Abstract This study reports the results of serial observations of simple haematological indices (haemoglobin concentration, white cell count and platelet count) in 25 patients who developed radiation bowel disease as a late complication of pelvic radiotherapy for malignancy. It is compared with a control group of 25 women patients who received pelvic radiotherapy but did not develop radiation bowel disease. There is a highly significant elevation in the platelet count (P<0·0001) at a time when the patients develop radiation bowel disease. The platelet count returns to normal after successful excision of the disease but the elevation recurs if further radiation disease develops in the urinary or gastrointestinal tracts. It is suggested that the platelet count may have a useful role in the diagnosis of radiation bowel disease.
Four cases of pulmonary veno‐occlusive disease are described. Two patients, who were brothers, had respiratory tract infections. The third patient had chronic active hepatitis and coeliac disease suggesting an abnormality of the immune system; the fourth patient had no obvious cause but presented initially with systemic hypertension. Three of the cases had been diagnosed initially as primary pulmonary hypertension either on open lung biopsy or clinically. In all cases the pulmonary arteries were abnormal with medial hypertrophy, intimal fibrosis and, in some cases, thrombosis in elastic pulmonary arteries. These findings suggest that pulmonary veno‐occlusive disease is not confined to veins and should be considered as a widespread pulmonary vascular disease. The range of aetiological factors indicate that it should not be considered as a single disease entity.
In March 1979 there was an explosion in a coalmine in Lancashire. As a result three men were found dead down the mine and a further seven men, all with extensive burns, died between the third and thirteenth day after the explosion. The lungs were studied in all the cases. Pulmonary infection was the commonest cause of death. Despite high levels of oxygen being given to these seven men, only one case showed a focal intra-alveolar fibrosis. In this case the inspired oxygen requirement came down before death. The toxicity of oxygen in the short term management of patients with severe trauma is questioned.
A new lung adenocarcinoma classification has been published by the International Association for the Study of Lung Cancer, the American Thoracic Society, and the European Respiratory Society. This new classification is needed to provide uniform terminology and diagnostic criteria, most especially for bronchioloalveolar carcinoma. It was developed by an international core panel of experts representing all 3 societies with oncologists/pulmonologists, pathologists, radiologists, molecular biologists, and thoracic surgeons.This summary focuses on the aspects of this classification that address resection specimens. The terms bronchioloalveolar carcinoma and mixed subtype adenocarcinoma are no longer used. For resection specimens, new concepts are introduced, such as adenocarcinoma in situ and minimally invasive adenocarcinoma for small solitary adenocarcinomas with either pure lepidic growth (adenocarcinoma in situ) and predominant lepidic growth with invasion of 5 mm or less (minimally invasive adenocarcinoma), to define the condition of patients who will have 100% or near 100% disease-specific survival, respectively, if they undergo complete lesion resection. Adenocarcinoma in situ and minimally invasive adenocarcinoma are usually nonmucinous, but rarely may be mucinous. Invasive adenocarcinomas are now classified by predominant pattern after using comprehensive histologic subtyping with lepidic (formerly most mixed subtype tumors with nonmucinous bronchioloalveolar carcinoma), acinar, papillary, and solid patterns; micropapillary is added as a new histologic subtype. Variants include invasive mucinous adenocarcinoma (formerly mucinous bronchioloalveolar carcinoma), colloid, fetal, and enteric adenocarcinoma.It is possible that this classification may impact the next revision of the TNM staging classification, with adjustment of the size T factor according to only the invasive component pathologically in adenocarcinomas with lepidic areas.
Acute cardiac allograft rejection is an immune-mediated response, hallmarked by cellular infiltration and myocyte damage in the transplanted heart. Cardiac biopsy sampling has been the 'gold' standard for routinely monitoring episodes of acute rejection. As cardiac biopsy is invasive, attention has focused on other non-invasive methods, such as serum analysis, for monitoring purposes. Tumour necrosis factor alpha (TNF-alpha) is a lymphocyte- and macrophage-derived cytokine that is pleiotropic in its actions. Its proinflammatory functions suggest that it may play an important role in initiating and orchestrating the rejection response. Studies demonstrating a correlation in the expression of TNF-alpha with the severity of the rejection episode have placed TNF-alpha as a prime candidate marker of rejection, and have prompted further study to elucidate these findings. This review discusses the limitations of the methodologies used to identify TNF-alpha, and how intragraft expression of TNF-alpha is not reflected in the serum. Furthermore, we describe how other stimuli besides the rejection response can affect TNF-alpha production, arguing against its use as a 'rejection-specific' marker. Nevertheless, genetic studies suggest that TNF-alpha may influence transplant outcome, and offer a new tool for studying the role of TNF-alpha in acute transplant rejection
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