BRIEFCLINICALOBSERVATIONS PERICARDIALEFFUSIONAS A MANIFESTATIONOF GIANT CELLARTERITIS Giant cell arteritis is a vasculitis that may involve medium-sized and large arteries in any organ system. It often presents atypically and poses a considerable diagnostic challenge. In the present case, the major manifestation of the disease was a pericardial effusion. A 65-year-old woman was admitted to the hospital with a lmonth history of dyspnea on exertion and pleuritic chest pain. She also complained of easy bruisability, nausea, constipation, diffuse myalgias, and a g-kg weight loss. Physical examination revealed a thin, acutely illappearing woman. Her vital signs included a blood pressure of 120/70 mm Hg without paradox, a regular heart rate of 72 beats/ minute, respirations of 16/minute, and a temperature of 37.2”C (99’F). There was no enlargement or tenderness of the temporal arteries on palpation. Results of the remainder of her physical examination were unremarkable. Pertinent laboratory data included a hemoglobin level of 10.7 g/dL with normochromic, normocytic indices; a normal white blood cell and platelet count; a Westergren sedimentation rate of 124 mm/hour; and an alkaline phosphatase level of 164 IU. A chest roentgenogram revealed moderate cardiomegaly without pulmonary congestion. An electrocardiogram was normal. After admission, the patient had four negative blood cultures and a negative urine culture. Her antinuclear antibody titer was positive at 1:320 with a speckled pattern. An echocardiogram done on the second hospital day revealed a moderately large anterior and posterior pericardial effusion with diastolic collapse of the right atrium, suggesting early tamponade [ 11. She remained he-

modynamically stable, however, and a pericardiocentesis was not necessary. Extensive further testing was unhelpful in establishing a diagnosis. On the ninth hospital day, the patient underwent a temporal artery biopsy that revealed a panarteritis with giant cells. Treatment with prednisone at a dosage of 60 mglday was initiated, and the patient clinically improved within 72 hours. A chest roentgenogram performed prior to discharge revealed a decrease in heart size. Six weeks after discharge, her sedimentation rate had returned to normal. A subsequent echocardiogram obtained at that time revealed essentially complete resolution of the pericardial effusion. Giant cell arteritis is a disease of the elderly, almost never occurring before age 50. Its prevalence is approximately 133 per 100,000 persons aged 50 and older [2]. The three most common symptoms of giant cell arteritis are headache, fever, and polymyalgia rheumatica, each appearing in approximately one third of patients [3]. However, like many other diseases of the elderly, the initial presentation of this entity may be very atypical. Involvement of the heart and great vessels has been reported in giant cell arteritis. Patients have been described with aortic arch syndrome causing claudication of one arm or leg, aortic insufficiency, and, uncommonly, coronary artery involvement [2,4]. The occurrence of pericardial effusion as a manifestation of giant cell arteritis has been reported in only three patients over the past 15 years [5,7]. In those cases, as in this one, the patients presented atypically and the pericardial effusion was discovered due to an abnormal chest radiograph or electrocardiogram. In only one of those cases was a pericardiocentesis performed, yielding “sterile






Pericardial involvement is known to be associated with other vasculitides including polyarteritis nodosa, rheumatoid arthritis, systemic lupus erythematosus, and hypersensitivity vasculitis [5]. In rheumatoid arthritis, silent pericardial effusions are seen on echocardiography in approximately 50% of patients. Although these are typically benign, they occasionally can progress to tamponade [8,9]. Whether tamponade would have eventually occurred without treatment in this patient is unknown. In summary, a 65-year-old woman with an atypical presentation of giant cell arteritis has been described. Her chief physical finding of a significant pericardial effusion was unusual and not suggestive of this disease at initial evaluation. The effusion resolved along with her elevated sedimentation rate following appropriate corticosteroid therapy, implying the same etiology for both. Giant cell arteritis should be considered in the differential diagnosis of idiopathic pericardial effusion, and possibly tamponade, in the elderly. JEANETTEPRESTON,M.D. MARK WARNER.M.D. Medical College of Virginia Richmond, Virginia 1. Gillam LD, Guyer DE, Gibson TC, King ME. Marshall JE. Weyman AE. Hydrodynamic compression of the right atrium: a new echocardiographic sign of cardiac tamponade. Circulation 1983; 68: 294-301. 2. Healey LA. The spectrum of polymyalgia rheumatica. Clin Geriatr Med 1988; 4: 323-31. 3. Partain K, Bradley J, Brandt KD. Polymyalgia rheumatica and giant cell arteritis. Indiana Med

1988; 81: 11-6. 4. Rai GS. Atypical presentation of temporal arteritis. J Am Geriatr Sot 1987; 35: 594-7. 5. Garewal HS, Uhlmann RF, Bennett RM. Pericardial effusion in association with giant cell arteritis. West J Med 1981; 134: 71-2. 6. Miller JP. Pericardial effusion and giant cell arteritis. Proc R Sot Med 1972; 65: 565. 7. Dupond JL. Temporal arteritis manifested as an acute febrile pericarditis. JAMA 1982; 247: 2371-2. 8. Franc0 AE, Levine HD. Hall AP. Rheumatoid pericarditis-report of 17 cases diagnosed clinically.

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BRIEF CLINICAL OBSERVATIONS Ann Intern Med 1972; 77: 837-44. 9. John JT, Hough A, Sergent JS. Pericardial disease in rheumatoid arthritis. Am J Med 1979; 66: 38590. Submitted


15. 1991, and accepted in revised form March 28, 1991

TRANSIENT ADRENOCORTICAL INSUFFICIENCYIN AIDS Adrenocortical insufficiency is a frequent, potentially serious complication of acquired immunodeficiency syndrome (AIDS) [l]. The most common offending infectious agents are cytomegalovirus, Cryptococcus, and Mycobacterium


Other noninfectious etiologies including Kaposi’s sarcoma and drugs have been identified [l]. The adrenocortical insufficiency encountered in patients with AIDS has previously been thought to be permanent; however, we report a patient in whom the adrenocortical insufficiency was transient and reversible, and he thus did not require long-term adrenocorticosteroid replacement therapy. The patient is a 49-year-old bisexual man with known AIDS who presented with a history of 1% weeks of fever, chest pain, and weakness. His only medication was zidovudine for 24 hours. Salient features on physical examination were a thin, trembling, disoriented, lethargic man, The temperature was 38.4”C (101.2”F), blood pressure 94/60 mm Hg (because of marked weakness, an evaluation of a postural change could not be performed), heart rate 12O/minute, and respiratory rate 24lminute. Laboratory values on admission included sodium 127 nmol/L, potassium 5.8 nmol/L, bicarbonate 17.2 nmol/L, chloride 103 nmol/L, creatinine 150.3 ~mol/L, blood urea nitrogen 5.6 nmol/L, and glucose 5.2 nmol/L. Because the clinical presentation 440

and biochemistry suggested adrenocortical insufficiency, a cosyntropin stimulation test (Cortrosyn, Organon Incorporated, West Orange, New Jersey) was performed using 25 U of cosyntropin intravenously with blood samples obtained prior to and 30 minutes after the infusion. The basal cortisol level was 160.1 nmol/L, which increased to 436.1 nmol/L on stimulation testing. A normal response is a stimulated cortisol value greater than 552 nmol/L at 30 minutes [2]. The patient received parenteral hydrocortisone and hydration, following which his electrolyte values, mental status, and blood pressure normalized. After 24 hours, the steroids were discontinued. The patient was discharged several days later feeling well. Five days after the initial admission, the patient was readmitted with chest, lower back, and lower extremity pain. Medications were zidovudine and topical nitrates. His blood pressure was 120158 mm Hg, pulse 84/minute, respirations 16/minute, and temperature 37.8”C (100.2’F). He was alert, oriented, and in no acute distress. Abdominal examination again showed hepatomegaly. He had some upper back tenderness bilaterally. Laboratory studies revealed the following values: sodium 138 nmol/L, potassium 3.6 nmol/L, chloride 107 nmol/L, and bicarbonate 25.9 nmol/L. A cosyntropin stimulation test showed a basal cortisol level of 328.4 nmol/L, which rose to 745.2 nmol/L in 30 minutes. The diagnosis of adrenocortical insufficiency in this patient was based upon his clinical presentation and response to hydrocortisone and confirmed by a cosyntropin test. The basal cortisol level in this ill patient was 160.1 nmol/L. This level is significantly below the basal cortisol level of 301.93 nmol/L reported in non-

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stressed, normal subjects [3]. The stimulated cortisol of 436.1 nmol/L is less than the level of 552 nmol/L accepted as the criterion for a normal peak cortisol [2]. Thus, the patient had adrenocortical insufficiency and rapidly responded to glucocorticoid replacement therapy. Transient adrenocortical insufficiency has not previously been noted to occur in AIDS. Whether this is a common phenomenon or not is unknown. To assess adrenocortical function in AIDS patients previously diagnosed as having adrenocortical insufficiency, in order to avoid possible long-term unnecessary corticosteroid therapy, we would suggest not abruptly discontinuing the glucocorticoid therapy, but switching to treatment with dexamethasone and then retesting with cosyntropin. ELISABETHHOROWITZ,M.D. JEFFREYL.MXLLER,M.D. LESLIEI.ROSE,M.D. Hahnemann University School of Medicine Philadelphia, Pennsylvania

l.Aron DC. Endocrine complications of the acquired immunodeficiency syndrome. Arch Intern Med 1989; 149: 330-3. 2. May ME, Carey RM. Rapid adrenocorticotropic hormone test in practice: retrospective review. Am J Med 1985; 79: 679-&o. 3. Hagg E, Asplund K. Lithner F. Value of basal plasma cortisol assays in the assessment of pituitaryadrenal insufficiency. Clin Endocrinol 1987; 26:

221-6. Submitted March 11,1991,

and accepted in revised form April 15, 1991

HEMORRHAGICBURSITIS COMPLICATINGTREATMENT WITH RECOMBINANTTISSUE PLASMINOGENACTIVATOR Recombinant tissue plasminogen activator (rt-PA) was developed with the hope of decreasing systemic fibrinolysis and secondary hemorrhagic complications while preserving the ability to lyse intracoronary thrombi in the setting of acute myocardial infarction [ 11. Although rt-PA has been

Pericardial effusion as a manifestation of giant cell arteritis.

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