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False positive sweat test, malnutrition, and the Mauriac syndrome
24 0
Brief clinical and laboratory observations
show mild obstructive pulmonary disease with normal arterial blood gas values. For the past two years, the hematocrit has been stable at 24%, with a reticulocyte count of 7.0% and a total bilirubin concentration of 2.0 mg/dl. He had no hepatosplenomegaly, cardiomegaly, or hyposthenuria. He has had one mild lower respiratory infection and no sickle crises. SPECIAL STUDY Nine children with sickle cell disease, confirmed by hemoglobin electrophoresis, had sweat chloride determinations by the quantitative pilocarpine iontophoresis method? The mean sweat chloride concentration was 22 mEq/1 with a range of 4 to 43 mEq/l. DISCUSSION The diagnoses in these two children seem firmly established. Both have significantly elevated sweat chloride values. In addition, the presence of meconium ileus (Patient I) and chronic lung disease (Patient II), together with the absence of elevated sweat chloride concentrations in nine other black children with sickle cell disease, are confirmatory findings. Cystic fibrosis, the most frequently lethal genetic syndrome in white children, 2 is now being recognized with greater frequency in the black population. 3-~ The most widely accepted incidence figure is one in 17,033 live black births? Sickle cell disease is the most common genetic disease in American blacks, with an estimated incidence of one in 625 live births$ Assuming an independent autosomal recessive mode of inheritance, the proba-
The Journal of Pediatrics February 1979 bility of cystic fibrosis and sickle cell disease occurring in the same black child is one in 10,625,000 live black births. Although early reports suggested a similar course for cystic fibrosis in blacks and in whites, more recent experience suggests a more benign course for the pulmonary disease of black patients if they survive infancy? Whether the additional problem of sickle cell disease will modify the clinical course of these patients is unknown. Further study of these two unique patients may possibly reveal some abnormality that will improve the understanding of the pathogenesis of cystic fibrosis. REFERENCES
1. Gibson LE, and Cooke RE: A test for concentration of electrolytes in sweat in cystic fibrosis of the pancreas utilizing pilocarpine by iontophoresis, Pediatrics 23:545, 1959. 2. Steinberg AG, and Brown DC: On the incidence of cystic fibrosis of the pancreas, Am J Hum Genet 12:416, 1960. 3. Kulczycki LL, Guin GH, and Mann N: Cystic fibrosis in Negro children, Clin Pediatr 3:692, 1964. 4. Kulczycki LL, and Shauf V: Cystic fibrosis in blacks in Washington, D.C., Am J Dis Child 127:64, 1974. 5. Heifer ET: Cystic fibrosis in black population, NY State Med J 74:2355, 1974. 6. Sultz HA, Schlesinger ER, and Mosher WE: The Erie County survey of long-term childhood illness: II. Incidence and prevalence, Am J Public Health 58:491, 1968. 7. Wintrobe MM, Lee GR, Boggs DR, Bithell TC, Athens JW, and Foerster J: Clinical hematology, ed 7. Philadelphia, 1974, Lea & Febiger, p 823.
False positive sweat test, malnutrition, and the Mauriac syndrome Robert Rosenfeld, M.D.,* Linda Spigelblatt, M.D., and Raymond Chicoine, M.D.,
Montreal, P.Q., Canada
AN ELEVATED SWEAT CHLORIDE LEVEL is the most reliable laboratory finding in cystic fibrosis. Other causes of elevated sweat electrolytes include untreated adrenal insufficiency, 1 glucose 6-phosphatase deficiency, glycogen-storage disease, ~ nephrogenic diabetes insipidus? ectodermal dysplasia with sensorimotor deafness,' and
From the Department of Pediatrics, Maisonneuve-Rosemont Hospital University of Montreal School of Medicine. *Reprint address: Maisonneuve-Rosemont Hospital, 5415 l'Assomption Blvd., Montreal, PQ, HIT 2M4 Canada.
hypoparathyroidism with pernicious anemia? Children with malnutrition have been reported with false positive sweat chloride values2 Children with mucopolysaccharidosis, ~ fucosidosis2 and hypothyroidism ~ have had transient high sweat chlorides while malnourished. Mauriac syndrome is characterised by hepatomegaly, glycogen infiltration of the liver, retarded sexual maturation, and short stature in diabetic children treated with insufficient insulin and diet. We report the first example of Mauriac syndrome, in a patient clinically malnourished and edematous, who had a transient false positive sweat test. 0022-3476/79/200240+03500.30/0 9 1979 The C. V. Mosby Co.
Volume 94 Number 2
Brief clinical and laboratory observations
CASE R E P O R T Patient M.R., a 6-year-old French Canadian girl, was admitted to our hospital in 1972 for fatigue, edema, polydipsia, and polyphagia. Two years earlier, she was found to have juvenile diabetes and was started on insulin daily. Her daily insulin dose was 2 units crystalline (Toronto) and 2 units NPH. The mother discontinued the insulin three weeks prior to admission. Examination revealed a malnourished, lethargic girl with short stature. (Her height was 102 cm, a 2 cm gain over 2 years; her weight was 16 kg, a 1 kg gain over 2 years.) She had a distended abdomen withhepatomegaly, edema of the lower extremities, and wasting of subcutaneous tissue. A random blood sugar concentration was 534 mg/dl. The COz combining power was 16.5 mEq/l. Total protein and electrophoretic pattern were normal. Serum albumin concentration was 4.22 gm/dl. Results of tests for stool fat, xylose absorption test, T,, and BUN were normal. Urinalysis showed no proteinuria. Cholesterol was 320 mg/dl (normal, 150 to 250). SGOT, SGPT and serum electrolyte values were normal. Liver biopsy was refused. Sweat chloride values are shown in the Figure; the initial values on day 3 were chloride 75.5 mEq/1 and sodium III mEq/1. Follow-up values of sweat electrolytes, after appropriate treatment with insulin and diet, returned to normal. Chloride concentrations of 33, 48, and 19.5 mEq/1 were obtained on day 11, 18, and 20, respectively. Within six months, both height and weight attained the 25% for age, and the abdominal distention and hepatomegaly regressed. At age 12 she is prepubertal and well. She weighs 37 kg and measures 142 cm. She is following dietary instructions. Her insulin requirements are remarkably small: 2 units of Toronto and 2-8 units NPH. Recently trypsin and chymotrypsin analysis in stool and T, (RIA) were normal. Plasma cortisol concentrations were 13 Fg/dl AM and 5 Fg/dl PM. METHOD Pilocarpine iontophoresis for sweat collection, as suggested by Gibson and Cooke, TM was utilized. The sweat was diluted with lithium sulfate. The sodium analysis was performed by flame photometry; chloride analysis by the mercurimetric method of Schales and Schales. 11 DISCUSSION The fact that sodium and chloride analyses were done by separate methods supports the validity of these findings. The range of sweat chloride concentrations for patients with cystic fibrosis in our hospital is 70 to 190 mEq/L The range of sweat chlorides in non-cystic fibrosis patients is 5 to 50 mEq/1. The range for sodium is 70 to 165 m E q / l for patients with cystic fibrosis. Sweat chloride values in our patient were done in view of the suspected malabsorption syndrome and the known association of diabetes and cystic fibrosis. The high sweat electrolyte value seemed to confirm this association. Normal stool fat excretion and normal xylose absorption ruled out a malabsorption syndrome. She was, however, clinically malnourished and edematous, despite normal
SWEAT ELECTROLYTE
I
I
I
I
I
i
10
15
20
25
Chloride
days
i
24 1
I I
I
I
I
I0
15
20
25
Sodium
Figure. Sweat chloride and sodium levels during the hospital ~tay. serum albumin values. The malnutrition can perhaps be explained by poor diet, and untreated diabetes. Our patient did not have evidence of Addison disease, storage diseases, or hypothyroidism, conditions known to cause high sweat chloride concentration during periods of malnutrition. Sweat electrolyte values return to normal in most of these patients as the state of nutrition improves, as in our patient. These findings suggest that the state of malnutrition and not the underlying disease is responsible for the high sweat chlorides. We speculate that the abnormal sweat tests in Morse's patients with familial hypoparathyroidism were due to malnutrition secondary to steatorrhea. Malnourished children who have a positive sweat test should have repeated sweat tests once the malnourished state has been reversed. This would eliminate error in the diagnosis of cystic fibrosis. REFERENCES
1. Conn JW: Electrolyte composition of sweat: clinical implication as index of adrenal cortical function, Arch Intern Med 83:416, 1949. 2. Harris RC, and Cohen HI: Sweat electrolytes in glycogen storate disease type I, Pediatrics 31:1044, 1963. 3. Lobeck CC, Barta RA, and Mangos JA: Study of sweat in Pitressin resistant diabetes insipidus, J PEDIATR 62:868, 1963. 4. Robinson GC, Miller JR, and Bensimon JR: Familial ectodermal dysplasia with sensorineural deafness and other anomalies, Pediatrics 30:797, 1962. 5. Morse WI, Cochrane WA, and Landrigan PL: Familial hypoparathyroidism with pernicious anemia, steatorrhea and adenocortical insufficiency: variant of mucoviscidosis, N Engl J Med 264:1021, 1971. 6. Mace JW, and Schanberger JE: Elevated sweat chlorides in a child with malnutrition, Clin Pediatr 10:285, 1971. 7. Durand P, Borrone C, Della CeUa (3, and Liotta A: Le mucopolisaccaridose, Recent Prog Med 44:28 l, 1968. 8. Durand P, Borrone C, Della Cella G, and Liotta A: Fucosidosis, J PEDIATR75:665, 1969. 9. Mardoff L: Elevated sweat chlorides and hypothyrodism, J PEDIATR73:244, 1968.
24 2
B r i e f clinical and laboratory observations
The Journal of Pediatrics
February I979 10. Gibson LE, and Cooke RE: A test for concentration of electrolytes in sweat in cystic fibrosis of the pancreas utilizing pilocarpine by iontophoresis, Pediatrics 23:545, 1959,
11. Schales O, and Schales SS: A Simple and Accurate Method for the determination of chloride in biological fluids, J Biol Chem 140:879, 1941.
Leukocyte alkaline phosphatase activity in the diagnosis of neonatal bacterial infections Hugo Donato, Enrique Gebara, Rodica H. de Cosen, and Osvaldo Gioseffi,* Buenos Aires, Argentina
L E U K O C Y T E A L K A L I N E P H O S P H A T A S E , determined
by cytochemical method, is increased in bacterial infections of the adult, but there are no data concerning infections in the neonatal period. The purpose of this study was to determine if LAP levels underwent changes during the course of neonatal bacterial infections, and to compare the results with conventional hematologic methods and with the nitroblue tetrazolium test. MATERIAL
AND METHODS
Material. Forty nine neonates, ages ranging from 3 to 28 days, were divided into two groups: (1) a control group, composed by 36 healthy newborn infants whose birth weight ranged from 2,400 to 4,350 gin, and (2) the infected group, composed by 13 newborn infants whose birth weight ranged from 1,170 to 5,210 gin, with severe bacterial infections (septicemia, meningitis, or pneumonia). Diagnostic criteria employed were as tbllows: (1) For septicemia-a positive blood culture or isolation of the organism from two or more cultures from different sites, and a clinical syndrome suggesting sepsis. (2) For meningitis-presence of two or more of the following findings simultaneously: positive culture of cerebrospinal fluid; more than 20 cells, predominantly neutrophils, in CSF; CSF glucose level less than 50% of glycemia simultaneously tested; presence of bacteria in CSF (Gram technique). (3) For pneumonia-clinical respiratory distress, and chest radiograph consistent with pneumonia. Methods. Capillary blood samples were withdrawn from each neonate for conventional hematologic procedures and cytochemical methods. In infected infants, determinations were performed prior to starting antibiotic therapy. Activity of LAP was studied according to the method From the Hospital Nacional A. Posadas *Reprint address: Seccion Hernatologia. Hospital Nacional Ale]andro Posadas. Martinez de Hozy Marconi, Villa Sarmiento, Pravinciade Buenos Aires, Argentina.
described by Kaplow.' One hundred consecutive segmented neutrophils were examined in each smear and rated from 0 to 4 according to the brown-black granular precipitate intensity within their cytoplasm. In our laboratory, normal adult scores are 85 _+ 13 (~ _+ SD). The NBT spontaneous reduction test was determined by the method of Park et al.'-' Abbreviations used BC: band count CSF: cerebrospinal fluid LAP: leukocyte alkaline phosphatase NBT: nitroblue tetrazolium NC: neutrophil count RESULTS Absolute neutrophil and band counts were significantly different in healthy and in infected infants (P < 0.001): 61.5% of infected newborn infants had levels above 6,000 neutrophils/mm 3 (~ + 2 SD) and 92.2% of the same group had levels above 1,000 bands/mm 3 (~ + 2 SD) (Table). Healthy infants had LAP scores significantly different (P < 0.001) from those of infected newborn infants-216 and 114, respectively (Table); 100% of healthy newborn infants had LAP scores ranging from 163 up to 270 (~ _ 2 SD), whereas all infected newborn infants had LAP scores below 160 (Figure). No significant difference was found in LAP activity between infected newborn infants who survived and those who died. LAP score did not show significant correlation with either the neutrophil and band counts or with the NBT test. The most frequent cytoplasmic abnormality was toxic granulation, found in 76.9% of infected neonates. Increased NBT spontaneous reduction by neutrophils was found in only 25% of infected newborn infants. In all, 92.2% of infected newborn infants had three or more positive results among those tests for the diagnosis of bacterial infection (LAP score, band and neutrophil 0022-3476/79/200242 +03500.30/0 9 1979 The C. V. Mosby Co.
Brief clinical and laboratory observations
show mild obstructive pulmonary disease with normal arterial blood gas values. For the past two years, the hematocrit has been stable at 24%, with a reticulocyte count of 7.0% and a total bilirubin concentration of 2.0 mg/dl. He had no hepatosplenomegaly, cardiomegaly, or hyposthenuria. He has had one mild lower respiratory infection and no sickle crises. SPECIAL STUDY Nine children with sickle cell disease, confirmed by hemoglobin electrophoresis, had sweat chloride determinations by the quantitative pilocarpine iontophoresis method? The mean sweat chloride concentration was 22 mEq/1 with a range of 4 to 43 mEq/l. DISCUSSION The diagnoses in these two children seem firmly established. Both have significantly elevated sweat chloride values. In addition, the presence of meconium ileus (Patient I) and chronic lung disease (Patient II), together with the absence of elevated sweat chloride concentrations in nine other black children with sickle cell disease, are confirmatory findings. Cystic fibrosis, the most frequently lethal genetic syndrome in white children, 2 is now being recognized with greater frequency in the black population. 3-~ The most widely accepted incidence figure is one in 17,033 live black births? Sickle cell disease is the most common genetic disease in American blacks, with an estimated incidence of one in 625 live births$ Assuming an independent autosomal recessive mode of inheritance, the proba-
The Journal of Pediatrics February 1979 bility of cystic fibrosis and sickle cell disease occurring in the same black child is one in 10,625,000 live black births. Although early reports suggested a similar course for cystic fibrosis in blacks and in whites, more recent experience suggests a more benign course for the pulmonary disease of black patients if they survive infancy? Whether the additional problem of sickle cell disease will modify the clinical course of these patients is unknown. Further study of these two unique patients may possibly reveal some abnormality that will improve the understanding of the pathogenesis of cystic fibrosis. REFERENCES
1. Gibson LE, and Cooke RE: A test for concentration of electrolytes in sweat in cystic fibrosis of the pancreas utilizing pilocarpine by iontophoresis, Pediatrics 23:545, 1959. 2. Steinberg AG, and Brown DC: On the incidence of cystic fibrosis of the pancreas, Am J Hum Genet 12:416, 1960. 3. Kulczycki LL, Guin GH, and Mann N: Cystic fibrosis in Negro children, Clin Pediatr 3:692, 1964. 4. Kulczycki LL, and Shauf V: Cystic fibrosis in blacks in Washington, D.C., Am J Dis Child 127:64, 1974. 5. Heifer ET: Cystic fibrosis in black population, NY State Med J 74:2355, 1974. 6. Sultz HA, Schlesinger ER, and Mosher WE: The Erie County survey of long-term childhood illness: II. Incidence and prevalence, Am J Public Health 58:491, 1968. 7. Wintrobe MM, Lee GR, Boggs DR, Bithell TC, Athens JW, and Foerster J: Clinical hematology, ed 7. Philadelphia, 1974, Lea & Febiger, p 823.
False positive sweat test, malnutrition, and the Mauriac syndrome Robert Rosenfeld, M.D.,* Linda Spigelblatt, M.D., and Raymond Chicoine, M.D.,
Montreal, P.Q., Canada
AN ELEVATED SWEAT CHLORIDE LEVEL is the most reliable laboratory finding in cystic fibrosis. Other causes of elevated sweat electrolytes include untreated adrenal insufficiency, 1 glucose 6-phosphatase deficiency, glycogen-storage disease, ~ nephrogenic diabetes insipidus? ectodermal dysplasia with sensorimotor deafness,' and
From the Department of Pediatrics, Maisonneuve-Rosemont Hospital University of Montreal School of Medicine. *Reprint address: Maisonneuve-Rosemont Hospital, 5415 l'Assomption Blvd., Montreal, PQ, HIT 2M4 Canada.
hypoparathyroidism with pernicious anemia? Children with malnutrition have been reported with false positive sweat chloride values2 Children with mucopolysaccharidosis, ~ fucosidosis2 and hypothyroidism ~ have had transient high sweat chlorides while malnourished. Mauriac syndrome is characterised by hepatomegaly, glycogen infiltration of the liver, retarded sexual maturation, and short stature in diabetic children treated with insufficient insulin and diet. We report the first example of Mauriac syndrome, in a patient clinically malnourished and edematous, who had a transient false positive sweat test. 0022-3476/79/200240+03500.30/0 9 1979 The C. V. Mosby Co.
Volume 94 Number 2
Brief clinical and laboratory observations
CASE R E P O R T Patient M.R., a 6-year-old French Canadian girl, was admitted to our hospital in 1972 for fatigue, edema, polydipsia, and polyphagia. Two years earlier, she was found to have juvenile diabetes and was started on insulin daily. Her daily insulin dose was 2 units crystalline (Toronto) and 2 units NPH. The mother discontinued the insulin three weeks prior to admission. Examination revealed a malnourished, lethargic girl with short stature. (Her height was 102 cm, a 2 cm gain over 2 years; her weight was 16 kg, a 1 kg gain over 2 years.) She had a distended abdomen withhepatomegaly, edema of the lower extremities, and wasting of subcutaneous tissue. A random blood sugar concentration was 534 mg/dl. The COz combining power was 16.5 mEq/l. Total protein and electrophoretic pattern were normal. Serum albumin concentration was 4.22 gm/dl. Results of tests for stool fat, xylose absorption test, T,, and BUN were normal. Urinalysis showed no proteinuria. Cholesterol was 320 mg/dl (normal, 150 to 250). SGOT, SGPT and serum electrolyte values were normal. Liver biopsy was refused. Sweat chloride values are shown in the Figure; the initial values on day 3 were chloride 75.5 mEq/1 and sodium III mEq/1. Follow-up values of sweat electrolytes, after appropriate treatment with insulin and diet, returned to normal. Chloride concentrations of 33, 48, and 19.5 mEq/1 were obtained on day 11, 18, and 20, respectively. Within six months, both height and weight attained the 25% for age, and the abdominal distention and hepatomegaly regressed. At age 12 she is prepubertal and well. She weighs 37 kg and measures 142 cm. She is following dietary instructions. Her insulin requirements are remarkably small: 2 units of Toronto and 2-8 units NPH. Recently trypsin and chymotrypsin analysis in stool and T, (RIA) were normal. Plasma cortisol concentrations were 13 Fg/dl AM and 5 Fg/dl PM. METHOD Pilocarpine iontophoresis for sweat collection, as suggested by Gibson and Cooke, TM was utilized. The sweat was diluted with lithium sulfate. The sodium analysis was performed by flame photometry; chloride analysis by the mercurimetric method of Schales and Schales. 11 DISCUSSION The fact that sodium and chloride analyses were done by separate methods supports the validity of these findings. The range of sweat chloride concentrations for patients with cystic fibrosis in our hospital is 70 to 190 mEq/L The range of sweat chlorides in non-cystic fibrosis patients is 5 to 50 mEq/1. The range for sodium is 70 to 165 m E q / l for patients with cystic fibrosis. Sweat chloride values in our patient were done in view of the suspected malabsorption syndrome and the known association of diabetes and cystic fibrosis. The high sweat electrolyte value seemed to confirm this association. Normal stool fat excretion and normal xylose absorption ruled out a malabsorption syndrome. She was, however, clinically malnourished and edematous, despite normal
SWEAT ELECTROLYTE
I
I
I
I
I
i
10
15
20
25
Chloride
days
i
24 1
I I
I
I
I
I0
15
20
25
Sodium
Figure. Sweat chloride and sodium levels during the hospital ~tay. serum albumin values. The malnutrition can perhaps be explained by poor diet, and untreated diabetes. Our patient did not have evidence of Addison disease, storage diseases, or hypothyroidism, conditions known to cause high sweat chloride concentration during periods of malnutrition. Sweat electrolyte values return to normal in most of these patients as the state of nutrition improves, as in our patient. These findings suggest that the state of malnutrition and not the underlying disease is responsible for the high sweat chlorides. We speculate that the abnormal sweat tests in Morse's patients with familial hypoparathyroidism were due to malnutrition secondary to steatorrhea. Malnourished children who have a positive sweat test should have repeated sweat tests once the malnourished state has been reversed. This would eliminate error in the diagnosis of cystic fibrosis. REFERENCES
1. Conn JW: Electrolyte composition of sweat: clinical implication as index of adrenal cortical function, Arch Intern Med 83:416, 1949. 2. Harris RC, and Cohen HI: Sweat electrolytes in glycogen storate disease type I, Pediatrics 31:1044, 1963. 3. Lobeck CC, Barta RA, and Mangos JA: Study of sweat in Pitressin resistant diabetes insipidus, J PEDIATR 62:868, 1963. 4. Robinson GC, Miller JR, and Bensimon JR: Familial ectodermal dysplasia with sensorineural deafness and other anomalies, Pediatrics 30:797, 1962. 5. Morse WI, Cochrane WA, and Landrigan PL: Familial hypoparathyroidism with pernicious anemia, steatorrhea and adenocortical insufficiency: variant of mucoviscidosis, N Engl J Med 264:1021, 1971. 6. Mace JW, and Schanberger JE: Elevated sweat chlorides in a child with malnutrition, Clin Pediatr 10:285, 1971. 7. Durand P, Borrone C, Della CeUa (3, and Liotta A: Le mucopolisaccaridose, Recent Prog Med 44:28 l, 1968. 8. Durand P, Borrone C, Della Cella G, and Liotta A: Fucosidosis, J PEDIATR75:665, 1969. 9. Mardoff L: Elevated sweat chlorides and hypothyrodism, J PEDIATR73:244, 1968.
24 2
B r i e f clinical and laboratory observations
The Journal of Pediatrics
February I979 10. Gibson LE, and Cooke RE: A test for concentration of electrolytes in sweat in cystic fibrosis of the pancreas utilizing pilocarpine by iontophoresis, Pediatrics 23:545, 1959,
11. Schales O, and Schales SS: A Simple and Accurate Method for the determination of chloride in biological fluids, J Biol Chem 140:879, 1941.
Leukocyte alkaline phosphatase activity in the diagnosis of neonatal bacterial infections Hugo Donato, Enrique Gebara, Rodica H. de Cosen, and Osvaldo Gioseffi,* Buenos Aires, Argentina
L E U K O C Y T E A L K A L I N E P H O S P H A T A S E , determined
by cytochemical method, is increased in bacterial infections of the adult, but there are no data concerning infections in the neonatal period. The purpose of this study was to determine if LAP levels underwent changes during the course of neonatal bacterial infections, and to compare the results with conventional hematologic methods and with the nitroblue tetrazolium test. MATERIAL
AND METHODS
Material. Forty nine neonates, ages ranging from 3 to 28 days, were divided into two groups: (1) a control group, composed by 36 healthy newborn infants whose birth weight ranged from 2,400 to 4,350 gin, and (2) the infected group, composed by 13 newborn infants whose birth weight ranged from 1,170 to 5,210 gin, with severe bacterial infections (septicemia, meningitis, or pneumonia). Diagnostic criteria employed were as tbllows: (1) For septicemia-a positive blood culture or isolation of the organism from two or more cultures from different sites, and a clinical syndrome suggesting sepsis. (2) For meningitis-presence of two or more of the following findings simultaneously: positive culture of cerebrospinal fluid; more than 20 cells, predominantly neutrophils, in CSF; CSF glucose level less than 50% of glycemia simultaneously tested; presence of bacteria in CSF (Gram technique). (3) For pneumonia-clinical respiratory distress, and chest radiograph consistent with pneumonia. Methods. Capillary blood samples were withdrawn from each neonate for conventional hematologic procedures and cytochemical methods. In infected infants, determinations were performed prior to starting antibiotic therapy. Activity of LAP was studied according to the method From the Hospital Nacional A. Posadas *Reprint address: Seccion Hernatologia. Hospital Nacional Ale]andro Posadas. Martinez de Hozy Marconi, Villa Sarmiento, Pravinciade Buenos Aires, Argentina.
described by Kaplow.' One hundred consecutive segmented neutrophils were examined in each smear and rated from 0 to 4 according to the brown-black granular precipitate intensity within their cytoplasm. In our laboratory, normal adult scores are 85 _+ 13 (~ _+ SD). The NBT spontaneous reduction test was determined by the method of Park et al.'-' Abbreviations used BC: band count CSF: cerebrospinal fluid LAP: leukocyte alkaline phosphatase NBT: nitroblue tetrazolium NC: neutrophil count RESULTS Absolute neutrophil and band counts were significantly different in healthy and in infected infants (P < 0.001): 61.5% of infected newborn infants had levels above 6,000 neutrophils/mm 3 (~ + 2 SD) and 92.2% of the same group had levels above 1,000 bands/mm 3 (~ + 2 SD) (Table). Healthy infants had LAP scores significantly different (P < 0.001) from those of infected newborn infants-216 and 114, respectively (Table); 100% of healthy newborn infants had LAP scores ranging from 163 up to 270 (~ _ 2 SD), whereas all infected newborn infants had LAP scores below 160 (Figure). No significant difference was found in LAP activity between infected newborn infants who survived and those who died. LAP score did not show significant correlation with either the neutrophil and band counts or with the NBT test. The most frequent cytoplasmic abnormality was toxic granulation, found in 76.9% of infected neonates. Increased NBT spontaneous reduction by neutrophils was found in only 25% of infected newborn infants. In all, 92.2% of infected newborn infants had three or more positive results among those tests for the diagnosis of bacterial infection (LAP score, band and neutrophil 0022-3476/79/200242 +03500.30/0 9 1979 The C. V. Mosby Co.