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   Table of Contents      
ARTICLES
Year : 1983  |  Volume : 31  |  Issue : 7  |  Page : 1049-1052

Growth hormone and diabetic retinopathy


Department of Ophthalmology, B.H.U., Varanasi, India

Correspondence Address:
R Singh
C-7. New Medical Enclave, Banaras Hindu University, Varanasi-221 005
India
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Source of Support: None, Conflict of Interest: None


PMID: 6544256

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How to cite this article:
Singh R, Agrawal J K, Kumar V, Raman R D. Growth hormone and diabetic retinopathy. Indian J Ophthalmol 1983;31, Suppl S1:1049-52

How to cite this URL:
Singh R, Agrawal J K, Kumar V, Raman R D. Growth hormone and diabetic retinopathy. Indian J Ophthalmol [serial online] 1983 [cited 2020 May 26];31, Suppl S1:1049-52. Available from: http://www.ijo.in/text.asp?1983/31/7/1049/29744

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Serum growth hormone (GH) abnormal­ities in diabetics have long been suggested to be responsible for the retinal changes.[1],[2],[3],[4] This casual association has furtherbeen supported by the relative infrequency of retinopathy in diabetics with growth hormone deficient states[5],[6]. Knoph and Co-workers[7] observed significantly higher than mean fasting growth hormone concentrations in diabetics with retinopathy than those without the retinal changes. Passa and his associates[6] demon­strated exaggerated growth hormone respo­nses to muscular exercise in patients with diabetic with diabetic retinopathy. However, such a correlation could not be established between the levodopa stimulated growth hormone response and the presence or absence of diabetic retinopathy[9]. Moreover, the relationship between the growth hormone responses and the, severity of diabetic reti­nopathy is also not well defined.

In the present work, fasting and the levodopa stimulated growth hormone responses have been studied in diabetics with and without retinopathy as well as in normal healthy controls. Further, the growth hormone response have also been correlated with the severity of diabetics and the grade of diabetic retinopathy.


  Method and materials Top


Twenty three diabetic patients and 8 age matched healthy controls have been studied. The diabetic state was confirmed on fasting blood sugar (FBS) level (140 mg.) or after an oral glucose tolerance test (OGTT)[10]. The controls were selected from the persons attending the ophthalmic out patients for the refractive errors. In them also diabetes mellitus was excluded by the OGTT. The diabetic retinal changes were graded accord­ing to the criteria of Schie and Albert[11]. The duration of diabetes was ascertained on the basis of history of definitive symptoms and/or previous FBS or OGTT results. The patients with FBS level of more than 200 mg. per cent were considered to be severe diabetic and those having values below this level were con­sidered as mild diabetic. The diabetic state was considered to be on good methabolic con­tols, if the FBS values were between 100-120 mg. per cent and/or post prandial blood sugar values were between 160-180 mg. percent Serum growth hormone levels were estimated in the fasting state and one hour after oral levodopa (500 mg.) administration[12]. The levodopa was given in the fasting state. The radioimmune assay of growth hormone was done using dextran coated charcoal[13].


  Observations Top


Amongst the 23 diabetics studied, retinal changes were found in 16 (69.5%) patients. In the remaining 7 (30.5%) fundus was normal. The mean age of diabetics with and without retinopathy was 52.8±11.5 years and 49.3±8.5 years, while that of the controls was 46.4±6.7 years respectively.


  DURATION AND SEVERITY OF DIABETES.AND RETINOPATHY Top


The duration of diabetes was less than 5 years in 56.5% and in the remaining it was known for more than 5 years. Diabetic state was mild (FBS<200 mg. %) in 30.4% and severe (FBS >200 mg. %) in the remaining 69.6%. The frequency of retinopathy was found to have no correlation either with the duration or the severity of the disease [Table ­1].

Serum Growth Hormone and Retinopathy

The mean growth hormone levels in the fasting state as well as after the levodopa stimulation were significantly higher in diabetes with and without retinopathy (p <0.01) as compared to healthy controls. However, in between the two diabetic groups there were no statistical differences [Table - 2]. But diabetics with retinopathy had greater (p <0.05) mean growth hormone response to levodopa as compared to control than there without retinopathy [Table - 2].

Growth Hormone Response and Severity of Diabetes and Retinopathy

The mean growth hormone response after levodopa administration was found to be statistically similar in patients with fasting blood sugar values below or above 200 mg. per cnet. Whereas diabetics with background retinopathy had significantly greater (p <0.01) response than those with proliferative retinal changes [Table - 3].


  Discussion Top


In the pathogenesis of diabetic retinopathy, many factors have been implicated[14]. Lundback et al[2],[3] while observing high and fluctuating levels of growth hormone con­sidered it to be the main cause of diabetic angiopathy and retinopathy. The infrequency of the retinal involvement in growth hormone deficient dwarfs with diabetes[5] and in idio­pathic haemachromatosis with diabetes hav­ing poor growth hormone responses[6] favours such a concept.

Some studies[15],[16],[17],[18] demonstrated elevated growth hormone levels, in patients of diabetes

mellitus. Hansen[17],[18] in addition, mentioned that response to exercise occures earlier and is greater in diabetics than that in the normal subjects. Knopf and Loworkers[7] observed significantly higher mean fasting growth hor­mone concentrations in diabetics with reti­nopathy than those without it. Passa and his associates[8] described significantly greater growth hormone response to muscular exer­cise in patients with diabetic retinopathy only. Holland et al[9] however, could not corre­late levodopa stimulated growth hormone response with the presence or absence of retinopathy. In the present study also, the mean serum growth hormone concentrations both in the fasting state (Group A : P < 0.01) as well as after the levodopa stimulation (Group A : p <0.01, Group B : p <0.01) were significantly higher in the diabetic groups as compared to the normal healthy controls but these were statistically similar in diabetics with and without retinopathy the mean growth hormone response to levodopa was, however, significantly greater (p <0.05) in patients with retinopathy only [Table - 2].

Although, this abnormal growth hormone dyanamics in diabetics have been correlated with blood sugar levels in the reported patient no such association could be established. The' mean growth hormone was similar inpatients' with FBS levels below or above 200 mg. per cent. The severity of retinopathy however. was found to be significant determinant of growth hormone response as patients with back­ground retinopathy had significantly greater (p <0.05) mean values, than those with pro­liferative retinal changes in (Talbe-3). To explain this association it has been proposed that the elevated growth hormone levels in diabetics enhances fatty acid catabolism with accumulation of sorbitol leading to basement membrane thickening and other changes secondary to sorbitol accumulation[21]. Alter­natively other growth hormone dependant mechanisms, viz. hepatic synthesis of large plasma pooteins including fibrinogen and alpha-2 globulins[19], altered basement mem­brane glycoprotein synthesis[22], accelerated platelet aggregation secondary to changes in a von-Willebrand factor activity , have also been suggested however, the precise bio­chemical mechanism of growth hormone action and its role in the pathogenesis of diabetic retinopathy still remains unclear.


  Summary Top


In the present study 23 diabetics (16 with retinopahy, 7 without retinopathy) and 8 non diabetic healthy controls were studied. Serum growth hormons were measured in the fasting state and one hour after levodopa administration.

The mean growth hormone levels were significantly higher in the diabetics as com­pared to controls, however there was no cor­relation between the mean growth hormone levels (either in the fasting state or after levodopa stimulation) and presence or absence of diabetic retinopathy although diabetics with retinopathy has significantly greater mean growth hormone response. The mean growth hormone was found to have no correlation with the fasting blood sugar levels. Diabetics with background retinopathy had significantly greater mean growth hormone than those with proliferative retinal changes.[23]

 
  References Top

1.
Powell, E.D.V.; Frantz, A.G., Ralkin, M.T. et al., 1966, New. Eng. J. Med. 275, 922.  Back to cited text no. 1
    
2.
Lundback, K: christensen, N.J., Jensen, V.A. et al., 1970, lencet. 2:131.  Back to cited text no. 2
    
3.
Lundback, K.: Christensen, N.J.,Jensen. V.A. et al., 1971, Danish. Med. Bull. 18:1.  Back to cited text no. 3
    
4.
Merimee, T.J.: Fineberg, S.E. and Hollander, W., 1973, Diabetes. 23:273.  Back to cited text no. 4
    
5.
Merimee, T.J.; Fineberg, S.E. and Hollander, W., 1973, Diabetes. 22:813.  Back to cited text no. 5
    
6.
Passa, P.; Rousselie, F.: Gauville, C. et al., 1977, Diabetes. 26:113.  Back to cited text no. 6
    
7.
Knoph, H.F.; Fajan, S.S., f'oyd J.C. et al., 1972, Diabetes. 21 (Suppll. 1):322.  Back to cited text no. 7
    
8.
Passa, P.; Granville, C. and Caniveb, P., 1974, Lan­cet. 2:27.  Back to cited text no. 8
    
9.
Holand, P.M.; Landers, M.B. III, Lebovits, A.E. et al., 1976, Amer. J. Ophthal. 82:208.  Back to cited text no. 9
    
10.
Fajan, S.S. and Conn, J.W., 1959, Ann.N.Y.Acad. Sciences. 82:208.  Back to cited text no. 10
    
11.
Scheie, H.G. and Albert, D.M.S., 1977, In textbook of ophthalmology W.B. Saunders, New York.  Back to cited text no. 11
    
12.
Lin. T. and Tucci. H., 1974, Ann. Inst. Med. 80: 464.  Back to cited text no. 12
    
13.
Meek, J.C.; Stoskoph, M.M. and Botinger, RE., 1970, Clin. Chem. 16:845.  Back to cited text no. 13
    
14.
Kohner, E.M. and Dollery, C.T., 1975, Diabetic retinopathy: In complicsation of diabets. Edied by H. and J. Jarret. pp 7-98. Edward Arnold, London.  Back to cited text no. 14
    
15.
Johnsen, K. and Hansen, A.P., 1969, Brit. Med. J. 2:356.  Back to cited text no. 15
    
16.
Hazen,T.C.;Lawren,A.M.andKristein,L.,1971,J. Lab. Med. Clin. 78:993.  Back to cited text no. 16
    
17.
Hansen, A.P., 1970 J. Clin. Invest. 43:1467.  Back to cited text no. 17
    
18.
Hansen, A.P., 1973, Diabetes. 22:619.  Back to cited text no. 18
    
19.
Little, H.L., 1976, Trans. Amerc. Ophth. Soc. 74: 573.  Back to cited text no. 19
    
20.
Hansen, A.P., 1971, J. Clin. Invest. 51:1806.  Back to cited text no. 20
    
21.
Bearumont, P. Schofield, P.J., Hollows, F.C. et al., 1971, Lancet. 1:579.  Back to cited text no. 21
    
22.
Albert, KC.M.M. and Hockaday, T.D.R., 1975, The Biochemistry of the complications of diabetes mellitus in. Complications of Diabetes. edited by H. Keen and J. Jannet. pp. 22:264, Edward Arnold. London.  Back to cited text no. 22
    
23.
Sad i, K.E.; Levine,J.W., Nair, R.M.S. et al., J. Clin. Endo. & Methals.  Back to cited text no. 23
    



 
 
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