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Edit ImageLathyrism India 1963
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JOURNAL Of THEINDIAN MEDICAL ASSOCIATION
CALCUTTA, AUGUST 16, 1963
LATHYRISM
yathyrism, a crippling disease, has been known
Ücenturies among the peasants in India, and the
í'Hindu literature in medicine has a mention of
s disorder. In the 17th century, it was attri-
to eating of the vetch, lathyrus and this
is yet generally held. It is mostly prevalent
|:India, though outbreaks have been reported
>m several European continental countries.ice the beginning of this century one finds fre-
lt reports of the disease, Having occurred in
lie or .epidemic form in several provinces,
tícularly Bihar, Madhya Pradesh and Uttar
idesh.1'10 Except for a few sporadic cases, the
ïse has not been encountered in West Bengal.11
:ent outbreak in this State investigated in
[ail by Chaudhuri et al.12 the report of which
irs elsewhere in this issue will, therefore, be
eiterest.
if, A. G.—Brit. Med. J., 2 : 707, 1903.^BUCHANAN, A.—Report of Lathyrism in the Central
ices in 1896-1902, 1904, Nagpur.toy, D. M.—Indian Med. Gaz., 8 6 : 263, 1951.LCTON, H. W.—Ibid., 57 : 241, 1922.
|HCCOMBIE YOUNG, T. C—Indian J. Med. Res., 15 :
£1927.
ÏANAPATHY, K. T. AND DwiVEDi, M. P.—Studies onEpidemiology of Lathyrism, Lathyrism Enquiry
i. Unit, Gandhi Memorial Hospital, 1961, Rewa
r, H.—Indian J. Med. Res., 18 : 51, 1930.
r JÎD, S. K.—Antiseptic, 41 : 514, 1944.¿RANJAN, N. P.—Ibid., 41 : 652, 1944.
glrfAI,, s . B.—Indian Med. Gaz., 84 : 468, 1949.FCHAUDHURI, R. N.—Annual Rep. Calcutta School
"Med., 1959-60, 1961, Supdt. Govt. Printing, WestGovt. Press, Alipore, p. 34.
AUDHURI, R. N., CHHETRI, M. K., SAHA, T. K.
P. P.—/. Indian M. A., 41 : 169, 1963.
The disease usually affects people belong-
ing to the lower income group who happen
to live principally on khesari dal. Human
lathyrism, also called neurolathyrism is charac-
terised by weakness, spasticity and rigidity of
the leg muscles with increased deep reflexes.
The higher functions, cranial nerves, trunk and
upper extremities escape so that the morbid ana-
tomy is confined to the lower dorsilumbar region
of the spinal cord. While most workers blamed
Lathyrus sativus seed itself for its neurotoxi-
city,13' 14> 15 other investigators16 incriminated
Vicia sativus seeds as the real offender, the toxic
principle being divicine. In any case the precise
causative agent has, however, not been identified.
Surprisingly enough and contrary to the popular
belief, patients with features of lathyrism have
been reported from South India in nonlathyrus
eating population.17"18 On theother hand, several
workers19'21 considered that deficiency of certain
factors in the diet, e.g., vitamin A or carotene,
tryptophane and methionine are in some way
related to the disorder. Metallic poisoning (sele-
nium, manganese, etc.) has also been incriminated
for the neurological features of the disease on the
basis of high selenium or manganese content of the
1 3 ACTON, H. W. AND CHOPRA, R. N.—Indian Med.
Gaz., 57 : 432, 1922.14 MEGAW, J. W. D. AND GUPTA, J. C.—Ibid., 62 : 299,
1927.15 JACOBY, H.—Ibid., 81 : 246, 1946.1 6 ANDERSON, I/. A. P., HOWARD, A. AND SIMONSEN, J.
L.—Indian J. Med. Res., 12 : 613, 1925.17 MINCHIN, R. L. K.—Brit. Med. J., 1 : 253, 1940.18 GOPALAN, C.—Trans. Roy. Soc. Trop. Med. Hyg.,
44 : 333, 1950.19 MEIVLANBY, E.—Nutrition and Disease, 1934, Oliver &
Boyd, London, p. 136.2 0 BASU, K. P., NATH, M. C , GHANI, M. O. AND
MUKHERJEE, R.—Indian J. Med. Res., 24 : 1027, 1937.3 1 RUDRA, M. N., CHOWDHURY, L. M. AND SINHA, S.
P.—Indian Med. Gaz., 87 : 89, 1952.
207
2Ô8 ]. INDIAN M. A., VOL. 41, NO. 4, AUGUST 16, 1963
Lathy rus sativus seeds.22"23 This is comparable to
hepatolenticular degeneration due to copper
poisoning.
It is thus obvious that there is still many gaps
in our knowledge regarding the aetiological back-
ground of the disease. The recent reported out-
breaks have been studied by Chaudhuri et al.11
clinically, epidemiologically and biochemically.
Floods and poverty had driven many inmates of
the particular rural area to cultivate khesari and
live exclusively on the cheap product seasonally
for 4-5 years during which period the disease
appeared in the community. Some members of the
affected family and many others in the area con-
suming similar food, however, escaped. The
authors suggest that the disease in some of these
individuals might have been subclinical or at bio-
chemical level only. In fact, slighter forms are
rarely ever recognised clinically or reported. Bas-
ing their conclusions on biochemical and haemato-
logical investigations the authors for the first time
point out that the disease may be the result of
antigen-antibody reactions, the auto-antigen being
related to the khesari protein and nervous tissue
complex. The hyperglobulinaemia, particularly
increased gammaglobulin, elevated ESR and posi-
tive thymol turbidity test all may be no doubt to
some such mechanism and, therefore, the present
work opens up a new field for investigation which
should ultimately establish or deny the suggested
view.
Autoimmune diseases, i.e., diseases resulting
from antigen-antibody reactions, the antibody
being produced against one's own cells are being
M RUDRA, M. N.—Nature, 170 : 124, 1952.23 SADASIVAN, T. S., SULOCHANA, C. B., JOHN, V. T.,
SUBBARAM, M. R. AND GOPAUN, C—Curr. Sei., 29 : 86,I960.
increasingly recognised. Collagen diseases occur',
ring in relation to the connective tissue, dissemi-
nated sclerosis occurring in relation to the myelin
sheaths of the central nervous system, Hashimoto's
disease occurring in relation to the thyroid gland
have been attributed to the same mechanism. It may
be that the antigen-antibody reaction in lathyrism
occurs in relation to the nervous tissue of the spinal
cord, the injurious effect depending upon prolonged
consumption of khesari and the activity of the auto-
immune mechanism, the site of predilection being
the most vulnerable part of the spinal cord, viz,,
dorsilumbar region.
The authors found that the subjects were tak-
ing khesari for 3-5 months every year during the
said period, and they think such periodical stimula-
tion of the antigen-antibody reaction important
for finally bringing about the overt clinical syn-
drome. Persons in whom the reactions are mild
may only show biochemical abnormality and herein
lies the slender possibility for the prophylaxis of
the disease. At this stage, besides elimination of
the sensitising agent from the diet, use of steroids
may halt the progress of the reactions which may
ultimately culminate in the disease. This no doubt
entails costly and comprehensive biochemical
survey of the inhabitants in the lathyrus growing
regions but is worth consideration, in view of the
fact that the end stage of the disease is crippling
to the sufferer and burdensome to the family and
the State. In any case, all measures to discourage
the use of lathyrus as the staple diet should be
taken,> and replacement of the poor cultivators'
lathyrus crops by paddy, especially during periods
of scarcity, will go a long way to prevent the
disease, as is borne out by the experiences gained
in the reported outbreak of West Bengal.