79
Infectious Diseases Newsletter 5(10) October 1986 Table 1. Time Course of Counts of Formed Elements in the Peripheral Blood. Date
Lcukocytes per ul
07/31 08/ 01 08/ 01 08/02 08/ 03 08/03 08/04 08/04 08/ 05
4,100
Neutrophils Mature Band 72% 24% 35% 20%
23% 44% 26% 53%
2,500
24%
3,700 5,600 4,100 4,700
35% 44% 53% 29%
2,200
1,600 2,200
Comment
A pancytopenia with fever coming on about 10 days after commencing therapy with T M P - S M X , without other apparent cause, was highly suggestive of adverse effect from the t h e r a p y - - a l m o s t surely due to the sulfamethoxazole. The timing was classic for both events with sulfonamides, as was resolution on withdrawal of the drug. While skin rash is said to be more frequent as an adverse reaction with T M P - S M X than with a sulfonamide given alone, there are no similar allegations regarding cytopenias or fever. The T M P may provoke adverse effects in persons deficient in f o l a t e - - n o t the case with our patient; moreover,
COMMENTS
Platelets (in thousands)
LymphocytesMonocytes Eosinophils Basophils Hematocrit 3% 25% 34% 26%
2%
0
0
40.3
6%
1%
0
34.1
129
3% 4%
1% 7%
1% 0
32.4 32.5
107 100
17%
50%
4%
4%
1%
34.1
122
14% 27% 18% 9%
43% 23% 23% 46%
5% 6% 5% 13%
2% 0 1% 3%
1% 0 0 0
36.4 35.3 35.6 37.2
164 155 149 179
megaloblastosis and thrombocytopenia are generally associated with the leukopenia. It is appropriate to note that the complaints that led to prescription of T M P - S M X were those of a lower urinary tract infection. Hence, it was inappropriate to have prescribed 10 days of therapy. Further, there has been good success from the use of T M P alone in the treatment of lower urinary tract infections, sparing the patient from exposure to S M X with its relatively greater potential for toxicity.
140
alone with trimethoprim-sulphamethoxazole in the treatment of respiratory and urinary infections with particular reference to selection of trimethoprim resistance. Lancet i: 1270-1273, 1980. Mandell GL, Sande MA: Sulfonamides, trimethoprim-sulfamethoxazole, and agents for urinary tract infections, AG Gilman, LS Goodman, TW Rail, F Murad (ed): The Pharmacological Basis of Therapeutics, 7th edition. New York, MacMillan, 1985, pp 1101-1102; 1106-1107. Ronald AR: Single dose treatment of urinary tract infection in females. Infect Dis Newsier 5:41-43, 1986. Paul D. Hoeprich, MD
Bibliography
Sacramento, California
Lacey RW, Lord VL, Gunasekera HK, et al: Comparison of trimethoprim
ON CURRENT PUBLICATIONS
Kato H. Ichinose E, Kawasaki N: Myocardial infarction in Kawasaki disease: Clinical analysis in 195 cases. J
Pediatr 108:923-927, 1986. Clinical data were analyzed from 195 children (141 males) with myocardial infarction complicalting Kawasaki disease. Infarctions usually occurred within the first year of illness; however, 27% had their infarcts more than one year after the initial illness. The myocardial infarctions were asymptomatic in 37% of the children. Death occurred during the first attack in 22%. In most of the fatal cases, obstruction in a coronary artery was found by coronary anglography. Although 43% of all survivors of the first or subsequent attacks were
well, the remainder were left with some kind of cardiac dysfunction. Comment
While it is known that the main cause of death in Kawasaki disease is myocardial infarction after thrombotic occulsion in a coronary aneurysm, it is said that deaths usually occurred within 60 days of illness. F r o m study of the largest number of Kawasaki patients with myocardial infarctions reported to date, Kato et al found that: 1) infarctions were evenly distributed throughout the first year after illness; and 2) infarction occurred in © 1986 Elsevier Science Publishing Co., Inc. 0278-2316/86/$0.00+ 2.20
asymptomatic children after an interval of several years in 25% of the children. Antithrombotic therapy, eg, with aspirin, is recommended to prevent any progresssion to ischemic heart disease (Pediatrics 63:175-179, 1979). More information is needed about the effect of treatment during the acute state of the disease on prevention of myocardial infarction. LKP D MMWR: Transfusion-associated human T-iymphotropic virus Type lll/lymphadenolmthy-associsted virus