the apex even without vasoactive maneuvers. On follow-up clinic visits two weeks and three months after discharge, the patient felt quite well, and auscultation of the heart revealed prominent late systolic click but no murmur. However, a late systolic munnur could again be precipitated by isometric exercise. DISCUSSION
Until the past few years, a late systolic murmur at the apex, preceded by a mid or late systolic click, was assumed to be innocent or extracardiac in origin. However, many recent studies in these patients have demonstrated late systolic mitral regurgitation in association with prolapse or ballooning of the mitral leaflets, usually the posterior leaflet into the left atrium,1,2,6,8 and intracardiac phonocatheter studies have localized the click and murmur to the region of the mitral valve and left atrium. 3 , . One of the complications of this syndrome described in the literature is that of subacute bacterial endocarditis, and instances of bacterial endocarditis have been reported in patients with a late systolic murmur, with or without a systolic click. 6, 1 However, to our knowledge, only one case of subacute bacterial endocarditis has been reported in a patient presenting only with a systolic, nonejection click without an associated murmur.s The patient presented previously by LeBauer et al 6 was strikingly similar to ours. Both presented with an erythematous, tender area near the ankle, and they both had normal results of cardiac examination except for a nonejection systolic click. Both their patients and ours developed a late systolic murmur during the course of treatment for endocarditis. This case is presented to emphasize the necessity for prophylaxis against endocarditis not only in those patients with both a nonejection systolic click and late systolic murmur but also in those patients with an isolated, nonejection, late systolic click. fu:FERENas
1 Barlow JB, Bosman LK: Aneurysmal protrusion of the posterior leaflet of the mitral valve: An auseulatory-electrocardiographic syndrome. Am Heart J 71:166-178, 1965 2 Criley JR, Lewis KB, Humphries JO, et al: Prolapse of the mitral valve: Clinical and cineangiographic findings. Br Heart J 28:488-496, 1966 3 Leon DF, Leonard JJ, Kroetz FW, et al: Late systolic murmurs, clicks, and whoops arising from the mitral valve. A transseptal intracardiac phonocardiographic analysis. Am Heart J 72:325-336, 1966 4 Ronan JA, Perloff JK, Harvey WP: Systolic clicks and the late systolic murmur. Intracardiac phonocardiographic evidence of their mitral valve origin. Am Heart J 70:319-325, 1965 5 Barlow JB, Bossman CK, Pocock WA, et all Late systolic murmurs and non-ejection ("mid-late") systolic clicks. An analysisof 90 patients. Br Heart J 30:203-218, 1968 6 LeBauer EJ, Perloff JK, KeIiher TF: The isolated systolic click with bacterial endocarditis. Am Heart J 73:534-537, 1967 7 Linhart JW, Taylor WJ: The late apical systolic murmur. Clinical hemodynamic and angiocardiographic observations. Am J CardioI18:164-168, 1966 8 Jeresaty RM: The syndrome associated with mid-systolic click and/or late systolic murmur, Analysis of 32 cases. Chest 59:643-647, 1971
CHEST, 66: 1, JULY, 1974
Recurrent Hodgkin's Disease Manifesting Roentgenographically as a Pleural Mass* Robert T. Bramson, M.D.; Michael A. Mikhael, M.D.; Stuart S. Sagel, M.D.; and John V. Forrest, M.D.
Two cases of p1eunJ.based Hodgkin's disease without antecedent or coincedent mediastinal adenopathy or parenchymal involvement are presented. This entity bas not previously been reported. 1be occurrence of a pleuralbased density in a patient with known Hodgkin's disease even without mediastinal 01' parenchymal involvement should lead to the snspidon of Hodgkin's disease. U pathologic documentation is required, this can be easily achieved by needle biopsy. This pleural form of the dlsease appears to respoad completely to chemotherapy. thoracic Hodgkin's disease and its radiographic I ntra manifestations are the subject of extensive reports.v''
Radiographically, intrathoracic Hodgkin's disease usually presents as enlarged mediastinal lymph nodes. Approximately 30 percent of patients eventually develop parenchymal Hodgkin's disease. 2, 3 Virtually all of these patients have had previous mediastinal lymph node enlargement or received radiation therapy to the mediastinum. Pleural involvement may occur, but this is almost always in conjunction with either mediastinal or parenchymal disease.t A subpleural form of Hodgkin's disease originating in the subpleural lymphatic tissue has been described, presenting radiographically as a pleural-based plaque." This form also was reported only in association with mediastinal or other parenchymal involvement. Two patients are presented, both of whom received previous mediastinal irradiation and initially had normal findings on chest roentgenograms. These patients were discovered on routine follow-up chest radiographs to have solitary pleural-based masses without evidence of mediastinal adenopathy or other parenchymal involvement.
CASE REPoRTS CASE 1 A diagnosis of Hodgkin's lymphoma, mixed cellularity type, was made by left cervical node biopsy in a 21-year-Old
woman in July, 1971. Chest radiographic findings at that time were normal. A staging laparotomy revealed disease in the spleen and splenic lymph nodes. The liver and periaortic nodes were disease free. She underwent total nodal irradiation from July, 1971 to October, 1971 without significant side effects. In June, 1972, she was found to have a right pleural mass lesion on a routine chest radiograph (Fig 1) and was readmitted to the hospital. The remainder of the chest was free of disease. Open biopsy of the pleural mass revealed a large mass of Hodgkin's lymphoma within the pleural space. She subsequently received chemotherapy for Hodgkin's disease, with resultant disappearance of the pleural mass.
·From the Mallinekrodt Institute of Radiology, Washington UniversitySchool of Medicine, St. Louis, Mo. Reprint requests: Dr. Bramson, MalUnckrodt Institute of Ra-
diology, 510 South Kingshighway, St. Louis 63110
RECURRENT HODGKIN'S DISEASE 89
DISCUSSION
FIGURE 1. Twenty-one-year-old woman with right pleuralbased massof Hodgkin's disease. CASE
2
A 37-year-old man was admitted to the hospital in April, 1972 with cervical lymph node enlargement. Biopsy revealed Hodgkin's disease. A chest roentgenogram indicated normal findings. Staging laparotomy disclosed no other evidence of Hodgkin's disease. He received a high cervical, full mantle, and periaortic node course of radiation therapy. The patient was asymptomatic when a routine followup chest radiograph showed a left pleural-based mass in April, 1973 (Fig 2). No other evidence of Hodgkin's disease was present in his chest. A cutting needle biopsy in May, 1973 showed malignant cells compatible with recurrent disease. Cyclophosphosphamide ( Cytoxan) therapy resulted in complete disappearance of the mass.
Hodgkin's disease in the chest usually presents with enlarged mediastinal lymph nodes. Primary parenchymal Hodgkin's disease is rare. Several different forms of pulmonary Hodgkin's disease have been descnbed.s-" Pleural involvement previously has been reported only in association with mediastinal adenopathy or parenchymal disease. A recently published series of 442 patients who were treated for Hodgkin's disease and observed for signs of relapse does not describe any case of solitary pleural-based involvement.' Undoubtedly, the appearance of pleural disease in the absence of mediastinal involvement in these two patients is related to the previous radiation therapy to the mediastinum. Presumably, these patients would have presented with pleural lesions and mediastinal involvement had not the previous therapy "destroyed" the Hodgkin'sforming tissue in the mediastinum. The present two cases showing solid pleural-based Hodgkin's disease without coincidental or antecedent mediastinal or parenchymal involvement are therefore extremely unusual. They demonstrate that Hodgkin's disease can have still another radiographic presentation from its more common form. The occurrence of a pleuralbased density in a patient with known Hodgkin's disease even without mediastinal or parenchymal involvement should lead to the suspicion of Hodgkin's disease. H pathologic documentation of recurrent disease is required, this can be easily achieved by needle biopsy. As documented in the two cases reported here, this form of disease appears to respond completely to chemotherapy. The paucity of cases of pleural-based Hodgkin's disease is difficult to explain. The proposed mechanism for the development and progression of Hodgkin's disease by some authorss-? suggests that it can start in the lymphatic structures either in the mediastinum or the peripheral pleural-located lymphatic tissue. H this mechanism is indeed true, it would be anticipated that
FIGURE 2. Posteroanterior and lateral view of 37-year-old man with left-sided mass, which on lateral view shows classic sign of posterior pleural-based density. Needle biopsy confirmed recurrent Hodgkin'sdisease.
90 BRAMSON ET AL
CHEST, 66: 1, JULY, 1974
more cases of pleural-based Hodgkin's disease would have presented. Exactly why this has not occurred more often is speculative. REFERENCES
1 CastelIino RA, Blank N, Cassady JR, et al: Roentgenologic aspect of Hodgkin's disease II. Role of routine radiographs in detecting initial relapse. Cancer 31:316-323, 1973 2 Fraser RG, Pare JAP: Diagnosis of Disease of the Chest. Philadelphia, WB Saunders, 1970 3 Greening RR: The Chest. Chicago, Yearbook, 1973, p 152 4 Moolten SE: Hodgkin's disease of the lung. Am J Cancer 21 :253-294, 1934 5 Stolberg HO, et al: Hodgkin's disease of the lung: Roentgenologic-pathologic correlation. Am J Roentgenol Radiwn Ther, Nucl Med 92:96-115, 1964 6 Whitcomb ME, et al: Hodgkin's disease of the lung. Am Rev Resp Dis 106:79-85, 1972 7 Wood NL, Coltman CA: Localized primary extranodaI hodgkin's disease. Ann Intern Med 78:113-118, 1973
Pulmonary Sporotrichosis* Roymond H. Eoers, M.D.,oO and Richard R. Whereatt, M.D. A 37-year-old salesman who developed a soft nodular infiltration in the upper lobe of his right hmg was fonnd to have pulmonary infectiou caused by Sporodnh sc:heuckii. This disease responded promptly to onlly administered potassium iodide. The disease presumed to have been caused by MPirated spores arising from a sphagnum mOl!l8 worm bed.
w.
S
porotrichosis, a disease caused by the fungus Sporothrix schenckii. is most commonly seen as a skin infection, traumatically induced, and is particularly common among gardeners, nurserymen and planters.' Although worldwide in incidence, Sporothrix schenckii is most common in the midwestern United States. Only 28 cases of pulmonary sporotrichosis have been reported in the United States, none in Wisconsin at the time of this report.s This is particularly unusual because the organism is found very readily in the bogs of central Wisconsin where sphagnum moss is abundant. It is harvested and shipped throughout the United States to be used to wrap seedling trees when shipping or storing. The mass absorbs and retains large quantities of fluids and thus is ideal for this purpose. It is also ideal as a growth medium for Sporothrix schenckii.
admitted to Holy Family Hospital. Manitowoc, Wis., for evaluation of his pulmonary symptoms. At the time of admission, he admitted to smoking up to three packs of cigarettes each day and to daily intake of a moderate amount of alcohol. A posteroanterior x-ray film of the chest demonstrated a small inflltration in the right upper lobe, which had not been seen on a previous chest film taken in 1969. Skin tests, including histoplasmin, blastomycin, coccidioidin and tuberculin intermediate PPD (purified protein derivative), were all negative. A second-strength PPD (250 TU) was reported as positive. 15 mm of induration. Sputwn specimens were collected for the routine Papanicolaou smears and cultured for fungi. as well as for acid-fast organisms. A broncboscopic examination revealed moderate to moderately severe erythema, asswned to be associated with his smoking. Bronchial washings were collected for Papanicolaou smears for cancer, fungi. and acid-fast organisms. Sputwn specimens were also sent to the Wisconsin State Laboratory of Hygiene Madison for further examinations. Planigrams of his right upper lung field revealed an upper lobe lesion which seemed larger than it was on the x-ray film taken ten days earlier; no evidence of cavitation was noted (Fig 1). A lateral tomogram indicated that the lesion was in the apical-posterior segment of the right upper lobe. His sedimentation rate was 40 mm/hr on admission and 50 mm/hr at the time of transfer to Maple Crest Sanatorium, Whitelaw. Wis., where the patient was admitted because of suspected tuberculosis. Shortly after admission, earlier cultures for fungi. sent to the Wisconsin State Laboratory, were reported as positive for Sporothrix 8chenckii. Two more sputwn cultures collected at the sanatoriwn were positive for the same organism, thus confirming the first culture. Cultures for acid-fast organisms were negative after eight weeks of incubation. After fungi were recovered from his sputwn, his history was pursued in greater depth to determine the source of this infection. Since it is known that sphagnum moss, as well as old wood, is the most common habitat of this organism, the patient's contact with moss as well as old wood was investigated. He stated
CASE REPoRT
A 37-year-old white man. a plywood company salesman, noted onset of inHuenzaIike symptoms in January, 1972. He had three episodes of associated chills, fever. fatigue, and weight loss. Initial therapy with antibiotics and antitussive medications was unsuccessful. On Jan 16, 1972 he was °From The Holy Family Hospital, Manitowoc, Wis. and Maple Crest Sanitarium, Whitelaw, Wis. oOMedical Director, Maple Crest Sanitarfum, Whitelaw. Reprint requests: Dr. EfJe1'8. Rocky KnoU Health Care Facility, PlyflUJflth. Wisconsin 53Q73
CHEST, 66: 1, JULY, 1974
FicURE 1. Posteroanterior view of chest taken on Jan. 25, 1972 showing inflltration in right upper lung field confirmed as pulmonary sporotrichosis by isolation of infecting organism.
PULMONARY SPOROTRICHOSIS 91