Document MMGe15y3O11oxnqj23L57qvza

es cob sion;ofl uiabijf artorS reseng s infi topla'2 Schtfj al. s wetg on aq ;s (Fig ion bj| placed did rii$ locyfej .vail oh nal ex case is of i arge iP'; BENIGN ASBESTOS PLEURISY--EISENSTADT 419 <vA 82. Higher-power photomicrograph of Fig 1 to show Ihlstiocytic macrophages with "foamy'' cytoplasm in ilptima and media. Note also prominence of plasma jrcells (arrows) in leukocytic exudate in artery wall ||{hematoxylin and eosin, X400). Comment |Microscopic abnormalities occurring in the renal easels of rejected human transplanted kidneys |Ve been well described.1'3 These changes seem to j&confined to the interlobular, arcuate, and inter- par arteries and arterioles, and vary with the ijgth 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 {fgibinrginoaulsondgeepropseitrioond,th2e5 intima.3 In to. 28 days, patients sur the vascular sage is more pronounced and more vessels are involved, with the main renal artery spared. At this ie the changes consist of medial necrosis, fibri- |jid necrosis, and intimal thickening. In addition, intima contains large vacuolated phagocytic fs which are distinctive, possibly plasma-cell de natives, and peculiar to this type of rejection jjjenomenon.' jfeJn the ureteral arteries of the two patients herein ported, severe vascular abnormalities were noted. |hese lesions are similar to those previously de- Mbed in renal arteries in transplant rejection.1'3 Rejection of the ureter may contribute to the physi- pgical failure of the renal transplant. phe ureteral vascular changes followed closely liter transplantation and consisted of focal round- 111 infiltration of the vessel wall, fibrinoid degen eration of the intima, and focal medial necrosis Ijil^ee 1). In the second patient, who survived for a fejger period of time (20 days, case 2), the vas- Tflar 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. Benio'n Asbestos Pleurisy N. It. I'Hsrti.slftrlt, 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- Sce 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 420 BENIGN ASBESTOS PLEURISY--EISENSTADT ly, extensive destruction of lung tissue leads to respiratory and cardiac failure. It is well known that pleural abnormalities are commonly found in asbestosis. Most experts believe that they are associated only with advanced pul monary disease; others describe them as secondary complications or even as coincidental lesions not directly connected with asbestos inhalation." In contrast to these observations we have been able to find a small number of patients with asbestosis who present primarily the clinical picture of pleurisy in the absence of any significant pul monary disease or respiratory dysfunction. Report of Cases Case l^-In September 1960, a 54-year-old insulator contact with asbestos for 15 years suffered from a left.l sided pleurisy. His chest x-ray revealed a small effusjon^j Because he had little discomfort, no thoracentesis done, and he was treated conservatively. However, in March 1961, a similar attack occurred orii the right side. At this time, chest pain, cough, malaise and* fever were quite severe, and a friction rub was noted, i-i thoracentesis yielded 500 cc serous fluid with 4% protein! and many lymphocytes; however, neither malignant cells nor microorganisms were encountered. The course was pt0i'{ longed, and finally an exploratory thoracotomy was done? The visceral pleura was as thick as an orange peel, and the pleural cavity was partly obliterated. Fibrous and hyaline! plaques covered the parietal pleura. The pathologist de-3 scribed large deposits of dense connective tissue in thaj pleura with inflammatory cell infiltration. A lung section! revealed thickening of the alveolar walls with macrophages! and asbestos bodies. ' Case 2.--A 58-year-old white male, working with asbestos! for 12 years was seen in consultation because of right-sidecM pleural effusion (Fig 1). The disease had been present fowj three weeks and had caused chest pain, fever, cough, andf dyspnea. Asbestos bodies in the sputum, a moderate leu! kocytosis, a fast sedimentation rate, and a positive latex_ test for rheumatoid arthritis were the only abnormal labofl ratory findings. Tests for tuberculosis and fungi gave nega-f tive results. A total of 30 cc of a blood-tinged exudate wan removed by thoracentesis. Two weeks later a thoracotomy^ clone because of persistent symptoms, revealed pleura plaques and adhesions. A lung'specimen, taken in addition! to the pleural biopsy, showed asbestos bodies. After decors tication and partial pleurectomy, the patient becamjf asymptomatic, and results of his chest x-ray were normals Eight months later the patient was seen again because <m fever and chest pain due to a left-sided pleural effusion. Hf was treated symptomatically and had completely recovered one month later. 1. Benign pleural asbestosis (case 2). 2. Malignant mesothelioma of pleura producing rib destruction. Note pleural calcifications. Two cases of malignant mesothelioma, obviousjj preceded by benign pleurisy, have been observed.^ CASE 3.--A 57-year-old refinery foreman," exposed to i bestos for a decade, was treated intermittently 12 years fS a severe pain in the hemithorax on the left. He had no al^ normal findings. One day, a routine chest x-ray revealedj spontaneous pneumothorax with a small pleural effusion^ Because of persistent symptoms a thoracotomy was dorjjj which showed pleural thickening, plaques, and adhesionf The correct diagnosis was not established until a year latijl when, during a barium x-ray of the colon, osteolytic lesioSj were discovered in the left lower side of the thorax. At tim time, malignant mesothelioma was found in the bone spdq men. The patient obviously had suffered from beni^j pleural asbestosis for about 12 years before the develop ment of his malignancy. This case was unusual inasmutf as a spontaneous pneumothorax was the first objective eVI dence of disease. This complication is rare but has been-a ported in association with benign 7 as well as malignant| asbestosis. Case 4.--In 1959, a 58-year-old foreman " who had supffl vised asbestos insulation for three decades was found-, have a malignant mesothelioma of the pleura on the.'Iff side. Ten years earlier he had been hospitalized fohL lateral pleural effusions. The diagnosis of tuberculosis Wffl entertained at this time but could never be proved. He h been under constant medical supervision because of the;fl pearance of streak-like pleural calcification following:^ attack of pleurisy (Fig 2). His autopsy showed benign, bestosis in all portions of the pleura not involved by J malignancy. Similar case histories have been found m literature dealing with asbestos and mesothelioma.4 160 JAMA, May 3, 1965 Vol 192, b< pie thf pie ser freq mot Mama, 'Urre noti 7o pr<f d hyfl logisf le Mil 'g eropH i aabJ ight- resenfi 3UghJ erate3j tive 1| mal I :avegffl udatejj racoti d plel i addljl ter da. t becjl e noffl lecaua 'usioti recoV ibviO ierve| sedt : year! \ad revea I effii was ;ti adhesjl year jj tic 1 ix. one b6 m bej > dev^T inasl? ectivejj a beejj (align iad founij n thd ed fpl ulosiaT d. Hejg of ttiflf ,owir> beniglfi ed bYJ ind na.4 192,:$ BENIGN ASBESTOS PLEURISY--EISENSTADT 421 pc ,,,0r nowhere has the benign disease of the pleura Cognised properly. Comment foie pathogenesis and the pathological findings of r-gn asbestos pleurisy do not differ fundamental izm those of classical asbestosis. Mechanical irri- or chemical influences may affect the pleura ,eU as the lung parenchyma. Strangely enough, ,^09 bodies have never been seen by us in the ral tissues. This observation, shared by the jority of the investigators/ in no way excludes restos as the causative agent. In addition, the Jden appearance of a unilateral or bilateral jlyral effusion after many years of exposure is fitte suspicious of a sensitivity response than of a feet local toxic reaction. pFhe clinical, laboratory, and x-ray picture of Ikural asbestosis does not differ significantly from Jit of any other form of pleural disease. The jfiurisy may be acute, subacute, or chronic; dry, pious, or hemorrhagic; unilateral, or bilateral. The oearance of an effusion on one side followed gorier or later by a similar one on the other seems be most characteristic of asbestosis. Streak-like lid patchy pleural calcifications on the x-ray films ||ye been known to be associated with various sili- Ttoses for a long time.5 Their presence may be Bjlpful in the diagnosis of asbestosis; however, they in be seen in asymptomatic patients, and are equently absent at the time of active pleuropul- johary disease. . jeThe history of prolonged exposure to asbestos pst is of greatest diagnostic significance. However, |ue to the secrecy of the various manufacturing processes the use of asbestos is not always known i the workmen nor to their physicians. Insulators, Jipefitters, and boilermakers who frequently come |n contact with this material may be under suspiiioh whenever respiratory disorders develop in jfcem. Unfortunately, many workers have changed |obs long before symptoms of active asbestosis ap- ear. , In the absence of any specific laboratory test the [mal diagnosis can only be established by thoracoto my, Fibrous, hyaline and calcified plaques, and remarkable thickening of the pleura with pleural Symphysis are highly suspicious to the experienced [pathologist. However, the presence of asbestos Bodies in the pulmonary parenchyma with or with out fibrosis has been generally accepted as the final criterion of asbestos disease. |> The differential diagnosis of asbestos pleurisy has i exclude tuberculosis, which has an almost identi fy course, and x-ray and laboratory appearance. |n addition, several other pathological entities pre|<mt a similar clinical picture and can only be .Ptinguished after exploration. The old dictum, Jpdiopathic pleurisy is tuberculous unless proven gatherwise," has often prevented a correct differentilation, IfeThe prognosis of benign pleural asbestosis is generally favorable. The disease is usually self limited and disappears within a period of weeks or months. However, sometimes the course is pro longed and occasionally, as demonstrated in cases 3 and 4, it is followed by pleural malignancy. Due to its self-limited course, asbestos pleurisy requires only symptomatic therapy. In the past, the recovery of the patient has probably been erroneously attributed to antibiotics and antituber culous drugs administered because of suggestion of infectious etiology. In recurrent and chronic pleural asbestosis, steroids may be of value for the anti inflammatory and antifibrotic effect. If none of the conservative methods are successful in the pro longed cases, pleurectomy should be recommended in order to avoid the development of malignancy. At a recent conference on asbestosis of the New York Academy of Science, C. Berkley, J. Churg, W. E. Smith, and I. J. Selikoff" have been able to demonstrate isolated asbestos fibers with the help of fluorochrome tagging and after electronic ashing in tissues not containing asbestos bodies. It is hoped that these new procedures may further clari fy the pathogenesis of pleural asbestosis. We have observed cases of benign idiopathic pleurisy as well as malignant mesothelioma among the same group of asbestos workers where the diagnosis of asbestosis could not be established because of absence of as bestos bodies. Summary The clinical picture of benign asbestos pleurisy differs greatly from that of classical asbestosis. It may occur in the absence of significant pulmonary disease and respiratory dysfunction. This entity must be considered in the differential diagnosis of any form of idiopathic pleurisy. The history of ex posure to asbestos will aid in directing the attention to this entity; however, the final diagnosis depends on a lung tissue specimen containing asbestos cor puscles or asbestos fibers. E. C. McRee, MD, Port Arthur, Tex, gave permission to publish case 1. References 1. Pendergrass, E.P.: Pneumoconiosis Problem, Springfield, III.: Charles C Thomas, Publisher, 1959. 2. American College of Chest Physicians: Report of Section on Nature and Prevalence Committee on Occupational Diseases of Chest, Dis Chest 45:107-111 (Jan) 1964. 3. Eisenstadt, H.B.: Asbestos Pleurisy, Die Chest 46:78-81 (July) 1964. 4. Wagner, J.C.; Sleggs, C.A.; and Marchand, P.: Diffuse Pleural Mesothelioma and Asbestos Exposure in North Western Cape Province, Brit J Induatr Med 17:260-271 (Oct) 1960. 5. Schneider, L., and Wimpfheimer, F.: Multiple Progressive Calcific Pleural Plaque Formation, JAMA 189:328-330 (July 27) 1964. 6. Eisenstadt, M.D., and Wilson, F.W.: Primary Malignanl Mesothelioma of Pleura, J Lancet 80:511-514 (Nov) 1960. 7. Wood, W.B., and Gloyne, S.R.: Pulmonary Asbestosis: Re view of 100 Cases, Lancet 2:1383-1385 (Dec 22) 1934. 8. Ehrenhaft, J.L.: Sensenig, D.M.; and Lawrence, M.S.: Meso theliomas of Pleura, J Thorac Cardioo Surg 40:393-409 (Sept) 1960. . 9. Berkley, S., et al: Detection and Localization of Mineral Fibers in Tissue, read before New York Academy of Science, Conference of Biological Effects of Asbestos, Oct 19-21, 1964. tlAMA, May 3, 1965 Vol 192, No 5 161