lung and Esophagus1

Cited by 103 publications

References 0 publications

Response of pig lung to irradiation with accelerated 12 C-ions

Response of pig lung to irradiation with accelerated 12 C-ions

The influence of a seventy-two hour gap on the acute response of mouse skin and oesophagus

Proliferation of Type II Pneumonocytes after X-irradiation

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