treated by surgical removal, bronchial artery embolization, or intracavitary instillation of antifungal drugs. Under unusual circumstances, however, the behavior of an aspergillorna may change from a chronic, benign lesion into an invasive, life-threatening infection, as in our patient. Two distinct pathologic patterns of invasion exist. The most dramatic is the rapidly developing acute invasive pulmonary aspergillosis, which is found almost exclusively in immunosuppressed and myelosuppressed patients," Cases like ours, without a predisposing immune compromise, are infrequently reported.?" In vitro testing has verified the critical role of phagocytic cells in host defense against Aspergillus, but some role for lymphocyte-directed, cellmediated immunity has also been proposed.' Both our case and that of Metzger et al3 demonstrate that acute invasive pulmonary aspergillosis can occur simultaneously with acute bacterial pneumonia with fever, nonproductive cough, pleuritic chest pain, and a pleural friction rub. The most common initial radiographic pattern in this situation is patchy bronchopneumonia at multiple peripheral sites. As the infectious process progresses, cavitation is seen in the areas of infiltration. A more indolent form of invasive aspergillosis, called chronic necrotizing pulmonary aspergillosis or semi-invasive pulmonary aspergillosis, has also been described. 8,9 This infection most commonly occurs in mildly immunocompromised hosts (eg, patients with diabetes mellitus and patients receiving low-dose corticosteroids) and progresses slowly over several months. The radiographic hallmark of this type of infection is the development of slowly evolving infiltrates with cavitary formation. These hosts, in contrast to those with the acute form, have a productive cough with positive sputum cultures for Aspergillus. It is interesting to consider the role of oxalic acid in this destructive and invasive process. The association of oxalic acid as a fermentation product of Aspergillus sp (most notably A niger) was 6rst reported in 1891 by Wehmer. 10 Nime and Hutchins!' describe not only the local destructive nature of calcium oxalate but also the systemic complications of acute widespread oxalosis. Kurrien and co-workers 12 reported an A niger fungus ball in a patient who died of massive hemoptysis. Oxalic acid was incriminated in the blood vessel destruction by identifying oxalate crystals by polarization. The appearance of black sputum with an acidic pH in pleural fluid, sputum, or cavitary washings should suggest the presence of A niger infection and/or invasion. We have described a patient with emphysema and a subsequent secondary infection with MAl. This resulted in formation of numerous caseating granulomas throughout the lung parenchyma with fibrotic cavitary lesions in both upper lobes. These lesions became secondarily colonized with Aspergillus, which existed in a chronic necrotizing state for several months. With the Aspergillus growth, the metabolic by-product oxalic acid may have caused further tissue destruction, which extended into the chest wall. This final insult from this invasive A niger infection led to respiratory failure and death in a patient whose pulmonary reserve was already severely compromised. REFERENCES 1 Young RC, Bennett JE, Vogel CL, Carbone P~ DeVita Yr. Aspergillosis: the spectrum of the disease in 98 patients. 872
Medicine 1970; 49:147-73 2 Bode FR, Pare J~ Fraser RG. Pulmonary diseases in the compromised host. Medicine 1974; 53:255-93 3 Metzger JB, Garagusi VF, Kerwin DM. Pulmonary oxalosis caused by Aspergillus niger: 1984; 129:501-02 4 Pennington JE. Aspergillus lung disease. Med Clin North Am 1980; 64:475-90 5 Williams OM, Krick JA, Remington JS. Pulmonary infection in the compromised host. Ann Rev Respir Dis 1976; 114:359-94 6 Cooper JAD, Weinbaum DL, Aldrich TK, Mandell CL. Invasive aspergillosis of the lung and pericardium in a nonimmunocompromised 33 year old man. Am J Med 1981; 71:903-07 7 Brown E, Freedman S, Arbeit R, Come S. Invasive pulmonary aspergillosis in an apparently non-immunocompromised host. Am J Med 1980; 69:624-28 8 Gefter WB, Weingrad TR, Epstein DM, Ochs RH, Miller WT. "Semi-invasive" pulmonary aspergillosis. Radiology 1981; 140: 313-21 9 Binder RE, Faling LJ, Pugatch RD, Mahasaen C, Snider GL. Chronic necrotizing pulmonary aspergillosis: a discrete clinical entity. Medicine 1982; 61:109-24 10 Raper KB, Fennell DI. The genus Aspergillus. Baltimore: Williams & Wilkins, 1965 11 Nime FA, Hutchins GM. Oxalosis caused by Aspergillus infection. Johns Hopkins Med J 1973; 133:183-94 12 Kurrien F, Green GH, Rowles SL. Localized deposition of calcium oxalate around a pulmonary Aspergillus niger fungus ball. Am J Clin Pathol 1975; 64:556-63
Acute Myocarditis in Fulminant Systemic Sclerosis· Barry S. Clemson, M.D.; Wayne R. Miller, M.D.; Luck~ M.D.; and john A. Fenss, M.D.
Jerry C.
Myositis and myocarditis have been reported in progressive systemic sclerosis, and these patients have had favorable therapeutic responses to intravenous pulse methylprednisolone. Thus far, premortem biopsy documentation of myocarditis and myocardial 6brosis has not been reported in such patients. We report the case of a patient with subacute congestive heart failure six months after she developed Raynaud's phenomenon. Clinical examination was typical of scleroderma but there was no proximal muscle weakness. She had elevated creatine kinase and MB-creatine kinase and laboratory evidence of hypothyroidism. Echocardiogram demonstrated four-chamber dilatation and severe left ventricular dysfunction. Cardiac catheterization revealed normal epicardial coronary arteries and severely decreased cardiac index. A skin biopsy specimen of the forearm was consistent with diffuse systemic sclerosis, and an endomyocardial biopsy specimen demonstrated mild 6brosis and lymphocytic in6ltrate. Her heart failure initially improved with digoxin, furosemide, and enaIaprii. She also received L-thyroxine and intravenous methylprednisolone. The heart failure progressed over the next six weeks and she died. Patients with scleroderma and new-onset heart failure (Chest 1992; 101:872-74) may have acute myocarditis. *From the Department of Medicine, Divisions of Cardiology and Rheumatology, The Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey, Pa. Reprint requests: Dr. Clemson, Hershey Medical Center, Division of Cardiology, Box 850~ Hershey~ lb 17033 Acute Myocarditis (Clemson at 81)
I
CHF = congestive heart failure
I
Although rare , clinically severe myocarditis has been reported in the setting of systemic sclerosis. U Such patients have been found to have a favorable response to intravenous pulse methylprednisolone therapy'> We describe a patient who presented with heart failure from myocarditis only six months after the onset of systemic sclerosis and who did not respond to intravenous pulse methylprednisolone therapy.
ft
CASE REPORT
A 27-year-oldwhite woman was in good health until she developed
Raynauds phenomenon and swelling of her hands and fingers. She
sought no medical attention until six months later when she
presented with a five-day history of worsening dyspnea on exert ion and orthopnea. She was transferred to our institution Ii,r evaluation of congestive heart failure (CHF) and a dilated heart . She denied dysphagia. dyspeps ia, and arthralgias . Her h\ood pres sure was 1101 80 mm Hg with a regular heart rate of 98 beats/min. On the cardiovascular examination, there was jugular venous distention and audible S3 and S. gallops. There were no murmurs or pericardial ruh. Her lungs were clear to auscultation. She had skin thickening extending from her fingers to midforearms and active Baynauds phenomenon. Her muscle strength was normal. and she had no evidence of arthritis. The CBC and electrolytes were normal. The BUN and creatinine were 21 and 1.0 mg/dl, respectively. Results of the urinalysis were normal . The creatine kinase (CK) was 685 IU (20 to 180 IU) with MB fraction 48 IU (0 to 18 IU), and the aldolase was 18.5 lUlL (00 to 8.0 lUlL). Her T. was 3.1 l1/idl, TSH was 69.2 I1U/ml. antithyroglobulin titer was 80 «160). and antimicrosomal thyroid titer was 1:6.400. The ESR was 1 mmlh, ANA titer was> 1:640 with a homogeneous pattern. anti-ds-DNA antibody was 3.8 Vlml (0 to 15), anti-ENA was negative, and anti-SCI-70 was negative. Coxsackie B ~)lIP antibody was
Medicine 1970; 49:147-73 2 Bode FR, Pare J~ Fraser RG. Pulmonary diseases in the compromised host. Medicine 1974; 53:255-93 3 Metzger JB, Garagusi VF, Kerwin DM. Pulmonary oxalosis caused by Aspergillus niger: 1984; 129:501-02 4 Pennington JE. Aspergillus lung disease. Med Clin North Am 1980; 64:475-90 5 Williams OM, Krick JA, Remington JS. Pulmonary infection in the compromised host. Ann Rev Respir Dis 1976; 114:359-94 6 Cooper JAD, Weinbaum DL, Aldrich TK, Mandell CL. Invasive aspergillosis of the lung and pericardium in a nonimmunocompromised 33 year old man. Am J Med 1981; 71:903-07 7 Brown E, Freedman S, Arbeit R, Come S. Invasive pulmonary aspergillosis in an apparently non-immunocompromised host. Am J Med 1980; 69:624-28 8 Gefter WB, Weingrad TR, Epstein DM, Ochs RH, Miller WT. "Semi-invasive" pulmonary aspergillosis. Radiology 1981; 140: 313-21 9 Binder RE, Faling LJ, Pugatch RD, Mahasaen C, Snider GL. Chronic necrotizing pulmonary aspergillosis: a discrete clinical entity. Medicine 1982; 61:109-24 10 Raper KB, Fennell DI. The genus Aspergillus. Baltimore: Williams & Wilkins, 1965 11 Nime FA, Hutchins GM. Oxalosis caused by Aspergillus infection. Johns Hopkins Med J 1973; 133:183-94 12 Kurrien F, Green GH, Rowles SL. Localized deposition of calcium oxalate around a pulmonary Aspergillus niger fungus ball. Am J Clin Pathol 1975; 64:556-63
Acute Myocarditis in Fulminant Systemic Sclerosis· Barry S. Clemson, M.D.; Wayne R. Miller, M.D.; Luck~ M.D.; and john A. Fenss, M.D.
Jerry C.
Myositis and myocarditis have been reported in progressive systemic sclerosis, and these patients have had favorable therapeutic responses to intravenous pulse methylprednisolone. Thus far, premortem biopsy documentation of myocarditis and myocardial 6brosis has not been reported in such patients. We report the case of a patient with subacute congestive heart failure six months after she developed Raynaud's phenomenon. Clinical examination was typical of scleroderma but there was no proximal muscle weakness. She had elevated creatine kinase and MB-creatine kinase and laboratory evidence of hypothyroidism. Echocardiogram demonstrated four-chamber dilatation and severe left ventricular dysfunction. Cardiac catheterization revealed normal epicardial coronary arteries and severely decreased cardiac index. A skin biopsy specimen of the forearm was consistent with diffuse systemic sclerosis, and an endomyocardial biopsy specimen demonstrated mild 6brosis and lymphocytic in6ltrate. Her heart failure initially improved with digoxin, furosemide, and enaIaprii. She also received L-thyroxine and intravenous methylprednisolone. The heart failure progressed over the next six weeks and she died. Patients with scleroderma and new-onset heart failure (Chest 1992; 101:872-74) may have acute myocarditis. *From the Department of Medicine, Divisions of Cardiology and Rheumatology, The Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey, Pa. Reprint requests: Dr. Clemson, Hershey Medical Center, Division of Cardiology, Box 850~ Hershey~ lb 17033 Acute Myocarditis (Clemson at 81)
I
CHF = congestive heart failure
I
Although rare , clinically severe myocarditis has been reported in the setting of systemic sclerosis. U Such patients have been found to have a favorable response to intravenous pulse methylprednisolone therapy'> We describe a patient who presented with heart failure from myocarditis only six months after the onset of systemic sclerosis and who did not respond to intravenous pulse methylprednisolone therapy.
ft
CASE REPORT
A 27-year-oldwhite woman was in good health until she developed
Raynauds phenomenon and swelling of her hands and fingers. She
sought no medical attention until six months later when she
presented with a five-day history of worsening dyspnea on exert ion and orthopnea. She was transferred to our institution Ii,r evaluation of congestive heart failure (CHF) and a dilated heart . She denied dysphagia. dyspeps ia, and arthralgias . Her h\ood pres sure was 1101 80 mm Hg with a regular heart rate of 98 beats/min. On the cardiovascular examination, there was jugular venous distention and audible S3 and S. gallops. There were no murmurs or pericardial ruh. Her lungs were clear to auscultation. She had skin thickening extending from her fingers to midforearms and active Baynauds phenomenon. Her muscle strength was normal. and she had no evidence of arthritis. The CBC and electrolytes were normal. The BUN and creatinine were 21 and 1.0 mg/dl, respectively. Results of the urinalysis were normal . The creatine kinase (CK) was 685 IU (20 to 180 IU) with MB fraction 48 IU (0 to 18 IU), and the aldolase was 18.5 lUlL (00 to 8.0 lUlL). Her T. was 3.1 l1/idl, TSH was 69.2 I1U/ml. antithyroglobulin titer was 80 «160). and antimicrosomal thyroid titer was 1:6.400. The ESR was 1 mmlh, ANA titer was> 1:640 with a homogeneous pattern. anti-ds-DNA antibody was 3.8 Vlml (0 to 15), anti-ENA was negative, and anti-SCI-70 was negative. Coxsackie B ~)lIP antibody was
