Growth in juvenile diabetes mellitus

Diabetologia, Jun 1972

Summary Height, weight, height velocity and skeletal maturity information was collected on a group of 94 juvenile diabetics in a mixed longitudinal study, and compared to a control population. Familial growth trends were taken into consideration where possible. Although the hormonal environment in the juvenile diabetic is probably unusual and fluctuating, there is no evidence that juvenile diabetes is likely to interfere with growth provided that a reasonable degree of control is maintained.

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Growth in juvenile diabetes mellitus

Growth in Juvenile Diabetes Mellitus 0 Department of Pediatrics, University of British Columbia , Vancouver , Canada Summary. Height, weight, height velocity and skeletal maturity information was collected on a group of 94 juvenile diabetics in a mixed longitudinal study, and compared to a control population. Familial growth trends were taken into consideration where possible. Although the hormonal environment in the juvenile diabetic is probably unusual and fluctuating, there is no evidence that juvenile diabetes is likely to interfere with growth provided that a reasonable degree of control is maintained. Growth; juvenile diabetic; maturation; height; weight; bone age Introduction T h a t chronic disease tends to interfere with growth is a widely accepted fact, although often the evidence for such belief is meagre. Juvenile diabetes mellitus m a y be considered a chronic metabolic disease; however it differs from such conditions as congenital cardiac disease or chronic renal disease in t h a t the abnormalities involve endocrine-metabolic relationships which are central to growth processes. In the literature of the early insulin era, references on growth and juvenile diabetes are numerous, and generally suggest subnormal growth is to be expected, although a few suggest "good control" ~11 result in normal growth. However in more recent years, since current modes of management have been adopted, references are rare, and further equally divided between the opinions t h a t juvenile diabetes, even if well controlled, is, [1--4] or is not, [ 5, 6 ] associated with growth disturbances. The object of the present mixed longitudinal s t u d y was to investigate whether growth disturbances were usually associated with controlled diabetes. Material and Methods The s t u d y population consists of a total of 94 juvenile diabetics ranging from three to t w e n t y years of age at the present time. Duration of diabetic state varied from 1 to 15 years. All subjects have been followed longitudinally over a period of at least one year, and some as long as four or five years. Subjects are normally seen three or four times a year. The great majority of heights have been recorded with a Harpenden stadiometer. Skeletal m a t u r i t y was determined from posteroanterior films of the left hand and wrist. M a t u r i t y is rated b y the method of Tanner [ 7 ]. Growth velocity was obtained from measurements over periods of at least one year. This is essential to eliminate the seasonal effects on growth rate [ 8 ]. Unfortunately it is not usually possible to schedule visits at exact intervals, and thus the seasonal effect has not been entirely excluded b u t at least minimized. Height and weight have been compared with the standards (3rd, 50th and 97th centiles) reported b y Tanner et al. (1966) [ 8 ]. I n a previous paper [ 9 ] we have reported the height and weight of healthy Vancouver school children using the same standards. Skeletal m a t u r i t y has been plotted and compared with the same control population. Skeletal m a t u r i t y films were available in 74 subjects. Information regarding growth patterns, final height, and age of menarche was sought on close relatives (siblings, parents and parent siblings). Useful data were obtained in f o r t y subjects. Discrepancies (of a n y sign and magnitude) between apparent skeletal m a t u r i t y and chronological age were examined in the light of family data. I n view of its greater precision and reliability, only menarchial age in female relatives was utilized. "Good control" is herein defined as absent or minimal giueosuria at most times; absence of ketosis or prolonged h e a v y giucosuria, except when infection is present; infrequent hypoglycemic episodes; and evidence of satisfactory adherence to a measured (but not weighed) dietary regimen, and urine testing. Insulin t h e r a p y should have been adjusted appropriate to urine testing findings. Results Achieved stature. Figs. 1 and 2 show achieved stature of all subjects at their most recent measurement. This cross-sectional method has been used b y almost all previous workers. I t will be seen from Table 16C E I 2 a t e s 1 that compared to the standards used, the skewing to the higher centfles seen in our control population is fully reflected in our female subjects, but not in our male subjects. This apparent excess of shorter males will be discussed below. I 16 n 42 52 42 52 18 16 14 ~12 9 males Family data. The reliability of family stature d a t a is open to question, as in few cases was it measured b y us. Stature of close relatives is described in Table 4. All male relatives and females, except for i m m a t u r e compared to the standards. H o w e v e r our control subjects of b o t h sexes showed a similar skewing, and we conclude t h a t the diabetic children show no significant abnormalities of skeletal maturation. Height velocity. We compared the height velocity in 76 subjects with the appropriate standard of Tanner et al. [ 8 ], and recorded the average centile status of the individual over the period of observation in Table 3. Some subjects showed considerable variation in their actual centile position from y e a r to year. This m a y be due to natural variations or measurement errors; it might also be due to fluctuations in diabetic control, although we have been unable to show a n y such correlation from our clinical records. siblings, show distributions similar to the control population. As will be seen f r o m Table 5, in a b o u t half the instances the bone age discrepancy of the diabetic is compatible with the family trend. I n those where the difference was not compatible, in the m a j o r i t y it was better t h a n (i. e. less than) the family trend. Discussion Serum growth hormone levels, which are high in u n t r e a t e d or inadequately treated juvenile diabetics, fall when control is established [ 10, 11 ]. However in longstanding diabetes, good control is often associated with higher growth hormone levels [11]. Recent reports demonstrate t h a t sleep-related plasma growth hormone elevation is normal in juvenile diabetics even in the presence of hyperglycemia [ 12 ]. Insulin also fulfills the criteria of a growth hormone; it is anabolie, promotes cell growth, and an insufficiency leads to growth stunting. Like somatotropin itself, we face the p a r a d o x t h a t the secretion and circulating levels of a m a j o r growth-promoting hormone are so variable, depending on the nutritional status of the individual at the m o m e n t . I t is clear t h a t insulin levels achieved in the t h e r a p y of juvenile diabetes are "unphysiological", in the sense t h a t t h e y cannot reflect rapidly changing metabolic needs. I t is likely t h a t the mean level of plasma insulin in a juvenile diabetic is usually less t h a n in a non-diabetic, since to avoid periods of incapacitating hypoglycemia during the post-absorptive phase, we accept a degree of hyperglycemia, and thus of hypoinsulinemia. Growth failure is certainly a feature of uncontrolled juvenile diabetes, this being p a r t of the "Mauriac s y n d r o m e " [ 13, 14 ]. A t present the possible interplay of these, at times, conflicting hormonal p a t t e r n s on growth cannot be perceived. The problem is whether " g o o d " control will p r e v e n t the growth retardation characteristic of undertreated juvenile diabetes. Nutritional factors are prominent among the requirements for optimal growth. The diabetic diet, with emphasis on variety, adequate caloric intake, and with its relatively high protein content (typically 20% of calories compared to the usual 12--15%) should also favour growth. The data on achieved stature are not in favour of poor growth in our subjects. Examination of individuals shorter than expected reveals familial factors in most instances. Height velocity data, although more difficult to interpret, are much more valuable than single determinations. Again no obviously abnormal trend is evident. We were not able to correlate fluctuations in height velocity with variation in diabetic control. Skeletal maturity patterns, allowing for familial trends, were again comparable to our control population. Included in this series were 11 subjects (7 male, 4 female), whose diabetic control status, even b y our moderate standards, was for prolonged periods judged unacceptable b y the criteria noted above. Of these, 8 were unusually short, and 7 markedly underweight. 0 n l y 4 had radiography, and while one showed much delay in bone maturation, two were normal and one was accelerated for age. None of these subjects had hepatomegaly. The apparent excess of shorter diabetic males compared to the control population must be contrasted with the growth rates of these males, which are normal when compared to the controls. Thus the shorter stature was not due to diminished growth rates during the period of observation. Familial factors certainly were responsible in some instances. Contrary to the observation of Bergqvist [ 1 ], there was no relationship between shorter stature and early onset of diabetes in our series. The poorly controlled short subjects noted above were also included in the series and affected the distribution of stature. I t is concluded t h a t diabetes mellitus, with adequate therapy, is not usually associated with growth delay or short stature. 1. Bergqvist , N. : The growth of juvenile diabetics . Acta endoer . 15 , 133 -- 165 ( 1964 }. 2. Larsson , Y. , Sterky , G. : Long-term prog~aosis in juvenile diabetes mellitus . Acta Pedlar . 51 , Suppl . 130 ( i962 ). 3. Knowles , H.C. , Guest , G.M. , Lampe , J. , Kessler , M. , Skillman , T. G. : The course of juvenile diabetes treated with an unmeasured diet . Diabetes 14 , 239 -- 273 ( 1965 ). 4. Sterky , G. : Growth patterns in juvenile diabetes . Acta pediat. Scandinav. Suppl . 177 , 80 -- 82 ( 1967 ). 5. Jackson , R.L. , Kelly , H.G. : Growth of children with diabetes mellitus in relationship to level of control of the disease . J. Pediat . 29 , 316 -- 328 ( 1946 ). 6. Joos , T.H. , Johnston , J.A.: A long-term evaluation of the juvenile diabetic . J. Pedlar . 50 , 133 -- 137 ( 1957 ). 7. Tanner , J.M. , Whitehouse, l%.H., Healey , M.J.]~.: A new system for estimating skeletal maturity from the hand and wrist . Paris: Int. Child. Centre ( 1962 ). 8. -- -- Takaishi , M. : Standards from birth to maturity for height, weight, height velocity and weight velocity: British children , 1965 . Arch. Dis. Childh. 41 , 454 -- 471 and 613 -- 635 ( 1966 ) 9. Birkbeek , J.A. : Growth standards for British Columbia children . Submitted for publication. 10. t-Iansen , A.P. , Johansen , K. : Diurnal patterns of blood glucose, serum free fatty acids, insulin, glucagon, and growth hormone in normals and juvenile diabetics . Diabetologia 6 , 27 -- 33 ( 1970 ). 11. Johansen , K. , Hansen , A.P. : Diurnal serum growth hormone levels in poorly and well-controlled diabetics . Diabetes 20 , 239 -- 245 ( 1971 ). 12. Parker , D.C. , l%ossman, L.G. : Sleep release of human growth hormone in treated juvenile diabetics . Diabetes 29 , 691 -- 695 ( 1971 ). 13. Mauriac , P. : Hepatomegalies de l' enfance avec troubles de la croissanee et du metabolisme des glucides . Paris Med . 2 , 525 -- 528 ( 1934 ). 14. Traisman , H.F. : Mauriae's syndrome. A complication of poorly managed diabetes . Clin. Ped . 8 , 520 -- 522 ( 1964 ).

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J. A. Birkbeck. Growth in juvenile diabetes mellitus, Diabetologia, 1972, 221-224, DOI: 10.1007/BF01212266