T H E J O U R N A L OF
PEDIATRIC S APRIL
1978
Volume 92
Number 4
MEDICAL PROGRESS Short stature. Part I David L. Rimoin, M.D., Ph.D.,* and William A. Horton, M.D.,
SXATUR~, the quantitative measure of height, varies widely within each ethnic group with a fairly normal distribution. Of the numerous patients whom the physi, clan encounters because of short stature, relatively few are pathologically small in the context of family and ethnic background. Thus it is imperative that the physician be able to differentiate pathologic short stature from the lower end of the normal curve before embarking on a complex diagnostic evaluation. We shall provide a pathophysiologic background for the evaluation of short stature by outlining the normal human growth curve, the physiologic mechanisms that participate in the growth process, and the manner in which these processes can be disturbed.
NORMAL H U M A N GROWTH A growth curve, common to all individuals, has characteristics which are shared by many other primates I ~ (Fig. 1); it is characterized by rapid fetal growth, quick deceleration of growth following birth, a period of relatively
Torrance, Calif.
slow but constant growth during childhood, a rapid growth spurt at puberty, and total cessation of growth With epiphyseal fusion. After birth, each individual appears to follow a growth curve that is largely dependent on genetic constitution, upon which environmental factors are superimposed. There is a strong tendency to maintain the individual growth curve; a major long-term insult to growth is required to alter growth potential permanently. A major illness will temporarily suppress the growth rate, but when the illness is cured or controlled, rapid compensatory growth occurs, returning the child to his original growth pattern, provided the insult has not lasted for an excessively long time. Abbreviations used U/L: upper to lower ratio hGH: human growth hormone
Supported in part by United States Public Health Service research and training grants (HD-05624, HD00417) and research grants from the National Foundation-March o f Dimes and the Easter Seal Research Foundation. *Reprint address: Department of Pediatrics, UCLA School o.1' Medicine, Harbor General Hospital Campus, 1000 W. Carson St., Torrance, CA 90509.
P e a k intrauterine growth velocity occurs at approximately four months of gestation. The decrease in growth rate during the latter half of pregnancy is probably due to a progressive decrease in cellular division and to uterine constraint on the fetus; the latter becomes increasingly more limiting as the fetus approaches term. Indeed, size at birth appears to be dependent more on maternal than on genetic factors, -~but by age one to two years, the child will have accelerated or decelerated his growth velocity until he reaches his genetic growth level. A number of maternal factors are known to alter fetal growth. These include maternal size; nutrition; illnesses such as toxemia, hyper-
0022-3476/78/0492-0523500.60/0 9 1978 The C. V. Mosby Co.
Vol. 92, No. 4, pp. 523-528
From the Division o f Medical Genetics, UCLA-Harbor General Hospital.
524
Rimoin and Horton
The Journal of Pediatrics April 1978
180-
160.
140E
U
I.-1-
(.9
120I00-
-1-
8060i
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., ., ., ., ., .,
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PEDIATRIC S APRIL
1978
Volume 92
Number 4
MEDICAL PROGRESS Short stature. Part I David L. Rimoin, M.D., Ph.D.,* and William A. Horton, M.D.,
SXATUR~, the quantitative measure of height, varies widely within each ethnic group with a fairly normal distribution. Of the numerous patients whom the physi, clan encounters because of short stature, relatively few are pathologically small in the context of family and ethnic background. Thus it is imperative that the physician be able to differentiate pathologic short stature from the lower end of the normal curve before embarking on a complex diagnostic evaluation. We shall provide a pathophysiologic background for the evaluation of short stature by outlining the normal human growth curve, the physiologic mechanisms that participate in the growth process, and the manner in which these processes can be disturbed.
NORMAL H U M A N GROWTH A growth curve, common to all individuals, has characteristics which are shared by many other primates I ~ (Fig. 1); it is characterized by rapid fetal growth, quick deceleration of growth following birth, a period of relatively
Torrance, Calif.
slow but constant growth during childhood, a rapid growth spurt at puberty, and total cessation of growth With epiphyseal fusion. After birth, each individual appears to follow a growth curve that is largely dependent on genetic constitution, upon which environmental factors are superimposed. There is a strong tendency to maintain the individual growth curve; a major long-term insult to growth is required to alter growth potential permanently. A major illness will temporarily suppress the growth rate, but when the illness is cured or controlled, rapid compensatory growth occurs, returning the child to his original growth pattern, provided the insult has not lasted for an excessively long time. Abbreviations used U/L: upper to lower ratio hGH: human growth hormone
Supported in part by United States Public Health Service research and training grants (HD-05624, HD00417) and research grants from the National Foundation-March o f Dimes and the Easter Seal Research Foundation. *Reprint address: Department of Pediatrics, UCLA School o.1' Medicine, Harbor General Hospital Campus, 1000 W. Carson St., Torrance, CA 90509.
P e a k intrauterine growth velocity occurs at approximately four months of gestation. The decrease in growth rate during the latter half of pregnancy is probably due to a progressive decrease in cellular division and to uterine constraint on the fetus; the latter becomes increasingly more limiting as the fetus approaches term. Indeed, size at birth appears to be dependent more on maternal than on genetic factors, -~but by age one to two years, the child will have accelerated or decelerated his growth velocity until he reaches his genetic growth level. A number of maternal factors are known to alter fetal growth. These include maternal size; nutrition; illnesses such as toxemia, hyper-
0022-3476/78/0492-0523500.60/0 9 1978 The C. V. Mosby Co.
Vol. 92, No. 4, pp. 523-528
From the Division o f Medical Genetics, UCLA-Harbor General Hospital.
524
Rimoin and Horton
The Journal of Pediatrics April 1978
180-
160.
140E
U
I.-1-
(.9
120I00-
-1-
8060i
......
I:I
., ., ., ., ., .,
III
18-
_z io: _
