Document VjdGY0vy7eM9EDnwn4bxMRK7N

mtra ten secuig arte? . ar al es con sion;ofl mabijf artarffl 1 resenfi a infi topla'J Schist al. s wetg on aij ;s (Fi| ion bj| placed did nif locytei .vail ofl nal ex case Is of'jj arge iP'; * BENIGN ASBESTOS PLEURISY--EISENSTADT 419 82'. Higher-power photomicrograph of Fig 1 to show ^histiocytic macrophages with "foamy" cytoplasm in ijfitlma and media. Note also prominence of plasma jrcells (arrows) in leukocytic exudate in artery wall jjljhematoxylin and eosin, X400). Comment ^Microscopic abnormalities occurring in the renal easels of rejected human transplanted kidneys |ye been well described.1'3 These changes seem to ^confined to the interlobular, arcuate, and inter ior arteries and arterioles, and vary with the ggth of survival and with vessel size. In the early ages, these lesions consist of a diffuse inflamma- cellular infiltrate made up chiefly of plasma Jls and lymphocytes, necrosis of the media, and Sessional fibrinoid necrosis of the vessel wall with Mbrinous deposit on the intima.3 In patients sur ging a longer period, 25 to. 28 days, the vascular aage is more pronounced and more vessels are gvolved, with the main renal artery spared. At this ?e the changes consist of medial necrosis, fibri|iid necrosis, and intimal thickening. In addition, intima contains large vacuolated phagocytic jpis which are distinctive, possibly plasma-cell de|yatives, and peculiar to this type of rejection sienomenon.3 jin the ureteral arteries of the two patients herein jported, severe vascular abnormalities were noted, piese lesions are similar to those previously de|&bed in renal arteries in transplant rejection.1'3 Rejection of the ureter may contribute to the physiwgical failure of the renal transplant. jThe ureteral vascular changes followed closely liter transplantation and consisted of focal roundill infiltration of the vessel wall, fibrinoid degenjpetion of the intima, and focal medial necrosis K^ee 1). In the second patient, who survived for a S|ger period of time (20 days, case 2), the vasIpar abnormalities in the ureter consisted of in- timal proliferation and degeneration, focal histio cytic infiltration of the media and intima, and medial necrosis. Infiltration of the artery wall by histiocytes with foamy cytoplasm (Fig 1) appears to be unique to the human renal transplantation rejection mechanism.3 These cells are large, have vacuolated cytoplasm which does not stain with the PAS reagent, and have small, ovoid, eccentri cally placed nuclei. Their origin may be from plasma cells.3 Summary Degenerative changes were present in the ureteral arteries in two patients who died after having undergone renal transplantation. These ab normalities are similar to those present in arteries in the kidney. The renal vascular rejection process has been previously described, whereas vascular rejection in the human ureter has not. Round-cell infiltration and focal necrosis of the media is pres ent in ureteral arteries in early rejection. Later findings include medial necrosis and infiltration of the media and intima with large vacuolated histio cytes and leukocytes. The histiocytes appear to be peculiar to the homotransplant rejection phe nomenon. Generic and Trade Names of Drugs Azathioprine--Imuran. Prednisone--Deltasone. Deltra, Meticorten, Paracort. Chloramphenicol--Chloromycetin. References 1. Darmady, E.M.; Offer, J.M.; and Stranack. F.: Study of Renal Vessels by Microdissection in Human Transplantation, Brit Med J 2:976-978 (Oct 17) 1964. 2. Dempster, W.J.; Harrison, C.V.; and Shackman, R.: Rejec tion Processes in Human Homotransplanted Kidneys, Brit Med J 2:969-976 (Oct 17) 1964. 3. Dunea, G.; Hazard, J.B.; and Kolff, W.J.: Vascular Changes in Renal Homografts. JAMA, 190:199-202 (Oct 19) 1964. Benign Asbestos Pleurisy fi. II. i`,isnt\huU, AID THE classical picture of asbestosis has been divided into several stages.' At first, there is a latent period of ten or more years during which asbestos bodies are formed around the asbestos fibers. During this time the patient is completely asymptomatic, and results of his chest x-ray are normal. This stage is followed by the gradual appearance of respiratory symptoms in the form of dyspnea, cough, expectora tion, and wheezing; the roentgenologist finds bilater- See also page 371. al pulmonary fibrosis. As the disease advances, systemic complaints are added, such as fatigue, malaise, weakness, anorexia, and weight loss. Final- From the Medical Clinic, Port Arthur, Tex. Reprint requests to 2301 Procter St, Port Arthur, Tex (Dr. Eisenstadt). |MA, May 3, 1965 Vol 192, No 5 SCF-FA-5675 159