BRIEF
CLINICAL
LABORATORY
AND
OBSERVATIONS
Studies in growth and development. XL Hemoglobin concentration in adolescents A preliminary study oJ American Negro college students K. P. Verghese, M.D., Dorothy B. Ferebee, M.D., Angella D. Ferguson, M.D., and Roland B. Scott, M.D.* XA,r A S H I N G T O N ~
1).
C,
wet preparation for sickling. The results of the study are summarized in Table I. The mean hemoglobin concentration was 13.8 Gm. per cent for males (range 9 to 17.5 Gm.) and 12.4 Gin. per cent for females (range 7.6 to 16 Gm.) If one accepts 12 Gm. per cent of hemoglobin as the lower limit of normal, then, i3.7 of the males and 52.7 per cent of the females can be categorized as being "anemic."
s E A R C I-I of the literature reveals a paucity of published data dealing with hemoglobin concentration in adolescent Negroes. 1-s This study provides information on 484 American Negro college studentst in the age range of 16 to 19 years.
A
METHOD
Freshmen students were selected at random for hemoglobin estimations during 2,063 routine physical examinations in 1964. These students were presumed to beIong to the middle socioeconomic group. There were 264 females and 220 males. They represented approximately one fourth of the total number of students examined. The cyanmethemoglobin method was utilized for the hemoglobin estimation. The subjects included in the study had a negative
DISCUSSION Similar studies from the literature are summarized in Table II. T h e study by Judy and Price s in 1958 of hemoglobin levels in normal adolescent girls revealed a mean hemoglobin level of 12.6 Gm. per cent. In 1954, Leonard 6 suggested 11.8 Gm. per cent as the lower limit of normal hemoglobin values for males. His subjects were Royal Air Force recruits between 17 and 21 years of age. In 1960, BrumfitV adopted 11.8 Gin. per cent as the lower limit of normal hemoglobin in males in his study of primary iron deficiency anemia in the Royal Army Medical Corps. Similarily, Seltzer 8 accepted a hemoglobin level of 12 Grn. per cent as the lower limit of normal in male and female adolescents. Inasmuch as sickle cell disease, the most
From the Department of Pediatrics and the University Health Service of the Howard University College oJ Medicine, and the Pediatric Service of Freedmen's Hospital. This project was supported, in part, by Public Health Service Grant HD-00645-2 ]rom the National Institute of Child Health and Human Development. *Address, Head, Dept. o] Pediatrics, Howard University School o] Medicine, Washington 1, D. C. "~Howard University is situated in Washington, D. C., with a total enrollment o[ more than 9,000. The student body is predominantly Negro and represents residents oJ 46 states, the District o~ Columbia, Virgin Islands, Puerto Rico, and over 78 loreign countries.
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Volume 67 Number 6
Brie[ clinical and laboratory observations
1 19 5
Table I. Distribution of cases by level of hemoglobin
Percentage
Males I
Hemoglobin (Gin. %)
No.
0.45 1 1.4 3 10.9 24 22.4 47 20.5 43 43.35 102 Mean, 13.8 Gm. % Range, 9- 17.5 Gm. % Standard deviation +- 1.5 Gm. %
< ~ < ,~ < ~
. No.
10 11 12 13 14 14
Females I Percentage
7 2.4 37 12.4 103 37.1 84 32.8 23 9.7 10 3.7 Mean, 12.4 Gin.% Range, 7.6-16 Gin.% Standard deviation + 1.1 Gin.%
Table II. Distribution of levels of hemoglobin a m o n g N o r t h American Caucasians
Author WintrobO
Year
Age
Males Hemoglobin Gin. % No. ~ean ] Range
1933 Medical 86 students 1935 14-30yr. 259 1938 17-19 yr. 20
16.0
Pett and Ogilvie ~ 1948 15-19yr. 88 Judy and Price 9 1958 Hamre and Mantting* 1942 16-25 yr. 137 *This study was done on Hawaiians.
Osgood2 Mugrage and Ander-
13.5-18.5
Age
Females ~ N~o. Hemoglobin Gin.% Mean t Range
Nurses
101
14.1
12-16.5
15.84 14-18 16.57 15.5-17.1
14-30 yr. 15-21yr.
152 95
13.8 14.5
11.5-16 13-6.6
13.8
10-16
17-19 yr. 11-19 yr.
40 121
12.7 12.6
10.1-15
15.1
11.83-17.2
son 3
frequently occurring hemoglobinopathy in Negro subjects, was excluded in our study, it has been presumed that the observed anemia was most probably due to iron deficiency. However, other blood disorders such as thalassemia, spherocytosis, megaloblastic anemia, and hemoglobinopathies other than sickle cell disease must also be considered as diagnostic possibilities. T h e high incidence of anemia in the girls can be attributed to such factors as the increase in d e m a n d for iron during the adolescent growth spurt, finicky eating habits, and the loss of iron in menstrual flow. I n discussing reasons that have been advanced to explain the poor eating habits observed a m o n g adolescents, Peckos and Heald 1~ point out that m a n y teenagers, particularly girls, have fears about becoming fat. SUMMARY
Hemoglobin concentrations were determined in 484 American Negro college stu-
dents between the ages of 16 and 19 years. Values for males ranged from 9 to 17.5 Gm. per cent (mean 13.8 _+ 1.5 Gin.). I n the females, the range was 7.6 to 16 Gin. per cent (mean 12.4 _+ 1.1 Gin.). Subjects included in the study had a negative test for sickling of the red blood cells. If one accepts 12 Gin. of hemoglobin as the lower limit of normal, 13.7 per cent of the males and 52.7 per cent of the females had presumptive iron deficiency anemia. However, before initiating therapy in the individual patient, the physician should give diagnostic consideration to other possible explanations for the anemia. REFERENCES
1. Wintrobe, M. M.: Blood of normal men and women. (Erythrocyte counts, hemoglobin and volume of packed red cells of 229 individuals), Bull. Johns Hopkins Hosp. 53: 118, 1933. 2. Osgood, E. E.: Normal hematologic standards, Arch. Int. Med. 56: 849, 1935. 3. Mugrage, E. R., and Anderson, M. I.: Red blood cell values in adolescents, Am. J. Dis. Child. 56: 997, 1938.
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Brie[ clinical and laboratory observations
4. Hamre, C. J., and Mantting, A. V.: Hematologic values for normal healthy men 16 to 25 years of age, J. Lab. & Clin. Med. 27: 1231, 1942. 5. Pett, L. B., and Ogilvie, G. F.: Hemoglobin level at different ages, Canad. M. A. J. 58: 353, 1948. 6. Leonard, B. J.: Hypochromic anemia in R.A.F. recruits, Lancet h 889, 1954.
7. Brumfitt, W.: Primary iron deficiency in young men, Quart. J. Med. 29: 1, 1960. 8. Seltzer, C. C., and Mayer, J.: Serum iron and iron-binding capacity in adolescents, Am. J. Clin. Nutrition 13: 354, 1963. 9. Judy, H. E., and Price, N. B.: Hemoglobin level and red blood cell count findings in normal women, J. A. M. A. 167: 563, 1958. 10. Peckos, P. S., and Heald, F. P.: Nutrition of adolescents, Children l h 27, 1964.
Qualitative changes in the cisternal and lumbar Tinal fluid following an intravenous injection of glucose in apparently "healthy"children R. D. Brooke Williams, M.D.,* and Frank Falkner, M.R.C.P. LOUISVILLE,
KY.
T H E B R A I N relies ahnost exclusively on carbohydrate as its source of energy; neuronal activity in the central nervous system is virtually dependent on glucose. We thought it valuable to investigate and assess the related "normal" patterns of entry of glucose into the spinal fluid in both the cisternal and lumbar regions and to contribute base-line data. U n d e r normal circumstances, the difference between concentrations of glucose in the blood and cerebrospinal fluid is attributed to the blood cerebrospinal fluid barrier, but the mechanisms involved have not been elucidated. There is evidence that the entry of glucose into the spinal fluid is dependent From the Department o[ Pediatrics, University o[ Louisville School o/Medicine, Louisville, Ky. This investigation was supported in part by the American Medical Association, Grant 299 and ERIC Grant 82; National Institutes o[ Health, Grants B1599 and B3570; and a grant [rom the American Cancer Society. *Address, University oJ Louisville School o[ Medicine, Department o[ Pediatrics, 226 East Chestnut Street, Louisville, Ky.
upon the transport of sugar via an intracellular pathway rather than by simple diffusion across the membranes of the blood CSF barrier. 1, ~, 3 T h e failure of brain glucose to increase proportionately when blood glucose is raised to very high levels is further evidence compatible with the concept of a rate-limited transport mechanism from the plasma into the central nervous system. ~ Although Geiger and his associates 4 suggest an active transport mechanism, there m a y be a finite capacity to a metabolic p u m p and it is possible that the limitations of metabolic mechanisms m a y explain certain differences between the plasma and cerebrospinal fluid. In view of Fishman's 2 recent work in the dog and our study 3 of the alterations in glucose transport in patients with complications of meningitis, we wanted to see if a uniform pattern of glucose transport occurred under normal circumstances. Using a standardized technique, in spite of the pressure changes caused by the removal of small amounts of cerebrospinal fluid from both sites and the rapidly changing blood levels and osmotic