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Complexities of Loeffler’s Syndrome
ATRIAL ARRHYTHMIAS RELATED TO TRAUMA TO SINOATRIAL NODE ACKNOWLEDGMENT: We are indebted to Mr. Milorad Ralevich for his technical assistance. REFERENCES
1 Lev M, Kinare SG, Pick A: The pathogenesis of atrioventricular block in coronary disease. Circulation 42:409-425, 1970 2 Cohn AE, Lewis T: Auricular fibrillation and complete heart-block. A description of a case of Adams-Stokes' syndrome, including the postmortem examination. Heart 4: 15-32, 1912-1913 3 Yater WM: Pathologic changes in auricular fibrillation and in allied arrhythmias. Arch Intern Med 43:808-834,1929
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4 Balsaver AM, Morales AR, Whitehouse FW: Fat infiltration of myocardium as a cause of cardiac conduction defect. Amer J CardioI19:261-265, 1967 5 Thomas MA, Wee AST: The sinus node in cor pulmonale. Israel J Med Sci 5:831-2, 1969 6 Hutter [r AM, Page DL: Atrial arrhythmias and lipomatous hypertrophy of the cardiac interatrial septum. Amer Heart J 82:16-21,1971 7 Paulin C, Rubin IL: Complete heart block with perforated interventricular septum following contusion of the chest. Amer Heart J 52:940-943,1956 8 Sims BA, Geddes JS: Traumatic heart block. Brit Heart J 31:140-142,1969
Complexities of Loeffler's Syndrome Forty years ago when Loeffler first reported pertinent observations (Beitr z Klin d Tuberk 79: 368, 1932) he could hardly anticipate the subsequent voluminous literature on the subject or designation of an eponymic entity with his name. Related acronyms followed: PIE (pulmonary infiltration with eosinophilia) and TLIE (transitory lung infiltration with eosinophilia). There is striking contrast between symptoms and x-ray findings. The former, general or pulmonary, may be mild or entirely absent. The disease may be detected on preemployment or enlistment examination. In victims of accidental death of some of these subjects, lung lesions were noted in the form of scattered areas of consolidation from few millimeters to 5 ern in diameter, bronchopneumonia or lobar pneumonia. They may involve one or more lobes. Histologic examination revealed numerous eosinophilic leukocytes, lymphocytes, histiocytes, fibroblasts, collagenous fibers, occasional giant cells. Pulmonary radiologic manifestations may be of homogeneous or uneven density, fluffy or heavy, round, triangular or of bizarre shape. Pleural effusion is infrequent. Complete clearing of the lung lesion may ensue within few days. Many agents may initiate this disease. They include parasitic infestation, mycoses, bacterial infections, several drugs, contrast medium, smoke inhalation in
CHEST, VOL. 61, NO.4, APRIL, 1972
fire fighters. Rarely, repeated occurrence may be seen in the same person. Also, its termination in fatal polyarteritis nodosa has been recorded. Ford observed one case of Loeffler's syndrome in about 300 patients with bronchial asthma (Am Rev Resp Dis 93: 797, 1966). Loeffler's syndrome is considered a hypersensitivity disease. Pepys et al suggested (Nature 184:1328, 1959) that precipitins of the blood might be instrumental in its development. Others believe that eosinophils participate in the disposal of the antigen-antibody complex. It is of interest that extract of eosinophils from the blood of horses subjected to allergenic sensitization has antihistaminic properties. To be sure, a great deal more corroborative information is needed for the clarification of the basic immunologic mechanism of this syndrome. As a corollary, mention should be made of another clinical entity with Loeffier as its eponym: Loeffler's endocarditis, that is, parietal fibroplastic endocarditis with eosinophilia. Its characteristic pathologic changes are: pronounced thickening and fibrosis of the parietal endocardium of either or both ventricles, with occasional mitral or tricuspid insufficiency due to involvement of the papillary muscles and chordae tendineae (Loeffier, W: Schweiz med Wchnschr 66:817, 1936). Andrew L. Banyai, M.D.
1 Lev M, Kinare SG, Pick A: The pathogenesis of atrioventricular block in coronary disease. Circulation 42:409-425, 1970 2 Cohn AE, Lewis T: Auricular fibrillation and complete heart-block. A description of a case of Adams-Stokes' syndrome, including the postmortem examination. Heart 4: 15-32, 1912-1913 3 Yater WM: Pathologic changes in auricular fibrillation and in allied arrhythmias. Arch Intern Med 43:808-834,1929
335
4 Balsaver AM, Morales AR, Whitehouse FW: Fat infiltration of myocardium as a cause of cardiac conduction defect. Amer J CardioI19:261-265, 1967 5 Thomas MA, Wee AST: The sinus node in cor pulmonale. Israel J Med Sci 5:831-2, 1969 6 Hutter [r AM, Page DL: Atrial arrhythmias and lipomatous hypertrophy of the cardiac interatrial septum. Amer Heart J 82:16-21,1971 7 Paulin C, Rubin IL: Complete heart block with perforated interventricular septum following contusion of the chest. Amer Heart J 52:940-943,1956 8 Sims BA, Geddes JS: Traumatic heart block. Brit Heart J 31:140-142,1969
Complexities of Loeffler's Syndrome Forty years ago when Loeffler first reported pertinent observations (Beitr z Klin d Tuberk 79: 368, 1932) he could hardly anticipate the subsequent voluminous literature on the subject or designation of an eponymic entity with his name. Related acronyms followed: PIE (pulmonary infiltration with eosinophilia) and TLIE (transitory lung infiltration with eosinophilia). There is striking contrast between symptoms and x-ray findings. The former, general or pulmonary, may be mild or entirely absent. The disease may be detected on preemployment or enlistment examination. In victims of accidental death of some of these subjects, lung lesions were noted in the form of scattered areas of consolidation from few millimeters to 5 ern in diameter, bronchopneumonia or lobar pneumonia. They may involve one or more lobes. Histologic examination revealed numerous eosinophilic leukocytes, lymphocytes, histiocytes, fibroblasts, collagenous fibers, occasional giant cells. Pulmonary radiologic manifestations may be of homogeneous or uneven density, fluffy or heavy, round, triangular or of bizarre shape. Pleural effusion is infrequent. Complete clearing of the lung lesion may ensue within few days. Many agents may initiate this disease. They include parasitic infestation, mycoses, bacterial infections, several drugs, contrast medium, smoke inhalation in
CHEST, VOL. 61, NO.4, APRIL, 1972
fire fighters. Rarely, repeated occurrence may be seen in the same person. Also, its termination in fatal polyarteritis nodosa has been recorded. Ford observed one case of Loeffler's syndrome in about 300 patients with bronchial asthma (Am Rev Resp Dis 93: 797, 1966). Loeffler's syndrome is considered a hypersensitivity disease. Pepys et al suggested (Nature 184:1328, 1959) that precipitins of the blood might be instrumental in its development. Others believe that eosinophils participate in the disposal of the antigen-antibody complex. It is of interest that extract of eosinophils from the blood of horses subjected to allergenic sensitization has antihistaminic properties. To be sure, a great deal more corroborative information is needed for the clarification of the basic immunologic mechanism of this syndrome. As a corollary, mention should be made of another clinical entity with Loeffier as its eponym: Loeffler's endocarditis, that is, parietal fibroplastic endocarditis with eosinophilia. Its characteristic pathologic changes are: pronounced thickening and fibrosis of the parietal endocardium of either or both ventricles, with occasional mitral or tricuspid insufficiency due to involvement of the papillary muscles and chordae tendineae (Loeffier, W: Schweiz med Wchnschr 66:817, 1936). Andrew L. Banyai, M.D.