398 Thorax 1992;47:398-399

After treatment with prednisone (1 mg/kg a Pleural effusion as day) there was rapid symptomatic improve- ment and after a week the left pleural shadow

manifestation of on the chest radiograph had virtually resolved. Thorax: first published as 10.1136/thx.47.5.398 on 1 May 1992. Downloaded from Two years later the patient was still taking temporal arteritis corticosteroids (5 mg/day) and was symptom free.

PATIENT 2 S Romero, P Vela, I Padilla, J Rosas, A previously fit 71 year old woman was admit- ted to hospital with a one month history of C Martin, I Aranda temporal headache, fatigue, and jaw claudica- tion. A few days later she developed right pleuritic chest pain and a productive cough. On examination she had bilateral temporal artery Abstract thickening, though the pulses were preserved, Two patients with temporal arteritis who and signs ofa right pleural effusion. Laboratory presented with pleural effusion are repor- findings included a haemoglobin concentration ted. Both had an exudate that responded of 9 9 g/dl, a white cell count of 15 x 109/l to prednisolone treatment. (86% neutrophils, 11% lymphocytes, and 3% monocytes), a platelet count of 69 x 109/1, and an erythrocyte sedimentation rate of 126 mm in About 9 % of patients with giant cell arteritis the first hour. Tests for antinuclear antibodies have prominent respiratory tract symptoms, and rheumatoid factor gave negative results. and in 4% they are the initial manifestation.' The chest radiographs showed loss of the Pleural effusions are rare, only seven reports costophrenic angle and thickening of the having been published,`7 four ofwhich give no oblique fissure on the right. Abdominal details of the effusion. We describe two ultrasound examination showed no abnor- patients presenting with a pleural effusion. mality. Thoracocentesis yielded serous fluid that showed no specific features on micro- biological or cytological examination. The Case reports pleural fluid white cell count was 3-2 x 109/1

PATIENT 1 (45% neutrophils, 5% lymphocytes, 8% hys- A 67 year old woman, previously symptom tiocytes, and 42% mesothelial cells); tests for

free, presented with a three month history of antinuclear antibodies and rheumatoid factor http://thorax.bmj.com/ malaise, weight loss, shoulder girdle pain, gave negative results. Other laboratory data are frontoparietal headache, jaw claudication, shown in the table. A temporal artery biopsy cough, scanty sputum, and left pleuritic chest specimen showed histological changes com- pain. On examination she had a tender, pulse- patible with giant cell arteritis. less, slightly thickened right temporal artery, Treatment with prednisone (1 mg/kg a day) and decreased breath sounds and diminished was started and caused rapid symptomatic and vocal fremitus in the left lower chest. The radiological improvement. She was still taking was prednisone (10 mg/day) and was symptom free haemoglobin concentration 10-3 g/dl, on September 29, 2021 by guest. Protected copyright. white cell count 8-4 x 10/l (62% neutrophils, when last seen 18 months later. 30% lymphocytes, and 8% monocytes), and Laboratory data on the two patients (normal values in platelet count 520 x 109/1. Her erythrocyte parentheses) sedimentation rate was 86 mm in the first hour, and she had no antinuclear antibodies Patient No: 1 2 or rheumatoid factor. Sputum culture was SERUM negative for Mycobacterium tuberculosis. The Protein(6-4-8g/dl) 6-2 7 chest radiograph and computed tomogram Alkaline phosphatase (98-279 629 643 U/1) showed a small left pleural effusion. Fibreoptic Lactate dehydrogenase (230- 304 330 bronchoscopy and abdominal computed 460 U/1) tomography and ultrasound all gave normal Cholesterol (120-250 mg/dl) 176 187 results. Thoracocentesis serous fluid Carcinoembryonic antigen 0 5 1-2 yielded (< 10 ng/ml) that showed no specific features on micro- Complement biological and cytological examination. The C3 (60-130 mg/dl) 120 214 pleural fluid white cell count was 0-6 x 109/l C4 (16-42 mg/dl) 37 44 (43% neutrophils, 12% lymphocytes, 10% PLEURAL FLUID macrophages, and 33% mesothelial cells), with Glucose (mg/dl) 100 99 Alicante, Spain no antinuclear antibodies or rheumatoid factor. Protein (g/dl) 3-2 4-1 S Romero Lactate dehydrogenase (U/1) 170 1085 P Vela Other serum and pleural fluid laboratory data Amylase (U/1) 32 87 I Padilla are shown in the table. The pleural biopsy Cholesterol (mg/dl) 58 79 J Rosas specimens showed atypical mesothelial hyper- Carcinoembryonic antigen 0 5 2-5 C Martin plasia in nodules mixed with (ng/ml) I Aranda arranged inflam- Carbohydrate antigen matory cells (figure 1). A biopsy ofthe temporal (15-3 ng/ml) 5 20 Reprint requests to: artery showed myointimal proliferation with a Fetoprotein (IU/ml) < 1 <1 Dr S Romero, Complement C Italia 30, Esc 2, 1 D, disruption of the internal elastic lamina, dense 03003 Alicante, Spain C3 (mg/dl) 36 92 chronic inflammatory cellular infiltration, and C4 (mg/dl) 18 26 Accepted 15 November 1991 giant cells. Pleural effusion as mamfestation oftemporal arteritis 399

C4 levels in the pleuralfluid were relatively high but within the range found in our laboratory in fluid from patients with a pleural exudate due to various other causes, including neoplasms. Thorax: first published as 10.1136/thx.47.5.398 on 1 May 1992. Downloaded from Histological study of the pleura in patients with effusions associated with temporal arteritis is limited to samples obtained by blind pleural biopsy. The changes found in two previous cases and in ours were non-specific, though our attention was drawn to the intense mesothelial :.' reaction, which initially suggested the possi- - > ~~~~ .. bility of neoplasia. The presence of vascular changes in the pleura could not be excluded owing to the limited area sampled and the focal nature of this type of arteritis. In the only patient with a pleural effusion on whom a necropsy was carried out2 no reference was made to the histological appearances of the pleura.

Pleural biopsy specimen with mesothelial hyperplasia: nodule of hyperplasic mesothelial The cytological findings in our patients were cells mixed with inflammatory cells. (Haematoxylin and eosin.) also non-specific. Although a low mesothelial cell count has been reported to suggest tuber- culosis,'0 a high count is not associated with any Discussion particular disease. Two patients with typical features of temporal A coexisting disease as a cause ofthe effusion arteritis were seen over a relatively short period is very unlikely, in our cases as in others, as the of time with a pleural effusion at the time of patients had undergone thorough clinical in- diagnosis. Identification ofthe cause of a pleural vestigation, which showed no other abnor- exudate is not always easy and 20% of cases mality, and substantial lasting improvement remain undiagnosed after conventional inves- occurred with corticosteroids. tigations, including cytology and biopsy.8 The characteristics of the pleural effusion are mentioned in three previous reports. 7 The effusion in all three cases was an exudate with a 1 Larson TS, Hall S, Hepper NGG, Hunder GG. Respiratory high protein content, but no reference was tract symptoms as a clue to giant cell arteritis. Ann Intern http://thorax.bmj.com/ made to lactate dehydrogenase activity. The Med 1984;1O1:594-7. 2 Cooke WT, Cloake PCP, Govan ADT, Colbeck JC. Tem- pleural fluid in our two cases comply with poral arteritis: A generalized vascular disease. Q J Med Light's criteria for an exudate-namely, ratio 1946;15:47-75. 3 Hamilton CR, Shelly WM, Tumulty PA. Giant cell arteritis: of protein in pleural fluid/serum above 0 5, a Including temporal arteritis and polymyalgia rheumatica. ratio for lactate dehydrogenase above 0-6, and/ Medicine 1971;50:1-27. or lactate dehydrogenase more than two thirds 4 Gallois P, Falconnet M, Dhers A, Plauchu G, Cavallero G, Cognet JB. Aspects cliniques de la maladie de Horton en the upper limit of normal for serum lactate medecine interne. A propos de 56 observations person- dehydrogenase. There was a predominance nelles. Med of Lyon 1979;241:837-42. on September 29, 2021 by guest. Protected copyright. 5 Routier G, Dutoit A, Carpentier M, et al. La maladie de polymorphonuclear cells in our patients as in Horton. Aspects actuels. J Sci Med (Lille) 1981;99:1-12. two of the previous studies; the third study7 6 Luthier F, Tourliere D, Rouchon JP, Divonne FF, Caplan initially showed a predominance of lympho- F, Bardet M. Manifestations pleurales de la maladie de Horton. A propos d'un cas. Rev Mid Intern 1988;9:304-5. cytes and after numerous relapses a predomin- 7 Turiaf J, Valere PE, Gubler MC. Pleuresie recidivante au ance of eosinophils, which could be due to cours d'une arterite temporale. Poumon Coeur 1967;23: 633-51. repeated thoracocenteses.9 The concentration 8 American Thoracic Society. Guidelines for thoracocentesis of glucose in the exudate, not mentioned in and needle biopsy of the pleura. Am Rev Respir Dis 1989; other studies, was similar to that in the serum in 140:257-8. 9 Adelman M, Albelda SM, Gottlieb J, Haponik EF. Diag- our patients. nostic utility of pleural fluid eosinophilia. Am J Med In our cases tests for several tumour markers 1984;77:915-20. 10 Spriggs AI, Boddington MM. Absence of mesothelial cells and non-organ specific antibodies gave negative from tuberculous pleural effusions. Thorax 1968;15: and unhelpful results. The complement G3 and 169-71.