Reference intervals for serum granulocyte colony-stimulating factor levels in children.

OBJECTIVE: To determine age-adjusted reference intervals for children for serum granulocyte colony-stimulating factor (G-CSF) levels. DESIGN: We determined the serum G-CSF levels of 168 disease-free children who were term neonates to 15 years of age with a highly sensitive chemiluminescent enzyme immunoassay. RESULTS: The lowest values (5 ng/L) exceeded the detectable limit (1 ng/L) of this assay technique. The G-CSF levels were highest on the day of birth (mean +/- SD 147 +/- 146 ng/L); thereafter values decreased to 46 +/- 33 ng/L in the early neonatal period and to 23 +/- 10 ng/L in the late neonatal period. The G-CSF levels both on the day of birth and in the early neonatal period were significantly higher than in all older age groups. No significant differences were found among any of the age groups after 4 weeks of age. The G-CSF values were correlated with both blood leukocyte counts (r = 0.496, p < 0.0001) and neutrophil counts (r = 0.547, p < 0.0001). In children older than 4 weeks of age (n = 128), the 95% reference interval for G-CSF values was 5 to 42 ng/L. CONCLUSIONS: Our study in disease-free children revealed that change in serum G-CSF levels are age dependent and are correlated with neutrophil counts. Determination of reference intervals for the neonatal period requires further study.

Internal potassium shift in premature infants: cause of nonoliguric hyperkalemia.

To study the pathophysiology of nonoliguric hyperkalemia, we measured serum potassium concentration and external K balance (intake and excretion), and estimated internal K balance (a shift from intracellular space to extracellular space) in 24 nonoliguric premature infants during the first 72 hours after birth. Data were analyzed from two aspects: gestational age (group 1, 24 to 28 weeks, n = 9; group 2, 29 to 32 weeks, n = 9; group 3, 33 to 36 weeks, n = 6) and postnatal age (0 to 72 hours). Serum K concentration rose from baseline (0 hour) to 24 hours in groups 1 and 2 (p < 0.01) but did not rise in group 3. The external K balance was negative in all groups during the study period, and was more negative in the more premature infants (group 1 > group 2 > group 3) during the second 24 hours. There was a significant difference (p < 0.01) between the internal K balance of the three groups during the first 24 hours (group 1 > group 2 > group 3), and the K shift decreased significantly (p < 0.05) during the study period in groups 1 and 2. The more premature the infants, the larger the K shift and the larger the rise in serum K concentration during the first 24 hours, and the more negative the external K balance after 24 hours. These data indicate that K loading caused by the K shift associated with prematurity produces a rapid rise in serum K concentration, resulting in an increase in urinary K excretion. We conclude that an internal K shift inversely proportional to gestational and postnatal age is the primary cause of nonoliguric hyperkalemia in very premature infants.

Classification of chronic granulomatous disease on the basis of monoclonal antibody-defined surface cytochrome b deficiency.

Flow cytometric quantitative analysis of cytochrome b on outer surface membrane and of oxidative product formation in polymorphonuclear leukocytes (PMNLs) from patients with chronic granulomatous disease was carried out with the use of monoclonal antibody against cytochrome b of human neutrophils and 2', 7'-dichlorofluorescin diacetate. Cytochrome b was present on the outer surface membrane of PMNLs in normal individuals, and its absence on the outer surface membrane was of value in the diagnosis and classification of chronic granulomatous disease. This study has shown that a major type of chronic granulomatous disease is one of the monoclonal antibody-defined surface membrane diseases.

Clinical characteristics of myocardial infarction following Kawasaki disease: report of 11 cases.

Between 1979 and 1984, 11 patients with myocardial infarction following Kawasaki disease were seen in our hospital. There were seven boys and four girls, aged from 3 months to 6 years. This cardiovascular complication developed in the early stage, from 19 days to 6 months of illness, in all but three patients. Significant clinical symptoms were recognized in only five patients. Two patients died, the conditions of two are well controlled with anticongestive therapy, and the remaining patients are asymptomatic. The diagnosis of myocardial infarction was confirmed by the following clinical findings: typical ECG patterns (10/11), abnormality of the left ventricular wall movement by serial two-dimensional echocardiography (9/10), elevated value of cardiac enzymes (6/6), perfusion defect by thallium 201 myocardial scintigraphy (6/8), and coronary artery occlusion or ventricular aneurysm by angiocardiography (9/9). All patients had markedly dilated and multiple coronary aneurysms during the course of the illness. Because myocardial infarction is frequently associated with the rapidly dilating coronary artery during the acute stage, ECG monitoring, preparation of resuscitation equipment, and use of antithrombotic agents are recommended for those high-risk patients. When a myocardial infarction has been diagnosed, measures including cardiac monitoring, use of vasodilators, inotropic agents, and urokinase may be valuable.

High incidence of aortic regurgitation following Kawasaki disease.

Among 131 patients with Kawasaki disease who underwent cardiac examinations from December 1979 to July 1984, six (4.6%) had aortic regurgitation documented on aortography. A protodiastolic murmur typical of aortic regurgitation was heard in four patients. Both cardiac enlargement on chest roentgenogram and ECG signs of left ventricular hypertrophy were demonstrated in only half of the patients. Of five patients who underwent a second angiographic study 1 year later, two no longer had aortic regurgitation; pulsed Doppled echocardiography at this point revealed aortic regurgitant flow in the remaining three patients. All patients had associated coronary artery aneurysms, and two patients developed subsequent myocardial infarction. The development of aortic regurgitation following Kawasaki disease has been considered to be causally related to the carditis that most frequently occurs during the acute stage of the illness. Our data indicate that aortic regurgitation is not rare but is an important additional cardiovascular complication of Kawasaki disease.