Pericardial cryptococcal disease in acquired immune deficiency syndrome

LETTERS TO THE EDITOR al pulmonary complication. The authors concluded by comparing these lesions with similar lesions found in ankylosing spondylitis. I suggest that this conclusion is strengthened by a report of a finding commonly associated with ankylosing spondylitis, saprophytic Aspergillus mycetomata within such cavities, in a patient with rheumatoid arthritis (Petrie JP, Caughey DE: Bilateral apical fibrobullous disease complicated by bilateral Aspergillus mycetomata in rheumatoid arthritis. NZ Med J 1983; 96: 7-8).

PERICARDIAL CRYPTOCOCCAL DISEASE IN ACQUIRED IMMUNE DEFICIENCY SYNDROME To the Editor: In their review of infectious complications in the acquired immune deficiency syndrome (AIDS), Grant and Armstrong (Am J Med 1986; 81 [suppl IA]: 59-72) have summarized infectious regional diseases and their management. We strongly recommend evaluation for pleural and pericardial causes in disseminated cryptococcal disease. We have recently observed cardiac tamponade in a 27year-old African man with AIDS. The patient, who lived in Zaire, was admitted to our institution in October 1985, for disseminated cryptococcal disease. Treatment with amphotericin B and fluocytosine resulted in prompt clinical improvement, and weekly maintenance therapy with amphotericin B was proposed. However, the patient was lost to follow-up, and treatment was discontinued. After three months, the patient was readmitted for fever, dyspnea, and pericarditis. Surgical pericardial drainage was performed within 24 hours, in view of clinical and hemodynamic cardiac tamponade. Recurrence of cryptococcal disease was documented on bronchoalveolar washing (large number of fungi) and by a high cryptococcal antigen titer in the cerebrospinal fluid. Hence, combined therapy with amphotericin B and fluocytosine was reinitiated. The patient was discharged from the intensive care unit on the fifth day. Pericardial[I], pleural- [2], and peritoneal-related [2] cryptococcal diseases have already been reported. Although unusual, these manifestations should be kept in mind, since they are potentially life-threatening, albeit treatable by a specific regimen. F. BRIVET, J. LIVARTOWSKI, Ph. HERVE, B. RAIN, J. DORMONT,

J.P.

Submitted

DlLTlAZEM OPPOSING

2.

M.D. M.D. M.D. M.D. M.D.

Zuger A, Louie E, Holzman R, et al: Cryptococcal disease in patients with the acquired immunodeficiency syndrome. Ann Intern Med 1986; 104: 234-240. Perfect J, Durack D, Gallis H: Cryptococcemia. Medicine 1983; 82: 98-109. Submitted

January

27, 1987, and accepted

APICAL FIBROCAVITARY LESIONS IN RHEUMATOID ARTHRlTlS

March

F.R.A.C.P.

February

WITHDRAWAL ViEWPOINT

24, 1987, and accepted

SYNDROME:

March

3, 1987

AN

To the Editor: We wish to differ with the conclusion of Kozeny et al (Am J Med 1986; 80: 1184-I 186) in which they implicated a diltiazem withdrawal syndrome in the pathogenesis of acute myocardial infarction. They described a patient presenting with uremia, chest pain, and increased MB creatine phosphokinase levels who was treated with diltiazem and nitrates, and in whom MB creatine phosphokinase values were re-elevated when treatment was discontinued. We believe the use of such anecdotal evidence as support for withdrawal phenomena is fraught with many pitfalls: and controlled studies [ 1,2] to date have failed to demonstrate true diltiazem withdrawal. It is important to distinguish between true withdrawal phenomena (as have been described with propranolol [3,4]) and a simple return to the original pretreatment baseline or to a new baseline state in cases in which the underlying disease process has progressed. The terms “withdrawal” or “rebound” are often used interchangeably and usually imply the appearance of signs and symptoms qualitatively different from (withdrawal) or quantitatively in excess of (rebound) the original disease state once therapy is abruptly discontinued. For example, when insulin therapy is suddenly terminated in a patient with well-controlled insulin-dependent diabetes, the development of high blood glucose levels is an expected consequence of a return to the untreated state and is not regarded as evidence of “insulin withdrawal syndrome” or an “insulin rebound.” Similarly, it can be argued that the acute myocardial infarction (or ischemia leading to myocardial infarction) described by Kozeny et al was already in progress on admission, even before therapy with diltiazem and nitrate was initiated. The authors themselves acknowledged the probability of an ongoing, spasm-related ischemic process or

Hopital Antoine B&l&e 92141 Clamart, France 1.

PETRIE,

Queen Elizabeth Hospital P.O. Box 1342 Rotorua, New Zealand

3, 1987

OF THE LUNG

To the Editor: The recent article reviewing apical fibrocavitary lesions of the lung in rheumatoid arthritis (Am J Med 1986; 81: 741-746) presents most of the pertinent data on this unusu-

June

1987

The American

Journal

of Medicine

Volume

82

1273