L. (1974). Thorax, 29,[262][263][264]. A common factor in hypertrophic osteoarthropathy. Two cases of oesophageal disease with hypertrophic osteoarthropathy are presented. The unusual site of the primary lesion has prompted a review of the literature and led to the conclusion that there is a common innervation accounting for a common afferent arc which is an integral and basic part of the mechanism in this disorder.The pathogenesis of hypertrophic osteoarthro-barium swallow showed the presence of a sliding pathy (HO) remains an enigma. It may be hiatus hernia. Oesophagoscopy revealed the presence associated with disease in a variety of organs and of severe confluent, ulcerative oesophagitis from in a wide range of pathological conditions in the cardia to the level of the aortic arch. those organs. We present two unusual and rare Repair of the hiatus hernia was carried out in causes of HO and propose a common factor in all cases of HO. CASE REPORTS PATIENT 3. M. A 78-year-old woman presented in 1959 with a three-month history of increasing dysphagia. For four to five months before admission she had noted swelling and stiffness in both ankles and wrists. Pitting oedema was easily demonstrable on the dorsum of the feet, ankles, and lower part of the legs and on the dorsum of the hands. Radiographs showed well-marked periosteal new bone formation on the tibiae, fibulae (Fig. 1), radii, and ulnae. Chest films and bronchoscopy were normal; in particular there was no evidence of bronchial carcinoma. Oesophagoscopy and biopsy revealed an adenocarcinoma in the middle third of the oesophagus.In view of the patient's age and frailty no operative intervention was undertaken and she died shortly after.PATIENT S. L. A 51-year-old man presented with a 10-year history of heartburn, especially at night; vomiting, occasionally with blood, was noted several times. From 1969 he had had aerophagy and slight dysphagia referred to the lower half of the sternum. From 1968 he had swollen and stiff ankles, stiff knees and wrists, and marked finger and toe clubbing.The chest film appearances were normal, but radiographs of the femora, tibiae, fibulae, and radii (Fig. 2
Methods of light and electron microscopy were employed to determine the exact nature of the chondroid portions of the benign mixed tumor of salivary gland. Although these regions could not be distinguished from normal hyaline cartilage when examined with the light microscope, no normal or metaplastic chondrocytes could be identified when the ultrastructure of these regions was examined with the electron microscope. Instead, neoplastic myoepithelial cells embedded in a matrix quite similar to that of immature hyaline cartilage were found to be present. It is concluded that in the benign mixed tumor neoplastic myoepithelial cells undergo partial metaplasia enabling them to produce a typical chondroid matrix. Further, because of the similarity in structure and function between myoepithelial cells and visceral smooth muscle cells, it is suggested that the myoepithelial cell is of mesenchymal origin and, therefore, after metaplasia entirely capable of producing a mesenchymal mucin.
TREATMEINT o01 ASTHMA BY t3LThA-IOLET LG{ i reason of the greater wealth of ultraviolet rays in the solar spectrum at those heights. Unfortunately, even this mechainism fails to explain all the clinical phenomena. For example, Case I, during his asthmatic attack, was apparently suffering from acute suprarenal dysfunction which means either that there was an inadequacy of dopasubstance, or else that the suprarenals were failing to convert it to adrenaline. The fact that he did not pigment in an Addisonian manner does not necessarily indicate the latter; it may have been too slight to be noticeable. He was given suprarenal extract (empirically) by mouth, and this was followed by improvement. But we do not know the real effect of suprarenal extract given by mouth. It may be the adrenaline content that is absorbed, or a ferment-in which the suprarenals are temporarily deficient-for converting dopa-substance into adrenaline. Whichever it may be, the whole scheme breaks down when the patient-on regaining his suprarenal function and normal blood pressure-develops an attack of asthma. One would have expected him to do this earlier, when his adrenaline production was at a low ebb. The only possible (and to my mind rather weak) plea is that he may not have had the allergic provocation during that time. Then the coma by which Case II distinguished himself cannot be explained by this mechanism. Summary 1. The beneficial effects of actinotherapy in cases of asthma cannot be attributed alone to the suggestibility of the patient. 2. At present no theory can be propounded which covers all the clinical observations. 3. The most striking clinical observation-that is, the relation between immunity and pigmentation-leads me to propound a theory involving the relation of adrenaline and melanin. 4. It is perhaps noteworthy that in none of these twelve asthmatic patients or in any of the fifty to sixty patients treated by ultraviolet rays for other conditions has pulmonary tuberculosis manifested itself either during treatment or subsequently.
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