-
CORRESPONDENCE
CALCIFICATIONOF VASCULAR sponsiveness a characteristic feature of this condition [1,2]. In LESIONSIN TAKAYASU’S general, an improvement in conDISEASE To the Editor: In the article by Ninet et al (Am J Med 1990; 88: 13-20) on subclavian and axillary involvement in temporal arteritis and polymyalgia rheumatica, a statement was made that lack of calcification in their patients’ vascular lesions favored an inflammatory process rather than atheromatous plaque. Although I agree with this, I and my colleagues have previously published a case report (Mengis CL, Dubilier W, Barry KG. The aortic arch syndrome of Takayasu. Am Heart J 1958; 55: 435-42) of a young woman with Takayasu’s disease, a condition with similar microscopic features, that shows that the lesions can also calcify, even in young patients. Veterans
CHRIS L. MENGIS, M.D. Administration M;fed;;: Walla
Submitted
February
Walla, Washington 16, 1990, and accepted
March 6, 1990
TREATMENT OF SWEET’S SYNDROME
To the Editor: The discussion in the clinicopathologic conference on Sweet’s syndrome (Am J Med 1989; 87: 671-6) contained an erroneous statement with respect to the therapy of Sweet’s syndrome; specifically, it was stated that “since this [oral potassium iodide] is a relatively benign treatment, it is certainly the drug of choice.” Actually, the vast majority of patients with Sweet’s syndrome reported in the literature have been treated with oral corticosteroids, and the near-universal success of this modality has virtually made corticosteroid re396
September
1990
The American
Journal
stitutional symptoms is noted within hours after the first dose, and resolution of skin lesions begins within 1 to 2 days [1,3]. Oral corticosteroid therapy is therefore considered the therapeutic gold standard for both idiopathic and malignancy-associated Sweet’s syndrome [3,4]. Also, it is important for physicians requesting dermatologic consultation regarding the management of these patients to realize that corticosteroids are usually recommended as the treatment of choice. To the best of our knowledge, only a small number of individuals with Sweet’s syndrome have been reported who were successfully treated with potassium iodide [5-71. Further, although side effects are infrequent, administration of this compound is not without the risk of drug-related toxicity. In particular, potassium iodide can produce adverse cutaneous and systemic reactions: acne, eczematous eruptions, erythema nodosum, urticaria, angioedema, iododerma, purpura, vasculitis, fever, polymyalgias, pulmonary infiltrations, periarteritis nodosa, hypothyroidism (Wolff-Chaikoff effect), and exacerbation of dermatitis herpetiformis [8-10]. Because of the limited experience with potassium iodide in treating patients with Sweet’s syndrome, it is perhaps most appropriate for this agent to be considered as a corticosteroid-sparing therapeutic modality and/or as an alternative therapy for those individuals in whom systemic corticosteroids are contraindicated. PHILIP R. COHEN, M.D. Dermatology Clinic Pasadena, Texas RAZELLEKURZROCK,M.D.
Pasadena
of Medicine
Volume
89
University of Texas M.D. Anderson Cancer Center Houston, Texas 1. Cohen PR, Kurzrock R. Sweet’s syndrome and malignancy. Am J Med 1987; 82: 1220-6. P.Cohen PR, Kurzrock R. Chronic myelogenous leukemia and Sweet syndrome. Am J Hematol 1989; 32: 134-7. 3. Cohen PR, Almeida L. Kurzrock R. Acute febrile neutrophilic dermatosis. Am Fam Physician 1989; 39: 199-204. 4. Cohen PR, Talpaz M. Kurzrock R. Malignancyassociated Sweet’s syndrome: review of the world literature. J Clin Oncol 1988; 6: 1887-97. 5. Horio T, lmamura S. Danno K. Furukawa F, Ofuji S. Treatment of acute febrile neutrophilic dermatosis (Sweets syndrome) with potassium iodide. Dermatologica 1980; 160: 341-7. 6. Horio T. Danno K. Okamoto H, Miyachi Y, Imamura S. Potassium iodide in erythema nodosum and other erythematous dermatoses. J Am Acad Dermatol 1983; 9: 77-81. 7. Myatt AE. Baker DJ, Byfield DM. Sweet’s
syn-
drome: a report on the use of potassium iodide. Clin Exp Dermatol 1987; 12: 345-9. 8. Bruinsma W. A guide to drug eruptions: the file of side effects to the skin (1982-1987). The File of Medicines, Oosthuizen. The Netherlands, 1987: 79. 9. Curd JG. Milgrom H, Stevenson DD. Mathison DA, Vaughan JH. Potassium iodide sensitivity in four patients with hypocomplementemic vasculitis. Ann Intern Med 1979: 91: 853-7. 10. Johnson TM, Rapini RP. The Wolff-Chaikoff effect: hypothyroidism due to potassium iodide. Arch Dermatol 1988; 124: 1184-5. Submitted
January 12,1990,
and accepted
May 31, 1990
DIAGNOSISOF DEEPVEIN THROMBOSISON THE BASIS OF CLINICAL FINDINGS To the Editor: I read with interest the article by Landefeld et al (Am J Med 1990; 88: 382-8) on acute proximal deep vein thrombosis (DVT). This excellent clinical study somewhat supports the clinical dictum that the diagnosis of acute DVT made on the basis of symptoms and physical findings is notoriously inaccurate. There is, however, some hope that this situation can improve. Clinical experience suggests that if the symptoms involve the left lower extremity they are more likely to be diagnostic of true DVT than if the symptoms involve the right
CORRESPONDENCE
CALCIFICATIONOF VASCULAR sponsiveness a characteristic feature of this condition [1,2]. In LESIONSIN TAKAYASU’S general, an improvement in conDISEASE To the Editor: In the article by Ninet et al (Am J Med 1990; 88: 13-20) on subclavian and axillary involvement in temporal arteritis and polymyalgia rheumatica, a statement was made that lack of calcification in their patients’ vascular lesions favored an inflammatory process rather than atheromatous plaque. Although I agree with this, I and my colleagues have previously published a case report (Mengis CL, Dubilier W, Barry KG. The aortic arch syndrome of Takayasu. Am Heart J 1958; 55: 435-42) of a young woman with Takayasu’s disease, a condition with similar microscopic features, that shows that the lesions can also calcify, even in young patients. Veterans
CHRIS L. MENGIS, M.D. Administration M;fed;;: Walla
Submitted
February
Walla, Washington 16, 1990, and accepted
March 6, 1990
TREATMENT OF SWEET’S SYNDROME
To the Editor: The discussion in the clinicopathologic conference on Sweet’s syndrome (Am J Med 1989; 87: 671-6) contained an erroneous statement with respect to the therapy of Sweet’s syndrome; specifically, it was stated that “since this [oral potassium iodide] is a relatively benign treatment, it is certainly the drug of choice.” Actually, the vast majority of patients with Sweet’s syndrome reported in the literature have been treated with oral corticosteroids, and the near-universal success of this modality has virtually made corticosteroid re396
September
1990
The American
Journal
stitutional symptoms is noted within hours after the first dose, and resolution of skin lesions begins within 1 to 2 days [1,3]. Oral corticosteroid therapy is therefore considered the therapeutic gold standard for both idiopathic and malignancy-associated Sweet’s syndrome [3,4]. Also, it is important for physicians requesting dermatologic consultation regarding the management of these patients to realize that corticosteroids are usually recommended as the treatment of choice. To the best of our knowledge, only a small number of individuals with Sweet’s syndrome have been reported who were successfully treated with potassium iodide [5-71. Further, although side effects are infrequent, administration of this compound is not without the risk of drug-related toxicity. In particular, potassium iodide can produce adverse cutaneous and systemic reactions: acne, eczematous eruptions, erythema nodosum, urticaria, angioedema, iododerma, purpura, vasculitis, fever, polymyalgias, pulmonary infiltrations, periarteritis nodosa, hypothyroidism (Wolff-Chaikoff effect), and exacerbation of dermatitis herpetiformis [8-10]. Because of the limited experience with potassium iodide in treating patients with Sweet’s syndrome, it is perhaps most appropriate for this agent to be considered as a corticosteroid-sparing therapeutic modality and/or as an alternative therapy for those individuals in whom systemic corticosteroids are contraindicated. PHILIP R. COHEN, M.D. Dermatology Clinic Pasadena, Texas RAZELLEKURZROCK,M.D.
Pasadena
of Medicine
Volume
89
University of Texas M.D. Anderson Cancer Center Houston, Texas 1. Cohen PR, Kurzrock R. Sweet’s syndrome and malignancy. Am J Med 1987; 82: 1220-6. P.Cohen PR, Kurzrock R. Chronic myelogenous leukemia and Sweet syndrome. Am J Hematol 1989; 32: 134-7. 3. Cohen PR, Almeida L. Kurzrock R. Acute febrile neutrophilic dermatosis. Am Fam Physician 1989; 39: 199-204. 4. Cohen PR, Talpaz M. Kurzrock R. Malignancyassociated Sweet’s syndrome: review of the world literature. J Clin Oncol 1988; 6: 1887-97. 5. Horio T, lmamura S. Danno K. Furukawa F, Ofuji S. Treatment of acute febrile neutrophilic dermatosis (Sweets syndrome) with potassium iodide. Dermatologica 1980; 160: 341-7. 6. Horio T. Danno K. Okamoto H, Miyachi Y, Imamura S. Potassium iodide in erythema nodosum and other erythematous dermatoses. J Am Acad Dermatol 1983; 9: 77-81. 7. Myatt AE. Baker DJ, Byfield DM. Sweet’s
syn-
drome: a report on the use of potassium iodide. Clin Exp Dermatol 1987; 12: 345-9. 8. Bruinsma W. A guide to drug eruptions: the file of side effects to the skin (1982-1987). The File of Medicines, Oosthuizen. The Netherlands, 1987: 79. 9. Curd JG. Milgrom H, Stevenson DD. Mathison DA, Vaughan JH. Potassium iodide sensitivity in four patients with hypocomplementemic vasculitis. Ann Intern Med 1979: 91: 853-7. 10. Johnson TM, Rapini RP. The Wolff-Chaikoff effect: hypothyroidism due to potassium iodide. Arch Dermatol 1988; 124: 1184-5. Submitted
January 12,1990,
and accepted
May 31, 1990
DIAGNOSISOF DEEPVEIN THROMBOSISON THE BASIS OF CLINICAL FINDINGS To the Editor: I read with interest the article by Landefeld et al (Am J Med 1990; 88: 382-8) on acute proximal deep vein thrombosis (DVT). This excellent clinical study somewhat supports the clinical dictum that the diagnosis of acute DVT made on the basis of symptoms and physical findings is notoriously inaccurate. There is, however, some hope that this situation can improve. Clinical experience suggests that if the symptoms involve the left lower extremity they are more likely to be diagnostic of true DVT than if the symptoms involve the right
