Pulmonary Dysfunction in Rheumatoid Arthritis and Systemic Lupus Erythematosus

Pulmonary Dysfunction in Rheumatoid Arthritis and Systemic Lupus Erythematosus* ALBERT D. NEWCOMER, M.D.,** NORMAN

G. G.

R.

DREW MILLER, M.D., F.C.C.P.t

HEPPER, M .D.t AND

EARL T . CARTER,

M.D.t

Rochester, Minnesota

F

OR A NUMBER OF YEARS, PULMONARY

involvement has been known to occur frequently in systemic lupus erythematosus and occasionally in rheumatoid arthritis. Although numerous clinical and pathologic descriptions of these conditions exist, information concerning their pulmonary pathophysiology has been scarce. This report presents I 3 cases of rheumatoid disease and eight of systemic lupus erythematosus associated with pulmonary complications with special emphasis on abnormalities of pulmonary function. Inasmuch as these two conditions may resemble each other clinically, especially in their early phases, it seems appropriate to consider the altered pulmonary function of both in the same report. MATERIAL AND METHODS

The 13 patients with rheumatoid arthritis and the eight with lupus erythematosus, seen between 1950 and 1961, had pulmonary function studies because of abnormalities on roentgenograms of the thorax. Of the 13 patients with rheumatoid arthritis, six were classified as having classic and seven as definite rheumatoid arthritis according to the revised (1958) diagnostic criteria of the American Rheumatism Association.' On examination, all 13 had typical articular deformities, and nine had characteristic changes on roentgenograms of the joints. The flocculation test for the rheumatoid factor was reactive for the five patients tested. The ages of the 13 patients -Presented at the Interim Clinical Meeting, American College of Chest Physicians, Portland, Oregon, November 30-December 2, 1963. --Fellow in Medicine, Mayo Foundation. tSection of Medicine, Mayo Clinic and Foundation.

562

ranged from 45 to 69 years, and eight were men. In the eight patients with lupus erythematosus, the diagnosis was made on the basis of: (1) a positive L. E. clot test in the seven patients so tested, and (2) a characteristic clinical course. All eight patients scored high enough to justify the diagnosis when the clinical criteria of Winslow and associates' were applied. The ages ranged from 40 to 59 years, and the group included six men and two women. Thus, we classified each of the patients into one of the two groups, although we realized that there are many intermediate forms in the continuum of collagen disease. A serologic overlap existed in that four of the 13 patients with rheumatoid arthritis had a positive result with the L. E. clot test. Patient 9 (Table 1), who had a positive L. E. clot test and rheumatoid factor, had a biopsy of the lung that showed interstitial fibrosis and lymphocytic infiltration and a biopsy of a subcutaneous nodule from the elbow that showed rheumatoid granulomatous changes. Patient 4, who also had positive tests for the L. E. cell and the rheumatoid factor, had a biopsy of synovial membrane that showed rheumatoid villous synovitis. In patient 13, who had a positive L. E. clot test, a flocculation test for rheumatoid factor was not done; but he had characteristic subcutaneous rheumatoid nodules. The difficulties in serologic differentiation of these two conditions have been pointed out by others.'" Although we were arbitrary in establishing the two groups, we include both groups in one series because of the potential serologic overlap. An attempt was made in every case to exclude other causes of the pulmonary

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PULMONARY DYSFUNCTION IN RHEUMATOID ARTHRITIS AND SLE

TABLE

I-CHBST X-RAY FINDINOS AND DATA ON PuLIlONAilY FUNCTION IN 21 PATIENTS WITH RHSUMATOID ARTHRITIS OR SYSnMIC Lupus ERYTHEMATOSUS

Data on Pulmonary FunctionS Sao.

E c

X-ray Findings Rh.umaloid G,oup I 48,F Mild, diffuse, hazy density with small scattered nodules 2 54,M Mild, reticular density in lower ~ of both lung field. 3 58,M Mild , reticular, nodular denaity in both upper lung fields 4 54,M Moderate, diffuse hazinesa in both lower lung field. 5 53,F Mild, reticular, hazinesa in both lower lung fields 6 61,M Moderate. diffuae, mottled haziness with nodularity 55,F Mild, basal-lateral

«

9

53,M

47,M

10 69,M

11 45,F

12 59,F 13 50,M

84

96

87

30

8

7.8

73

135

89

40

12

85

160

105 40

14 18

87

175

110 40

76

85

78

30

54

93

64

30

61

89

68

34

11

70

148

90

42

17

54

110

70

17

67

128

17

50

9.6

39

16 16

15

20 11

1959 22 Severe, diffuae honeycombing 1961 27 Severe, diffuse, mottled hazinesa with ama!1 bilateral effusions 16

Lupus G,oup 14 56,F Mild , diffuse, hazy denaity left base 15 15 4O,M Mild, linear denaity right midlun~ field and pleural 14 thickenmg, right base

16 61,F 17 51,M

18 40,M 19 57,M

20 21

53,M 51,M

Moderate, bilateral basilar denaity 36 Peripheral, basilar, hazineu compatible with pleural thickening 22 Moderate to severe bilateral patchy density 18 Moderate, reticular baailar density and pronounced cardiomegaly 12 Minimal basilar den.ity Moderate, diffuse denaity and bilateral pleural thickening

~%

,0

12

7.9 10 8.6

0 Ii'l

>":::l1 tw:et

8.5

on left 21 Moderate, diffuse reo ticulonodu1ar density with bullous emphyaema of both upper lungs 14 Severe hazinesa with superimposed honeycombing

Mild, basilar, diffuae hazinesa Mild] diffuae, reticular denJIty greater in lower half of each lung

r

17

haziness, greater

8

l:?

>

~E

ice

.sC$ -

.!l~

106 0.5

98

(5 min .) 98

1.5

95

95

118 0.6

97

1.33

2.5

97

2.00

100 0.7

97

0.6

98

5.00

108 0.7

96

1.51

92

80

74

1.7

94

36

124 0.7

92

83

39

76 0.5

95

125

68

46

28

1.3

95

119

60

53

59

1.2

96

9.2

44 185

86

61

69

3.8

95

9.6

83

166

104

40

78

3.0

95

37

117

59

55

92

0.7

95

30

100

48

15

31

115

54

58

48

0.4

96

10

44

103

59

44

67

0.4

94

13

51

57

26

89

0.4

94

10 6.7

98

86

9.8

55

81

62

33

87

6.9

43

150

71

56

46

2.5

98

29

239

68

69

18 2.8

95

97

95

(2 .5 min .) 91 (0 .8 min .)

85

(1.2 min .)

90

(0 .5 min.] 85 (1.0 min .) 94 (1.6 min .) 84 (1.2 min.) 92 (0 .9 min.) 99 (3 min .)

2.22 1.82

2.50

(nor. >19) 7.3 (nor. >21) 6

4.00 1.67 .43

(nor. >15) 3.3 2.50 0.67 1.25

2.85

85

(1.8 min .) 92 (1.4 min.) 93 (1.3 min .) 75 (1 .5 min.) 91 (1.7 min.) 95 (0 .6 min .)

93.4

1.11 1.33 4.0 1.81 0.32 0.43

*Abbreviationa : Resp .=respirationa/minute ; Vent .=ventilation (L./min.); VC=vitai capacity (~r cent of normal) ; RV=residuai volume (per cent of normal) ; TC=totai capacity (per cent of normal} ; MBC =maximum breathing capaci!r. (per cent of normal) ; Sao.=per cent saturation of hemoglobin with oxygen in arterial blood ; Doo=diffu.ing capacity for carbon monoxide (mi./min./mm.Hg) ; and MMF= maxima1 midexpiratory flow (L./aec.) . tNormal is Jesa than 2.5 per cent.

NEWCOMER, MILLER, HEPPER AND CARTER

changes. Eighteen biopsies were performed in 11 cases. Examination of sputum for malignant cells and cultures of sputum, gastric contents, and tissues for tubercle bacilli and fungi were carried out in most cases. Studies of respiratory function consisted of determinations of vital capacity, total lung capacity, residual volume with our modification of the open-circuit technic of Darling, discussed by Miller and colleagues,' maximal midexpiratory flow,' maximum breathing capacity/ and arterial oxygen saturation recorded by an ear oximeter' during rest and during exercise (9inch step, 15 cycles per minute). The pulmonary diffusing capacity for carbon monoxide was measured during exercise by a modification of a steady state method ("Dco-IV") of Bates, Boucot and Dormer.' Values for rate of carbon monoxide uptake and alveolar (end-tidal) tension were measured during the third minute of breathing 0.1 per cent carbon monoxide in air and of a standard exercise (9-inch step, 15 cycles per minute) . Normal standards are based on studies done in our laboratory." RESULTS

Thirteen patients in the series showed a restrictive defect with diminished vital and total capacities and normal or only moderately decreased maximal breathing capacity (Table 2) . Twelve patients demonstrated arterial oxygen saturation below 94 per cent : two while at rest and ten only with exercise. Four patients with rheumatoid arthritis were unable to exercise in the laboratory because of pain and deformity of the extremity. The carbon monoxide diffusing capacity was quite low for the three hypoxic patients so studied. Only four patients showed obstructive features, and all of these had associated major restrictive changes. Two of the four had a history of asthmatic bronchitis. The results of the pulmonary function studies of three patients (No.2, 3 and 4, Table 1) were considered normal in spite of an increased

Diseasesof the Chest

residual volume since this change is often seen in older age groups. Each of the three had diffuse reticular densities on the roentgenogram of the thorax . Less than one third of the series had hyperventilation at rest. The abnormalities on the roentgenogram of the thorax were quite variable and included both parenchymal and pleural changes (Table 1) . The parenchymal abnormalities included increased peripheral markings with or without honeycombing and nodule formation, and the pleural involvement included thickening or effusion or both. Some patients showed both parenchymal and pleural lesions. The abnormalities were less extensive or less generalized in the four patients whose pulmonary volumes were in the predicted normal range than in those with definite defects of function. Eleven patients had biopsy. In most of these, the findings were nonspecific and were useful only in eliminating other pathologic conditions. Four patients (No.6, 9, 10 and 18) had lung biopsy. In patient 6, this showed marked dilatation of peripheral bronchi and nonspecific chronic inflammatory changes in the walls. In patient 9, the biopsy revealed marked interstitial edema, fibrosis with honeycombing, and focal lymphocytic infiltration. The biopsy findings in patients 10 and 18 are included in the illustrative case reports. Biopsies of scalene lymph nodes showed nonspecific inflammatory changes. A subcutaneous nodule showed granulomatous rheumatoid changes (patient 9). Synovial biopsy showed changes consistent with rheumatoid arthritis (patients 1 and 4) and moderate subacute synovitis (patient 14) . Pleural and pericardial biopsies showed nonspecific inflammatory changes (patients 12 and 14). All patients in the rheumatoid group had significant articular symptoms. In 11 of the 13, the arthritis preceded the pulmonary symptoms by two months to 45 years. In the two other patients, the onset of articular symptoms followed the pulmo-

~~~~':be~6i~"

565

PULMONARY DYSFUNCTION IN RHEUMATOID ARTHRITIS AND SLE

TABLE 2-CLASSIFICATION OF CHANGES IN PULMONARY FUNCTION IN 21 PATIENTS WITH INVOLVEMENT OF THE LUNGS DUE TO RHEUMATOID ARTHRITIS OR SYSTEMIC Lupus ERYTHEMATOSUS

Arterial Os Saturation <94 PerCent

Type of Change Patients. Number

None

Rheumatoid arthritis Systemic lupus erythematosus

13

4

8

Total

21

Group

Combined Restrictive and Restrictive Obstructive At Rest

7

2

0

6

2

4

13

4

nary symptoms by one and one-half and two years. All of the patients with abnormal pulmonary function had respiratory symptoms . Eleven complained of cough, which usually was nonproductive. Nine had dyspnea on exertion . Five had chest pain, which was pleuritic in four . All eight patients with lupus erythematosus had febrile episodes, dyspnea on exertion, and pain in the chest. Four had cough, seven had articular symptoms, and two had a rash. Eighteen of the 21 patients in the series had pulmonary abnormalities on physical examination; these consisted usually of basilar rales, but some patients with primarily pleural abnormalities had decreased breath sounds and diminished chest expansion. Four patients with rheumatoid disease were treated with corticosteroids because of the pulmonary involvement . Patient 9 was treated for six months; this resulted in an increase in vital capacity of 33 per cent, in total lung capacity of 17 per cent, and in exercise period from 0.8 to 3.6 minutes with an arterial oxygen saturation of 84 per cent. The diffusion capacity for carbon monoxide increased from 6 to 10 ml.j min.Zmm.Hg (23 to 35 ml. is normal) . While receiving 1.5 mg. of dexamethasone daily, patient 12 showed no objective improvement in function despite a subjective decrease in pulmonary symptoms and patient 10 had worsening of pulmonary function and increased x-ray evidence of chest disease. Patient 11 was treated for two years, with resulting symptomatic improve-

Only on Exertion

5 5 2

10

ment and some improvement in the appearance of the roentgenogram; the measurements of pulmonary function were not repeated. REPORT OF ILLUSTRATIVE CASES

CASE 10 A 69-year-old cattle salesman was first seen at the Mayo Clinic in July, 1959; rheumatoid arthritis was diagnosed. He recalled having had an attack of polyarthritis involving most of his joints in 1914 when he was 24 years old which confined h im to bed for three months. He had noted a moderate cough with sputum in 1952, and by 1958 the cough had become worse and mild dyspnea on exertion became apparent. He had smoked cigars moderately for many years. His arthritis remained quiescent from 1914 until three months before he was 'seen in 1959. The flare-up involved his hands and wrists, and the patient had responded promptly to corticosteroid

.....

FIGURE 1: (Case 10) Thorax showing disseminated reticular density with a honeycombed appearance .

NEWCOMER, MILLER, HEPPER AND CARTER

therapy. He described a mild, nonspecific pain in the right anterior portion of the chest. Examination revealed rather typical, but mild, rheumatoid involvement of the hands, wrists, ankles, and knees, but no subcutaneous nodules. Clubbing of the fingers was present. Scattered, crackling rales were heard throughout both lungs. Hemoglobin concentration was 13.2 gm. per 100 ml. of blood. The leukocytes numbered 9700 per cubic millimeter, and the erythrocyte sedimentation rate was 94 mm. in one hour (Westergren method) . There was mild proteinuria. The serologic test (VDRL) for syphilis was not reactive, and L. E. clot test was negative. Repeated smears and cultures of the sputum revealed no fungi or tubercle bacilli. The roentgenogram of the thorax showed a disseminated reticular density with a honeycombed appearance involving both lungs (Fig. 1). The roentgenographic appearance of the hands and wrists was normal. Pulmonary function studies revealed a restrictive defect with a decrease of arterial oxygen saturation to 90 per cent after 1.2 minutes of exercise. A biopsy of a scalene node showed inflammatory reaction, and a biopsy of the lung showed marked interstitial fibrosis associated with foci of organizing pneumonitis and pronounced thickening of the walls of the blood vessels with an organizing thrombus in one small artery (Fig. 2). Cultures of the lymph node and the lung for tubercle bacilli, fungi, and Brucella organisms revealed no growth. The patient continued to take 0.75 mg. of dexamethasone twice daily until he returned two years later because of progressive dyspnea. Symptoms involving the joints remained quiescent. The roentgenogram of the thorax showed

Diseases of the Chest

more pulmonary involvement. The flocculation lest for the rheumatoid factor was reactive, and the result of the L. E. clot test remained negative. The pulmonary volume had decreased further, and the arterial oxygen saturation decreased to 85 per cent after 0.5 minute of exercise. The carbon monoxide diffusing capacity was 3.3 ml./min. /mm.Hg (normal> 15). CASE

18

A 40-year-old rancher from Wyoming registered at the Mayo Clinic in August, 1961. He had been in excellent health until May, 1961, when he noted sudden pain involving all peripheral joints. Two weeks later, left lateral pleuritic pain and severe dyspnea appeared on exertion. He had a low-grade fever and lost 15 pounds during the next two months . During this time, roentgenograms of the thorax revealed progressive opacification of the midportions of both lungs. Physical examination revealed a cyanotic, chronically ill man with moist rales in the lower half of each lung. The joints were normal. The hemoglobin concentration was 16.2 gm., and the leukocyte count was 5800 per cubic millimeter with a normal differential leukocyte count. The erythrocyte sedimentation rate was 35 mm. in one hour (Westergren method). The urine was normal. The serologic test for syphilis was not reactive. The results of the L. E. clot test were positive on four occasions. The flocculation test for the rheumatoid factor was nonreactive. The serum protein electrophoretic fractions were normal, except for an albumin value of 2.82 gm. per 100 ml. Roentgenograms of the thorax showed bilateral, diffuse, patchy infiltration, which was more evident in the central

2: (Case 10) Specimen from lung showing marked interstitial fibrosis and foci of organizing pneumonitis. There is pronounced thickening of the walls of the blood vessels with an organizing thrombus in one small artery (hematoxylin and eosin; x27) .

FIGURE

~~~~~~6i~4"

PULMONARY DYSFUNCTION IN RHEUMATOID ARTHRITIS AND SLE

slight clearing. On dismissal, the patient was following a schedule of gradually decreasing doses of corticosteroids to be continued under medical supervision . COMMENT

---~

3 : (Case 18) Thorax showing diffuse, patchy infiltration and a small amount of fluid and pleural reaction in both costophrenic angles.

FIGURE

areas, and a small amount of fluid and pleural reaction in both costophrenic angles (Fig. 3) . Pulmonary function studies revealed restrictive changes with arterial oxygen saturation of 94 per cent at rest and 75 per cent after only 1.3 minutes of exercise. A biopsy of the lingula demonstrated multicentric subacute and chronic pneu monitis (Fig. 4). Cultures of the sputum, lung, and bone marrow for tubercle bacilli and fungi revealed no growth. After ten days of therapy with 10 mg. of prednisone four times daily, symptomatic improvement was marked and a roentgenogram showed

Since Ellman and Ball" first described widespread pulmonary lesions in rheumatoid arthritis, many reports of such cases have appeared in the literature. These authors aptly suggested the term "rheumatoid disease" because of the widespread nature of this mesodermal condition, and since the respiratory tract contains considerable amounts of connective tissue, one would logically expect pleural and pulmonary involvement . Although Aronoff and associates" expressed doubt that such an entity as rheumatoid disease of the lung existed, most authors agree that both specific necrobiotic pulmonary inflammatory lesions and, more commonly, nonspecific ones may be associated with rheumatoid arthritis. Only a few authors have referred to pulmonary function studies in rheumatoid and lupus erythematosus pulmonary disease. Andersen and Moersch" reported briefly on two patients with rheumatoid arthritis, one having a restrictive defect and the other an obstructive change with arterial desaturation with exercise. The same au-

(he-

NEWCOMER. MILLER, HEPPER AND CARTER

thors commented on a lupus erythematosus patient showing decreased volumes and expiratory slowing. Brinkman and Chaikof" presented a case of rheumatoid arthritis involving decreased vital capacity and arterial oxygen saturation. Ognibene" reported on two patients with rheumatoid disease with restrictive defects, one of whom had severe cor pulmonale. Morgan,I' Cudkowicz and associates,IT and Doctor and Snider" reported single cases of rheumatoid disease with brief mention of pulmonary function. The last two reports included data suggesting a diffusion defect. The two groups in the present study showed similar changes in pulmonary function. The differences were only in degree with the abnormalities among cases of lupus erythematosus being more pronounced. In individual patients, no consistent relationship was found between the severity of restrictive changes and the degree of hypoxemia. Thus, in some instances greatly reduced vital capacity was associated with normal saturation, while in others, moderately reduced vital capacity was associated with definite hypoxemia. The changes in lung volumes can be explained readily by restriction following pleural effusion, pleural thickening, thickening and rigidity of the costoarticular parenchymal structures, or any combination of these. That the medium and major airways are largely spared is documented by the only occasional and, even then, mild reduc tion in estimates of maximal expiratory flow. These mild reductions may be attributable to muscular weakness. Hypoxemia probably resulted both from thickening of considerable portions of the diffusing surface by interstitial fibrosis and from edema. Additional factors contributing to hypoxemia could include reduction in diffusing surface area by nodules and limitation of ventilation-perfusion adjustment with exercise. The pathologic changes in rheumatoid lung disease that produce these changes in function are both specific and nonspecific. Rubin l ' found that the most frequent ab-

Diseases of the Chest

normality in rheumatoid disease of the lung was a pleuritis appearing as a small serous effusion. Rickards and Barrett," in reviewing .the literature on pathologic changes in rheumatoid lungs, found reports on 11 patients showing nonspecific fibrosing pneumonitis and 26 patients showing necrobiotic foci of the rheumatoid type, the majority of this latter group having associated pneumoconiosis. The typical rheumatoid nodule contains a core of hyalinized collagen that is surrounded by inflammatory cells and fibroblasts which may show a palisade arrangement. The biopsy of the lung for three patients in the rheumatoid group showed only nonspecific fibrosing pneumonitis and no typical rheumatoid nodules. The walls of the blood vessels in patient 9 showed marked thickening. This particular process may become so severe that pulmonary hypertension accompanied by obliterative disease of the small pulmonary arteries and arterioles may occur," Baggenstoss" observed that when distinctive lesions are found in systemic lupus erythematosus, they are most commonly in the kidneys or heart, and that no pathognomic lesions are found in the lungs. Purnell and co-workers" reviewed 54 cases of lupus erythematosus at necropsy and found that the pulmonary changes included terminal bronchopneumonia, hemorrhage, pleural effusions, pulmonary edema, inflammatory exudates within alveolar walls, acute fibrinous pleuritis, pleural fibrosis, and thickening, in the order of decreasing frequency. We were interested in determining whether therapy could reverse the observed changes in function . Reports in the literature indicate that there has been a variable response to corticosteroid therapy for rheumatoid disease of the lung; also in our four patients so treated, the results were variable. Although subjective improvement was noted in three of four patients, only one had an increase in lung volume and some improvement in diffusion.

~~~~~6i~"

PULMONARY DYSFUNCTION IN RHEUMATOID ARTHRITIS AND SLE

The dangers of undesirable side effects of corticosteroid administration, particularly in the patients with rheumatoid arthritis, cannot be overemphasized. Such therapy should be undertaken only when the pulmonary symptoms demand or when it is evident that the progression of the pulmonary disease will lead to significant impairment of function. SUMMARY

Pulmonary function was studied in 13 cases of rheumatoid disease and eight of systemic lupus erythematosus associated with roentgenographic evidence of pulmonary involvement. The most common abnormality noted was a reduction of lung volumes associated frequently with arterial oxygen unsaturation. These changes possibly were due to pleural effusion, restrictive pleuritis, parenchymal involvement, or any combination of these. Corticosteroid administration was attended by variable results. RESUMEN Se estudi6 la funci6n pulmonar en 13 casos de artritis reumatoide y en ocho de lupus eritematoso generalizado, en los que habia evidencia radiografica de compromiso pulmonar. La anormalidad mas comun fue la reducci6n de los vohimenes del pu1m6n a los que se asoci6 frecuentemente falta de saturaci6n arterial de oxigeno. Estos cambios son posible que se debiesen a derrame pleural, pleuritis restrictiva 0 retractil , invasi6n del parenquima pulmonar 0 las combinaciones de estas condiciones. La administraci6n de corticosteroides fue seguida de resultados diversos. RESUMt

La fonction pulmonaire a ete etudiee dans 13 cas d'affections rhumatismales et 8 cas de lupus

erythemateux dissemine associe a la preuve radio graphique d'atteinte pulmonaire. L'anomalie notee Ie plus comrnunement fut la reduction des volumes pulmonaires frequemment associee a la desaturation oxygenee arterielle. Ces alterations sont imputables a l'epanchement pleural, a l'atteinte parenchymateuse ou a toute association de ces alterations. L'administration de corticosteroides fut suivie de resultats variables. ZUSAMMENFASSUNG Lungenfunktionspriifungen erfolgten an 13 FlUlen rheumatischer Erkrankung und 8 Fallen von

generalisiertem Lupus erythematodes in Verbindung mit rontgenologischem Nachweis von pulmonaler Mitbeteiligung. Die am haufigsten beobachtete Abweichung vom normalen Befund war eine Verringerung der Lungenvolumina, hliufig verkniipft mit arterieller Sauerstoffunterslittigung. Moglicherweise waren diese Veranderungen zuriickzufiihren auf einen pleuralen Ergu~, auf eine restriktive Pleuritis, auf eine Beteiligung des Lungenparenchyms oder auch auf Kombination dieser Befunde miteinander. Eine CorticosteroidBehandlung war von wechselhaften Ergebnissen begleitet. REFEIlENCES ROPES, M. W., BENNETT, G. A., COBB, S., JACOX, R. AND JESSAIl, R. A.: "1958 Revision of Diagnostic Criteria for Rheumatoid Arthritis," Arth . and Rheumat., 2 : 16, 1959. 2 WINSLOW, W. A., PLoss, L. N. AND LoITMAN, B.: "Pleuritis in Systemic Lupus Erythematosus: Its Importance as an Early Manifestation in Diagnosis," Ann. Int. M ed., 49 : 70, 1958. 3 HIJMANS, W., DONIACH, D., ROITT, I. M. AND HOLBOIlOW, E. J.: "Serological Overlap Between Lupus Erythematosus, Rheumatoid Arthritis, and Thyroid Auto-immune Disease," Brit. Med . t-. 2 :909 , 1961. 4 ROBEIlTSON, J. L. AND BRINKMAN, G. L. : "Nodular Rheumatoid Lung Disease," Am . J. Med ., 31 :483 , 1961. 5 MILLEll, R. D., BIlIDGE, E. V., JIl., FOWLEll, W. S., HELMHOLZ, H. F., JIl., ELLIS, F. H., Jil. AND ALLEN, G. T .: "Pulmonary Function Before and After Pulmonary Resection in Tuberculous Patients," J. Thor. Surg., 35 :651, 1958. 6 LEAUALLEN, E. C. AND FOWLEIl, W. S. : "Maximal Midexpiratory Flow," Am . Rev . Tubere., 72: 783, 1955. 7 BALDWIN, E. DEF., COUIlNAND, A. AND RICHAIlDS, D. W., JR.: "Pulmonary Insufficiency: Physiological Classification, Clinical Methods of Analysis, Standard Values in Normal Subjects," Medicine, 27:243, 1948. 8 WOOD, E. H. AND GERACI, J. E.: "Photoelectric Determination of Arterial Oxygen Saturation in Man," J. Lab . and Clin. u,«, 34 :387, 1949. 9 BATES, D. V., DoUCOT, N. G. AND DORMER, A. E.: "The Pulmonary Diffusing Capacity in Normal Subjects," I. Physiol., 129:237, 1955. 10 CONNOIl, P. J . : "The Measurement of the Carbon Monoxide Diffusing Capacity of the Lung," Thesis, Graduate School, University of Minnesota, 1960. 11 ELLMAN, P. AND BALL, R. E. : "'Rheumatoid Disease' with Joint and Pulmonary Manifestations," Brit. Med . J., 2: 816, 1948. 12 ARONOFF, A., BYWATERS, E. G. L. AND FEARNLEY, G. R.: "Lung Lesions in Rheumatoid Arthritis," Brit. M ed. J., 2: 228, 1955. 13 ANDEIlSEN, H. A. AND MOEIlSCH, H . 1.: "Pulmonary Manifestations of Collagen Diseases," In GoIlDON, B.: Clinical Cardiopulmonary Physiology, Grone & Stratton, Inc., New York, 1957.

57°

NEWCOMER, MILLER, HEPPER AND CARTER

14 BRINKMAN, G. L. AND CHAtKOF, L. : "Rheumatoid Lung Disease: Report of a Case which Developed in Childhood," Am. Re v. Resp , Dis., 80: 732, 1959. 15 OoNIBENE, A. J.: "Systemic 'Rheumatoid Disease' with Interstitial Pulmonary Fibrosis," A.M.A. Arch . Int. Med ., 105: 762, 1960. 16 MOROAN, W. K. C. : "Caplan's Syndrome : An Interesting Clinicopathological Occurrence,"Ann. Int. Med ., 55 :667, 1961. 17 CUDKOWJCZ, L., MAooFF, I. M. AND ABELMANN, W. H.: "Rheumatoid Lung Disease: A Case Report which Includes Respiratory Function Studies and a Lung Biopsy," Brit. J. Dis. Chest, 55:35, 1961. 18 DOCTOR, L. AND SNIDER, G. L. : "Diffuse Intentitial Pulmonary Fibrosis Associated with Arthritis," Am . Rev. Resp. Dis., 85 :413 , 1962. 19 RUBIN, E. H .: "Pulmonary Lesions in Rheumatoid Disease with Remarks on Diffuse Inter-

D iseases of the Chest

stitial Pulmonary Fibrosis," Am . J. Med ., 19: 569, 1955. 20 RICKARDS, A. G. AND BARRETT, G. M . : "Rheumatoid Lung Changes Associated with Asbestosis," Thorax, 13: 185, 1958.

21 GARDNER, D. L., DUTHIE, J. J. R., MACLEOD, J. AND ALLAN, W. S. A.: "Pulmonary Hypertension in Rheumatoid Arthritis: Report of a Case with Intimal Sclerosis of the Pulmonary and Digital Arteries," Scottish Med. J., 2 : 183, 1957. 22 BAOOENSTOSS, A. H . : "Visceral Lesions in Disseminated Lupus Erythematosus," Proc. Staff Meet., Mayo Clin., 27 :412, 1952. 23 PURNELL, D. C., BAOOENSTOSS, A. H . AND OLSEN, A. M.: "Pulmonary Lesions in Disseminated Lupus Erythematosus," Ann. Int. Med ., 42:619, 1955. For reprints, please write Section of Publications, Mayo Clinic, Rochester, Minnesota 55901.

ESOPHAGEAL OBSTRUCTION It would seem that endoscopically Inserted Intraluminal tubes are a useful adjunct to the other techniques available for the management of esophageal carcinoma . It Is possible In this relatively simple and safe manner to provide a patient passage for food and to eliminate regurgitation. Such tubes are useful for lesions at any level and of any length. The Souttar tube can be used In conjunction with x-ray therapy. Most of our patients with lesions

considered Incurable by virtue of local extenslon were treated with radiation following insertion of the tube . Since the tube can become obstructed by particles of solid food. It Is Important to maintain the patient entirely on liquids and soft foods followIng Insertion. ] . M., KJNG. T . C. AND CANTULL, ] . R. : " Esophageal Obstruction," J. K."s.s M,J. St1(., 65:2n, 1964.

ZUU'ERWAN.

RESULTS OF DOMICILIARY TREATMENT IN AN URBAN TUBERCULOSIS CLINIC figures, regularity and adequacy In a community as a whole, though we should aim at 100 per cent results, especially In Individual cases. Conversion to take regular treatment (the treatment can be rates Increase with the Increase In the standard of made to continue for at least 12 months In 77 per regulartty of treatment. To ach1eve conversation rate at ~ per cent or above, replartty In medicine cent of the cases) . administration should be at least of the order of ~ Theoretically speaking, 98.2 per cent of patients per cent. It means body condones Irregularity of the can be converted In 12 months, If with Improved order of 20 per cent to the maximum . supervision all patients are made to take treatment with regularity for at least 12 months. Looking at MATHUR, K. C., SINGH. K. D., CHADAVAaTY. A•• BAlU, N. AND KHANDELWAL. M. L. : "Results of Domiciliary Treatment the cost Involved In providing a larger supervisory in an Urban TubercuJosis Oink." ]"JiIur J. Tdm .• 11:61. stsJr and realizing some weakness of human nature. one may for the present be content with the above 1964. In an urban clinic with average facJlJtles, '79.6 per cent of the patients can be made nonJnfectlve In 12 months. Of the total cases, 71.6 per cent can be made

HEART BLOCK Data on 61 children with complete heart block are presented. In at least half these patients, It may be assumed . with certainty. that the conduction disturbance was congenital In origin. In only seven are we certaln that the complete heart block developed after birth. Approximately SO per cent of the patients surely had assoc1ated congenital heart disease, and 16 per cent certainly did not. The atrial and the ventricular rates both decreased slgnlfl.cantly with

age. The duration of the QRS complexes of seven patients, three of them now dead, was 0.10 second or longer. The Increase In ventricular rate averaged just below 20 per cent after exercise and atropine whereas Isoproterenol caused an average Increase In ventricular rate of about SO per cent. NAXAWURA. P. P. AND NADAS. A. S.: "Complete Heart Blodt in Infants and Children,' N,w H"'lJ . J. MIJ. 270:1261. 1964.