CORRESPONDENCE
Second, absence of MA1 in the affected joint of Maricic and Alepa’s patient was confirmed merely by synovial fluid culture. Although results of synovial fluid culture are positive in approximately 80% of cases of tuberculous arthritis [5,9], data on nontuberculous mycobacteriosis are not as abundant. A diagnosis of nontuberculous mycobacterial septic arthritis or periarthritis was eventually established in 39 of 46 cases (85%) by surgically excised tissue. In only 15% was a diagnosis made by culture of joint or bursal fluid [lo]. I agree with Messner [ll] that the quickest and the most reliable method of diagnosis of mycobacterial arthritis is biopsy. I think that we need to know whether results of biopsy and culture of synovial tissue were also negative in Maricic and Alepa’s patient. Apart from this, Borrelia burgdorferi-an offending microorganism of Lyme disease-has recently been demonstrated in the synovial fluid of a patient with Lyme arthritis [El. The possibility exists that MA1 might have been identified in the patient described by Maritic and Alepa. Third, the authors state that the patient was a normal host. However, I suspect that she had an underlying illness, namely another form of arthritis such as a connective tissue disease, because she had Raynaud’s phenomenon and livedo reticularis. Mycobacterial arthritis might coexist with rheumatoid arthritis and systemic lupus erythematosus [5,10]. Last, in agreement with Poncet, I would like to recommend the term “nontuberculous mycobacterial rheumatism” rather than “reactive arthritis after MA1 infection.” HIDETO
Keio University
School
AKAMA,
M.D.
of Medicine
Tokyo,
Japan
1. Tsukamura
M, Kita N, Shimoide H, et al. Studies on the nontuberculous lung mycobacteriosis in Japan (report of the study in the year 1986 of the
136
January
1991
The American
Journal
Mycobacteriosis Research Group of the Japanese National Chest Hospitals)., [Abstract in English.] Kekkaku 1988; 63: 493-9. 2. lsaacs AJ. Sturrock RD. Poncet’s disease-fact or fiction? A re-appraisal of tuberculous rheumatism. Tubercle 1974; 55: 135-42. 3. Ford OK. Reiter’s syndrome: reactive arthritis. In: McCarty DJ, ed. Arthritis and allied conditions. 11th ed. Philadelphia: Lea & Febiger, 1989: 944-53. 4. Kolstoe J, Messner RP. Lyme disease: musculoskeletal manifestations. Rheum Dis Clin North Am
1989;15:649-56. 5. Berney S. Goldstein M, Bishko F. Clinical and diagnostic features of tuberculous arthritis. Am J Med
1972;53:36-42. 6. Cheatum DE, Hudman V, Jones SR. Chronic arthritis due to Mycobacterium infracellulare. Arthritis Rheum 1976; 19: 777-81. 7. Marchevsky AM, Damsker B, Green S, Tepper S. The clinicopathological spectrum of non-tuberculous mycobacterial osteoarticular infections. J Bone Joint Surg [Am] 1985; 67: 925-9. 8. Halleran WJ, Martin NL. Nontuberculous mycobacterial arthritis: report of a chronic case. J Kans Med Sot 1982; 83: 284-6. 9. Wallace R. Cohen AS. Tuberculous arthritis: a report of two cases with review of biopsy and synovial fluid findings. Am J Med 1976; 61: 277-82. 10. Hoffman GS, Myers RL. Stark FR, Thoen CO. Septic arthritis associated with Mycobacterium avium: a case report and literature review. J Rheumatol 1978; 5: 199-209. 11. Messner RP. Arthritis due to mycobacteria, fungi, and parasites. In: McCarty DJ. ed. Arthritis and allied conditions-textbook of rheumatology. 1 Ith ed. Philadelphia: Lea & Febiger, 1989: 1925-37. 12. Snydman DR, Schenkein DP. Berardi VP, Lastavita CC, Pariser KM. Borrelia burgdorferi in joint fluid in chronic Lyme arthritis. Ann Intern Med 1986; 104: 798-800. Submitted
June 15.1990,
and accepted
August 28, 1990
The Reply:
I would like to respond to the questions raised by Dr. Akama concerning the patient reported with reactive arthritis following MA1 infection. Although no biopsy or synovial culture of the joint was undertaken to definitively exclude direct infection, the fact that the joint inflammation completely disappeared after 1 week and remained so without administration of anti-inflammatory agents and well before antituberculous therapy was begun argued clinically against a direct infection. Therefore, no biopsy was done. Dr. Akama questions whether the patient had another form of arthritis or underlying connective tissue disease because she had Raynaud’s phenomenon and of Medicine
Volume
90
livedo reticularis. The patient has now been followed for 2 years with no evidence of other disease. His comment that most types of reactive arthritis are polyarticular may be true, but the dogmatic position he takes equating reactive arthritis with polyarthritis and infectious arthritis with monoarthritis is fallacious. There is no question that reactive arthritis including Reiter’s syndrome and Lyme disease may be monoarticular. Finally, with regard to his suggestion that this condition be called “nontuberculous mycobacterial rheumatism,” I fail to see how the term “rheumatism” is more clinically useful than “reactive arthritis.” J. MARICIC? M.D. University of Amona Tucson, Arizona
MICHAEL
USE OF /?-BLOCKERSIN THYROTOXICPATIENTS WITH HEART FAILURE To the Editor:
In their recent articles examining the relationship between the thyroid and the cardiovascular system, Levey and Klein (Am J Med 1990; 88: 642-6) as well as Ladenson (Am J Med 1990; 88: 638-41) propose that judicious use of /?blockers in thyrotoxic patients with heart failure may be beneficial, particularly in controlling rapid heart rate and tachyarrhythmias. However, the large potential risk associated with such use of P-blockers is illustrated by the findings of Ikram [1,2], who administered 2 mg of propranolol intravenously to seven thyrotoxic patients with heart failure and no underlying cause of heart disease other than the thyrotoxicosis itself. In these patients, administration of the pblocker caused the mean right atria1 pressure to increase from 11.9 to 20.6 mm Hg and the mean pulmonary artery diastolic pressure to rise from 13.6 to 28.2 mm
CORRESPONDENCE
Hg. If such dramatic increases in pulmonary artery diastolic pressure are reflective of similar changes in pulmonary capillary and venous pressures, as is usually the case, then severe pulmonary vascular congestion and pulmonary edema become likely. Consequently, Ladenson’s (Am J Med 1990; 88: 638-41) suggestion that hemodynamic monitoring during administration of pblockers in thyrotoxic patients with heart failure is “ideal” might well be amended to “essential,” and P-blockers should probably be employed in this circumstance only with great reluctance. ALLAN R. GLASS,M.D. Walter Reed Army Medical Center Washington, D.C. 1. lkram H. Haemodynamic effects of beta-adrenergic blockade in hyperthyroid patients with and without heart failure. Br Med J 1977; 1: 1505-7. 2. lkram H. The nature and prognosis of thyrotoxic heart disease. Q J Med 1985; 54: 19-28. Submitted
July 6. 1990, and accepted
August 28, 1990 (NOTE: The opinions and assertions stated herein are the private views of the author and are not to be construed as official or as reflecting the crews of the Department of the Army or the Department of Defense.)
The Reply:
The cardiovascular hemodynamits of patients with hyperthyroidism have been reviewed in the report by Klein (Am J Med 1990; 88: 631-7) that accompanied the articles referred to by Dr. Glass. The decision to use ,&adrenergic blocking agents in hyperthyroid patients must balance the potential benefit of increased diastolic filling and stroke volume against the risk of decreasing ventricular contractility. When signs of cardiac decompensation (failure) are related to exaggerated sinus tachyarrhythmias or atria1 fibrillation, the therapeutic index for this form of treatment is most often favorable. The report of Ikram (Dr. Glass’s reference 2) described a group of elderly patients without significant tachycardia, a subset of patients in whom no benefit from pro-
pranolol would have been anticipated and in whom an above-average risk for treatment was predictable. Furthermore, 2 mg of propranolol was administered by a right-heart catheter in that study. Under more common clinical circumstances (e.g., severely tachycardic patients with no reason to suspect intrinsic myocardial disease), ,&adrenergic blockade remains an important therapeutic option. For patients with unstable cardiovascular hemodynamics, oral or low-dose (1 mg) intravenous propranolol should be employed, as emphasized in our article, only under vigilant observation, which may require invasive hemodynamic monitoring. In future, short-acting P-adrenergic blockers, such as esmolol, should be evaluated as potentially superior agents for therapeutic trials in patients in whom the benefit-risk ratio is difficult to predict. GERALDS. LEVEY, M.D. Pittsburgh School of Medicine Pittsburgh, Pennsylvania IRWIN KLEIN, M.D. New York, New York PAUL ~.LADENSON,M.D. The Johns Hopkins Hospital Baltimore, Maryland
University
of
PHEOCHROMOCYTOMAIN A PATIENT WITH HYPERTHYROXINEMIA To the Editor:
Drs. Blodgett and Reasner (Am J Med 1990; 88: 302-3) recently reported a patient with a pheochromocytoma who presented with a hypermetabolic state, goiter, and elevated values on thyroid function studies; a hypertensive crisis following administration of a pblocker led to discovery of the pheochromocytoma. The authors presented convincing evidence that the hyperthyroxinemia was caused by the pheochromocytoma, and documented normalizaJanuary
1991
The American
tion of results of thyroid studies after appropriate management of the pheochromocytoma. The authors’ patient is very similar to a patient I saw several years ago (Ober KP: Hyperthyroidism or pheochromocytoma? NC Med J 1983; 44: 285-6), and in many ways supports their finding and interpretations. My patient was a 20-year-old woman who presented at 25 weeks of pregnancy with a 4.5kg weight loss, tachycardia, diaphoresis, goiter, and lid lag. Although she had a low triiodothyronine resin uptake, consistent with her pregnancy, of 28% (normal: 30% to 40%), she had a disproportionately elevated total thyroxine (T4) level of 30.0 pg/dL (normal: 4.5 to 11.5 pg/dL), with a free Tq index of 8.5 (normal: 1.7 to 4.7). A free T4 measurement was elevated at 3.3 ng/dL (normal: 0.8 to 2.3 ng/ dL). After P-blocker therapy with propranolol, she became acutely diaphoretic, developed a blood pressure of 300/180 mm Hg and a temperature of 41.1*C (106”F), had a tonic-clonic seizure, and developed ventricular tachycardia. Similar to the experience of Blodgett and Reasner, this led to evaluation for pheochromocytoma, with studies revealing the following values: urinary vanillylmandelic acid, 86 mg/24 hours (normal: 1 to 8 mg/24 hours), urine catecholamines 3,016 pg/24 hours (normal: 0 to 230 pg/24 hours), plasma dopamine 164 pg/ mL (normal: 0 to 90 pg/mL), epinephrine 203 pg/mL (normal: 0 to 55 pg/mL), and plasma norepinephrine 1,385 pg/mL (normal: 65 to 320 pg/mL). Computed tomography of the abdomen revealed a large adrenal mass. After resection of the pheochromocytoma, the patient had normal urinary catecholamines (107 pg/24 hours) and normal free Tq (1.3 ng/dL). I had theorized that my patient’s hyperthyroxinemia was most likely caused by either a Journal
of Medicine
Volume
90
137
Second, absence of MA1 in the affected joint of Maricic and Alepa’s patient was confirmed merely by synovial fluid culture. Although results of synovial fluid culture are positive in approximately 80% of cases of tuberculous arthritis [5,9], data on nontuberculous mycobacteriosis are not as abundant. A diagnosis of nontuberculous mycobacterial septic arthritis or periarthritis was eventually established in 39 of 46 cases (85%) by surgically excised tissue. In only 15% was a diagnosis made by culture of joint or bursal fluid [lo]. I agree with Messner [ll] that the quickest and the most reliable method of diagnosis of mycobacterial arthritis is biopsy. I think that we need to know whether results of biopsy and culture of synovial tissue were also negative in Maricic and Alepa’s patient. Apart from this, Borrelia burgdorferi-an offending microorganism of Lyme disease-has recently been demonstrated in the synovial fluid of a patient with Lyme arthritis [El. The possibility exists that MA1 might have been identified in the patient described by Maritic and Alepa. Third, the authors state that the patient was a normal host. However, I suspect that she had an underlying illness, namely another form of arthritis such as a connective tissue disease, because she had Raynaud’s phenomenon and livedo reticularis. Mycobacterial arthritis might coexist with rheumatoid arthritis and systemic lupus erythematosus [5,10]. Last, in agreement with Poncet, I would like to recommend the term “nontuberculous mycobacterial rheumatism” rather than “reactive arthritis after MA1 infection.” HIDETO
Keio University
School
AKAMA,
M.D.
of Medicine
Tokyo,
Japan
1. Tsukamura
M, Kita N, Shimoide H, et al. Studies on the nontuberculous lung mycobacteriosis in Japan (report of the study in the year 1986 of the
136
January
1991
The American
Journal
Mycobacteriosis Research Group of the Japanese National Chest Hospitals)., [Abstract in English.] Kekkaku 1988; 63: 493-9. 2. lsaacs AJ. Sturrock RD. Poncet’s disease-fact or fiction? A re-appraisal of tuberculous rheumatism. Tubercle 1974; 55: 135-42. 3. Ford OK. Reiter’s syndrome: reactive arthritis. In: McCarty DJ, ed. Arthritis and allied conditions. 11th ed. Philadelphia: Lea & Febiger, 1989: 944-53. 4. Kolstoe J, Messner RP. Lyme disease: musculoskeletal manifestations. Rheum Dis Clin North Am
1989;15:649-56. 5. Berney S. Goldstein M, Bishko F. Clinical and diagnostic features of tuberculous arthritis. Am J Med
1972;53:36-42. 6. Cheatum DE, Hudman V, Jones SR. Chronic arthritis due to Mycobacterium infracellulare. Arthritis Rheum 1976; 19: 777-81. 7. Marchevsky AM, Damsker B, Green S, Tepper S. The clinicopathological spectrum of non-tuberculous mycobacterial osteoarticular infections. J Bone Joint Surg [Am] 1985; 67: 925-9. 8. Halleran WJ, Martin NL. Nontuberculous mycobacterial arthritis: report of a chronic case. J Kans Med Sot 1982; 83: 284-6. 9. Wallace R. Cohen AS. Tuberculous arthritis: a report of two cases with review of biopsy and synovial fluid findings. Am J Med 1976; 61: 277-82. 10. Hoffman GS, Myers RL. Stark FR, Thoen CO. Septic arthritis associated with Mycobacterium avium: a case report and literature review. J Rheumatol 1978; 5: 199-209. 11. Messner RP. Arthritis due to mycobacteria, fungi, and parasites. In: McCarty DJ. ed. Arthritis and allied conditions-textbook of rheumatology. 1 Ith ed. Philadelphia: Lea & Febiger, 1989: 1925-37. 12. Snydman DR, Schenkein DP. Berardi VP, Lastavita CC, Pariser KM. Borrelia burgdorferi in joint fluid in chronic Lyme arthritis. Ann Intern Med 1986; 104: 798-800. Submitted
June 15.1990,
and accepted
August 28, 1990
The Reply:
I would like to respond to the questions raised by Dr. Akama concerning the patient reported with reactive arthritis following MA1 infection. Although no biopsy or synovial culture of the joint was undertaken to definitively exclude direct infection, the fact that the joint inflammation completely disappeared after 1 week and remained so without administration of anti-inflammatory agents and well before antituberculous therapy was begun argued clinically against a direct infection. Therefore, no biopsy was done. Dr. Akama questions whether the patient had another form of arthritis or underlying connective tissue disease because she had Raynaud’s phenomenon and of Medicine
Volume
90
livedo reticularis. The patient has now been followed for 2 years with no evidence of other disease. His comment that most types of reactive arthritis are polyarticular may be true, but the dogmatic position he takes equating reactive arthritis with polyarthritis and infectious arthritis with monoarthritis is fallacious. There is no question that reactive arthritis including Reiter’s syndrome and Lyme disease may be monoarticular. Finally, with regard to his suggestion that this condition be called “nontuberculous mycobacterial rheumatism,” I fail to see how the term “rheumatism” is more clinically useful than “reactive arthritis.” J. MARICIC? M.D. University of Amona Tucson, Arizona
MICHAEL
USE OF /?-BLOCKERSIN THYROTOXICPATIENTS WITH HEART FAILURE To the Editor:
In their recent articles examining the relationship between the thyroid and the cardiovascular system, Levey and Klein (Am J Med 1990; 88: 642-6) as well as Ladenson (Am J Med 1990; 88: 638-41) propose that judicious use of /?blockers in thyrotoxic patients with heart failure may be beneficial, particularly in controlling rapid heart rate and tachyarrhythmias. However, the large potential risk associated with such use of P-blockers is illustrated by the findings of Ikram [1,2], who administered 2 mg of propranolol intravenously to seven thyrotoxic patients with heart failure and no underlying cause of heart disease other than the thyrotoxicosis itself. In these patients, administration of the pblocker caused the mean right atria1 pressure to increase from 11.9 to 20.6 mm Hg and the mean pulmonary artery diastolic pressure to rise from 13.6 to 28.2 mm
CORRESPONDENCE
Hg. If such dramatic increases in pulmonary artery diastolic pressure are reflective of similar changes in pulmonary capillary and venous pressures, as is usually the case, then severe pulmonary vascular congestion and pulmonary edema become likely. Consequently, Ladenson’s (Am J Med 1990; 88: 638-41) suggestion that hemodynamic monitoring during administration of pblockers in thyrotoxic patients with heart failure is “ideal” might well be amended to “essential,” and P-blockers should probably be employed in this circumstance only with great reluctance. ALLAN R. GLASS,M.D. Walter Reed Army Medical Center Washington, D.C. 1. lkram H. Haemodynamic effects of beta-adrenergic blockade in hyperthyroid patients with and without heart failure. Br Med J 1977; 1: 1505-7. 2. lkram H. The nature and prognosis of thyrotoxic heart disease. Q J Med 1985; 54: 19-28. Submitted
July 6. 1990, and accepted
August 28, 1990 (NOTE: The opinions and assertions stated herein are the private views of the author and are not to be construed as official or as reflecting the crews of the Department of the Army or the Department of Defense.)
The Reply:
The cardiovascular hemodynamits of patients with hyperthyroidism have been reviewed in the report by Klein (Am J Med 1990; 88: 631-7) that accompanied the articles referred to by Dr. Glass. The decision to use ,&adrenergic blocking agents in hyperthyroid patients must balance the potential benefit of increased diastolic filling and stroke volume against the risk of decreasing ventricular contractility. When signs of cardiac decompensation (failure) are related to exaggerated sinus tachyarrhythmias or atria1 fibrillation, the therapeutic index for this form of treatment is most often favorable. The report of Ikram (Dr. Glass’s reference 2) described a group of elderly patients without significant tachycardia, a subset of patients in whom no benefit from pro-
pranolol would have been anticipated and in whom an above-average risk for treatment was predictable. Furthermore, 2 mg of propranolol was administered by a right-heart catheter in that study. Under more common clinical circumstances (e.g., severely tachycardic patients with no reason to suspect intrinsic myocardial disease), ,&adrenergic blockade remains an important therapeutic option. For patients with unstable cardiovascular hemodynamics, oral or low-dose (1 mg) intravenous propranolol should be employed, as emphasized in our article, only under vigilant observation, which may require invasive hemodynamic monitoring. In future, short-acting P-adrenergic blockers, such as esmolol, should be evaluated as potentially superior agents for therapeutic trials in patients in whom the benefit-risk ratio is difficult to predict. GERALDS. LEVEY, M.D. Pittsburgh School of Medicine Pittsburgh, Pennsylvania IRWIN KLEIN, M.D. New York, New York PAUL ~.LADENSON,M.D. The Johns Hopkins Hospital Baltimore, Maryland
University
of
PHEOCHROMOCYTOMAIN A PATIENT WITH HYPERTHYROXINEMIA To the Editor:
Drs. Blodgett and Reasner (Am J Med 1990; 88: 302-3) recently reported a patient with a pheochromocytoma who presented with a hypermetabolic state, goiter, and elevated values on thyroid function studies; a hypertensive crisis following administration of a pblocker led to discovery of the pheochromocytoma. The authors presented convincing evidence that the hyperthyroxinemia was caused by the pheochromocytoma, and documented normalizaJanuary
1991
The American
tion of results of thyroid studies after appropriate management of the pheochromocytoma. The authors’ patient is very similar to a patient I saw several years ago (Ober KP: Hyperthyroidism or pheochromocytoma? NC Med J 1983; 44: 285-6), and in many ways supports their finding and interpretations. My patient was a 20-year-old woman who presented at 25 weeks of pregnancy with a 4.5kg weight loss, tachycardia, diaphoresis, goiter, and lid lag. Although she had a low triiodothyronine resin uptake, consistent with her pregnancy, of 28% (normal: 30% to 40%), she had a disproportionately elevated total thyroxine (T4) level of 30.0 pg/dL (normal: 4.5 to 11.5 pg/dL), with a free Tq index of 8.5 (normal: 1.7 to 4.7). A free T4 measurement was elevated at 3.3 ng/dL (normal: 0.8 to 2.3 ng/ dL). After P-blocker therapy with propranolol, she became acutely diaphoretic, developed a blood pressure of 300/180 mm Hg and a temperature of 41.1*C (106”F), had a tonic-clonic seizure, and developed ventricular tachycardia. Similar to the experience of Blodgett and Reasner, this led to evaluation for pheochromocytoma, with studies revealing the following values: urinary vanillylmandelic acid, 86 mg/24 hours (normal: 1 to 8 mg/24 hours), urine catecholamines 3,016 pg/24 hours (normal: 0 to 230 pg/24 hours), plasma dopamine 164 pg/ mL (normal: 0 to 90 pg/mL), epinephrine 203 pg/mL (normal: 0 to 55 pg/mL), and plasma norepinephrine 1,385 pg/mL (normal: 65 to 320 pg/mL). Computed tomography of the abdomen revealed a large adrenal mass. After resection of the pheochromocytoma, the patient had normal urinary catecholamines (107 pg/24 hours) and normal free Tq (1.3 ng/dL). I had theorized that my patient’s hyperthyroxinemia was most likely caused by either a Journal
of Medicine
Volume
90
137
