|Year : 1979 | Volume
| Issue : 2 | Page : 1-9
Role of Vitamin A deficiency and protein-calorie malnutrition in keratomalacia and Bitot's spots (A clinicopathologic study)
CV Raghuveer1, Amrit L Aurora1, RK Puri2, Philomena Mathew1
1 Department of Pathology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605006, India
2 Department of Paediatrics, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605006, India
Amrit L Aurora
Department of Pathology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605006
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Raghuveer C V, Aurora AL, Puri R K, Mathew P. Role of Vitamin A deficiency and protein-calorie malnutrition in keratomalacia and Bitot's spots (A clinicopathologic study). Indian J Ophthalmol 1979;27:1-9
|How to cite this URL:|
Raghuveer C V, Aurora AL, Puri R K, Mathew P. Role of Vitamin A deficiency and protein-calorie malnutrition in keratomalacia and Bitot's spots (A clinicopathologic study). Indian J Ophthalmol [serial online] 1979 [cited 2020 Sep 29];27:1-9. Available from: http://www.ijo.in/text.asp?1979/27/2/1/31231
Keratomalacia and Bitot's spots are generally considered to be due to Vitamin-A deficiency. However, though Vitamin-A deficiency is commonly seen in several parts of the country, keratomalacia afflicts only a few. The role of protein deficiency in the genesis of these lesions is far from clear. A detailed study of 100 paediatric patients suffering from protiencalorie malnutrition was undertaken to assess the importance of protein-calorie malnutrition in the development of keratomalacia and Bitot's spots.
| Material And Methods|| |
A detailed clinical and a thorough ophthalmological examination were carried out in 100 paediatric patients suffering from protein-calorie malnutrition- All the cases with varying degrees of xerophthalmia were graded according to Doesschate's classification, as given in [Table - 1]. The Bitot's spots were classified into pearly and mucoid types. [Figure - 1],[Figure - 2]
The cases were classified into 6 groups depending on the degree of malnutrition, according to WHO classification [Table - 2]. There were 63 males and 37 females. The youngest patient was 10 months and the oldest 12 years old.
The following laboratory investigations were carried out:
1. Haematologic investigations
Haemoglobin estimation by Sahli's method, packed cell volume, total WBC count and peripheral blood smear study including differential WBC count.
Urine examination was carried out for albumin, sugar and microscopy.
3. Stool examination
Stools were examined for ova and cysts in 71 out of the 100 cases by saline and iodine methods.
4. Biochemical investigations
i) Estimation of serum iron and total iron binding capacity by Bathophenanthroline method.
ii) Estimation of serum carotenes and Vitamin-A by Carr-Price method.
iii) Estimation of serum proteins by Biuret method.
5. Liver biopsy studies
Liver biopsy could be obtained in only 25 out of the 100 cases. Apart from studying paraffin sections stained with hematoxylin and eosin (H and E), special stains like reticulin, periodic acid Schiff (P.A.S.) and Masson's trichrome were carried out by standard procedures, 7sub wherever indicated.
6. Conjunctival cytology was also studied and is being reported elsewhere.
| Results|| |
I. Clinical findings
In Group I there were 7 cases of which 6 had Bitot's spots and I case had only conjunctival xerosis. 3 of these 6 cases with Bitot's spots had bilateral lesions. One case had pearly type and 2 had pearly and mucoid types. Three cases with unilateral lesions were of the pearly type.
In Group II there were 14 cases of which 10 had Bitot's spots. Of the remaining 4 cases, 3 had conjunctival xerosis and night blindness, and I had only night blindness with no manifest eye changes. 6 out of the 10 cases with Bitot's spots had bilateral lesions. The Bitot's spots were of the pearly type except in one case where the left eye showed mucoid type. The remaining 4 cases with unilateral Bitot's spots were of the pearly type.
In Group III (Kwashiorkor cases) there were 5 cases of which only 2 had Bitot's spots, one of them had bilateral lesions. Both the cases with Bitot's spots were of the pearly type. The remaining 3 cases in the group had only conjunctival xerosis.
In Group IV (nutritional dwarfism cases), of the 29 cases, 20 had Bitot's spots, 2 had only conjunctival xerosis, I had conjunctival with corneal xerosis and 1 had Keratomalacia. 5 cases did not have any known symptom or sign of eye disease. Out of the 20 cases with Bitot's spots, 12 had bilateral lesions. 8 of these with bilateral lesions were of the mucoid type, 3 were of pearly type and in 1 there was pearly type in the right eye and mucoid type in the left eye. The remaining 8 cases with unilateral Bitot's spots had pearly type in 7 cases and mucoid type in 1 case.
In Group V (Marasmic-Kwashiorkor cases) there were 20 cases of which only 8 cases had Bitot's spots. 7 out of these 8 cases had bilateral lesions and I case had unilateral Bitot's spots. The Bitot's spots were of the pearly type in all the 8 cases. There were as many as 10 cases with conjunctival xerosis alone and 2 cases with Keratomalacia, one of which had Bitot's spots also.
In Group VI (Cases of Marasmus) there were 25 cases out of which 8 cases had no known clinical sign or symptom of eye disease. 10 cases had Bitot's spots and 4 had Keratomalacia. There were 2 cases with conjunctival xerosis and I case with corneal xerosis alone. 6 out of the 10 cases with Bitot's spots had bilateral lesions and all of them were of the pearly type. Of the 4 cases with unilateral Bitot's spots, 2 were of pearly type and 2 were of mucoid type.
Liver biopsy could be obtained in only 25 cases. The microscopic findings are given in [Table - 3]. The prominent changes in liver in the marasmic-Kwashiorkor group consisted of varying degrees of fatty change. [Figure - 3]. It was interesting to note that most of the cases belonging to the marasmus group on the other hand, showed evidence of nonspecific hepatitis with spur formation in the portal areas. [Figure - 4].
II Laboratory findings
The biochemical investigations in Group I [Table - 4] showed lower protein levels in cases with Bitot's spots as compared to the only case who did not have Bitot's spots. However as there was only one case in the group without Bitot's spots as against 6 with Bitot's spots, the biochemical parameters could not be compared statistically.
In Group II [Table - 5], cases with Bitot's spots showed a significantly lower value of total serum proteins and serum albumin than cases without Bitot's spots. The difference was statistically significant (P<0.001 and 0.1 respectively). The total iron binding capacity in cases with Bitot's spots was 323.6+79.756 μg/100ml as compared to 427.5+17.31 µg/100 ml in cases without Bitot's spots (P<0.05). Again, the serum Vitamin-A (corrected value) level in cases with Bitot's spots was lower (15.05+ 2.42 ug/ 100ml) as compared to cases without Bitot's spots (19.0+6.01 ug/100 ml).
In Group III [Table - 6] the total serum proteins and albumin levels were lower in cases with Bitot's spots, than in cases without Bitot's spots. There were only 2 cases in the group with Bitot's spots. The serum carotenes and Vitamin-A were lower in cases with Bitot's spots, than in cases without Bitot's spots.
In Group IV [Table - 7] the total serum proteins and total iron binding capacity showed lower values in cases with Bitot's spots than in cases without Bitot's spots. The other parameters viz. serum albumin, serum carotenes serum Vitamin-A and serum iron did not show significant differences between cases with and without Bitot's spots. The average haemoglobin value for cases with Bitot's spots was 8.06 G/ 100 ml and that for the only case with Keratomalacia was 3.5 G/ 100 ml.
In Group V cases with Bitot's spots, the total serum protein, total iron binding capacity and serum Vitamin-A were statistically lower compared to cases without Bitot's spots [Table - 8]. The average Haemoglobin values for cases with Bitot's spots was 7.6 G/100 ml and that for cases with Keratomalacia was 8.5 G/ 100 ml.
In Group VI [Table - 9], cases with Keratomalacia showed significantly low values for total serum proteins, serum iron and Vitamin-A as compared to cases without Keratomalacia. The average haemoglobin values for cases with Bitot's spots was 9.3 G/100 ml and for cases with Keratomalacia was 5.1 G/100 ml.
| Discussion|| |
Protein-calorie malnutrition affects every tissue and every cell in the body and is rampant in the pre-school children, especially in the developing nations.
Vitamin-A plays a vital role in the cellular growth and differentiation. The maintenance of integrity of epithelial cells and the metabolic functions of subcellular membranes is an important function of Vitamin-A (Adhikari et al). Keratinizing metaplasia is believed to be caused by Vitamin-A deficiency. However the relationship of Bitot's spots to Vitamin-A deficiency is controversial.
In the present study, out of the 100 cases 57 cases had Bitot's spots. The biochemical investigations in Group I showed a lower total serum proteins in cases with Bitot's spots as compared to cases without Bitot's spots. This finding is comparable to the results obtained by Bagchi' who studied 46 cases with Bitot's spots.
In Group II also cases with Bitot's spots showed a significantly lower value of total serum proteins, serum albumin and total iron binding capacity. The lower value for total iron binding capacity could be explained on the basis of protein deficiency in these cases, the binding protein itself becoming deficient. The lower serum Vitamin-A levels in cases with Bitot's spots could also be explained on the basis of hypoproteinemia in these cases. The .hypoproteinemia itself could have contributed to impaired absorption of Vitamin-A and hence its low levels in the blood.
The low levels of total serum proteins, albumin, serum carotenes and serum Vitamin-A in Group III cases with Bitot's spots could be due to a decreased absorption of Vitamin-A as a result of protein malnutrition or due to deficiency of carotenes and Vitamin-A . in the diet itself or a consequence of both the factors acting together.
In Group VI, cases with Keratomalacia showed significantly low values for total serum proteins, serum iron and Vitamin-A. There was thus a precipitous fall in serum Vitamin-A in Keratomalacia. Sinha believes that whatever may be the role of Vitamin-A, a simultaneous deficiency of protein might be necessary for the development of Keratomalacia. Perhaps the level of both Vitamin-A and protein in blood is gradually lowered so that the "stabilizing influence" on the tissues of the cornea is removed resulting in liquefaction of the cornea.
The present study indicated that vitamin-A and protein deficiency, especially the latter are significant factors in the causation of Bitot's spots and Keratomalacia. However these factors failed to account for the sudden and rapid necrosis of the cornea in Keratomalacia. It is not improbable that low serum iron and haemoglobin levels besides protein and Vitamin-A deficiencies adversely affected the metabolic activity of corneal epithelial cells. The collagenase, released suddenly from these degenerating cells was perhaps responsible for the sudden necrosis of the cornea.
| Summary|| |
One hundred cases belonging to the paediatric age group, suffering from protein-calorie malnutrition with or without manifest VitaminA deficiency were studied. It was shown that protein and Vitamin-A deficiency were important for the occurrence of Keratomalacia. The role of corneal collagenase as a probable inciting factor for the development of Keratomalacia has been suggested.
| Acknowledgement|| |
The authors extend their sincere thanks to the Director, JIPMER, Pondicherry for his permission to conduct this study and Roche Products Limited, Bombay, for providing Vitamin-A standard.
| References|| |
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Bagchi, K., 1959, J. Indian Med. Assoc.. 33, 401.
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Dacie, J.V. and Lewis, S.M., 1968, Practical Haematology, ELBS and J & A Churchill Ltd., London, pp. 45, 59 and 61.
Davidsohn, I. and Henry, J.B., 19;4, ToddSanford Clinical Diagnosis by Laboratory Methods, W.B. Saunders Company. p. 15.
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Rodger, F.C. and Sinclair, H.M., 1969, Metabolic and Nutritional Eye Diseases, Charles C. Thomas Publishers, U.S.A. p. 202.
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Varley, J., 1967, Practical Clinical Biochemistry, Arnold-Heinemann, pp. 473 and 608.
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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7], [Table - 8], [Table - 9]