7/29/2019 Lathyrism Biochem Serum Phosphatase 1946 Par Miles

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. tho fourth week of treatm ent, .«ecropsy showed- iliotypical thinning of the gut wall, with extensivedestruction of the mucosa of the colon and severesecon dary infection of th e colon wall. . •

The great majority of the remainder were not followedbeyond the point at which they became fit to travel.They then had haemoglobin values of 60% or more, hadlost their fever and diarrhcea, recovered an appetite

for food, and p ut on a good deal of weight. Areas ofskin ulceration were either healed, if small, or granula-ting. Patie nts who had been seriously ill were amnesicfor that period.

It is to be hoped that, when a similar clinical taskis next undertaken in an Indian famine, adequatelabora tory facilities will be at hand to enable the m aximalinformation to be obtained from the oppo rtunit y. .

SUMMARY

Indian famine is a special problem, because thepatients are usually already the victims of severaldebilitating pathological processes. They are oftenprofoundly ansemic and do not respond well or quicklyto liver and iron therap y. •

Mortality is very high among these very anaemic

patients, unless something can be done quickly toimprove the condition of their blood.Blood-transfusion, notoriously risky in ansemic people

is especially so among these debilitated famine victims.It does, however, offer the only method of saving manywhose condition cannot otherwise be controlled.

It follows that a safe technique for the administrationof blood was required, and a technique was adoptedwhich was bo th effective and safe. It em ploys ordin aryapparatus, is only a little more complex than'ordinarymetho ds of transfusion, and is very easy to manage whenassembled.

Details in the practical management are described,as the y are essential to success. : .

: Grateful acknowledgment is made to Dr. J. M. Smellie,late consulting physician to Eastern Command^ India, for

his interest and support, and to Drs. E. A. Wood andT.. N. S. Kurup for their collaboration in the use of themethod. . . . . - .. :. . . . . . . . . ..,'., .

SERUM PHOSPHATASE IN LATHYRISM

; •'-}•:"/.',.M\..N. B.TZDKA. ; EL. P . B H A T T A C H A E Y A U J ' , ; : '

From the Department of Medical Chemistry, Prince of Wales•••••;: •••:•.

:. • Medical College, Patna, India •'[•li:1i•.••...!•;.•.•,•.

' AXTH6TJ:GH lathyrisnxis an extremely disabling disease

and is fairly common in certain parts of the wbrld,particularly India, its aetiology, apart from its'associationwith a diet restricted to vetch-peas (dal), is still unknown .Several theories have been advanced—Acton (1922) citedby Young (1927), Anderson etal. (1925), Mellanby (1930),Geiger et al: (1933), Shah (1939)-^but all of the m' lack

a: convincing' experimen tal background. "According toJim&ieK Diaz et al. (1943) th e vetches contain a toxic sub-stance which antagoriises'some thermostable water-solublesub stanc e,' distinct from the known vitamins, w hich ispresent in certain foodstuffs. Lathyrism , they maintain,is due to massive doses of lathyrus peas and Ia6k, par-ticula rly, of foodstuffs of animal origin which furnishthe protective element. • ' , . . •

In view of the intimate relationship between vitaminBj and the nervous system, it is surprising that the stateof yitamin-Bi nutrition in lathyrism cases has not beeninvestigated so far, as lathyrism is the result of thedegeneration of pa rt of' the nervous system. We have ,made a comprehensive* survey of the state of v i t a m i n ^nutrition of lathyrism patien ts. It was soon evident th atthe diets of some of the patients were balanced and the.

! contents of their blood and urine were of an

order which might bo regarded as lying within normallimits.. It was thought that, though there might not.bean apparent vitaniin-Bj deficiency, there might be aphysiological one due to an unknown factor. We decidedto determine the serum-phosphatase levels of lathyrisnipatients. ' •: .

The serum phosphatase was determined by the methodof Bodan sky (1937). No magnesium ions were add ed, as

the native phosphatase value was of importance and noactiva tion was desirable. The values for nor mal sub jectsand lathyrism cases are given in the accompanying tab le,which shows that serum phosphatase in. lathyrism isconsistently and considerably higher than that in normalperson s. Out of the 10 cases investigated in not a singlecase does the serum phosphatase lie even on the border-line, and the minimal value is 228% higher than the

SERUM PHOSPHATASE

Serialno.

1

345(i

• 8

a10l i1 2

Mean

Median

IN NORMAL SUBJECTS AN D LATHYBISMCASES (ALL ABE MALES)

Normal subjects

Ago

(years)

22

50.2 44 030203 5

20273 52 3

2 6

Phosphatase(units)

2- 3

2 • i1 05-72-42-22-62-7i- 4)-8

•1

1-7

2-38

Lathyrism cases

Age(years)

20

I S40:!52024•> ^

IB45

30 .

Phoaphatase(unite)

38 -0

53-5Jfi-5 '42-535-S33 036-033-518-739-fi

38-7

maximum value in normal persons. The result is statis-tically significant. The possibility of such valuesoccurring by chance is less than 1 in 370.

It seems to us possible that the greatly increasedalkaline phosphatase which we have demonstrated inthe serum in lathyrism may possibly destroy the circu-lating cocarboxylase. ' If this is so, the patient may b«chemically saturated with aneurine but still functionallydeficient in vitamin B1# 'As a natural sequence to thisstate the nervous system may possibly degenerate.

We

suggest that the high serum phosphatase and aconsequent possible cocarboxylase deficiency in lathyrismare related to th e aetiology of the disease. We do notattem pt to explain how or why the serum phosphaterises in lathyrism. It is also possible that the h igh serumphosp hatase is the effect, an d not the cause, of lathyrism.It may be mentioned here that the inorganic-phosphateconten t of serum in lathyrism is unusually high. Usuallythe serum-phosphatase level is a measure of the severityof t h e dis ea se. .-_ ., , ._._. , ,. ,- ,' . - ; : : •-,:•, v ; . : , . , . , ; . ; . : ; - • •• ._> ,:\,r j

. - . . - . : , , ; , - : : ; - . ; ! : ; - / j . ; .'REFERENCES ; i W v , .; :;;;:.v. .-;;:;;Ur^--

Acton, H . W . (1922) Indian med. Oaz. 57, 241. • •••'-": -> • •: '- ;-i - ' • ' -Anderson, L. A. P . , Howard, A ., Simonsen, J_Jj.'(1925) Indian J.

med. Res. 12, 613. . " ,'."-.Bodansky, A. (1937) J. biol. Chem. 120, 167. • -

: ;- ,-;: •> i.;. •

Geiger, B. J., Steenbock, H., Parsons , H. T. (1933) J. Nutrit. 6,.427.Jimene z Diaz, C, Ortiz de Landazu ri, E., Roda, E . (1943) Rev. din.

. • espan. 8 , 1 5 4 . •;

'• -••• ' • ' • ' •:

Mellanby, E. (1930) Brit. med. J. i, 677. . . ,-Shah, S. B. A. (1939) Indian med. Qaz. 74, 385.Young, T. C. M. (1927) Indian J. m ed. Res. 15, 453. - ; : • . .

IN th e Times of April. 11 it was announced that Mr. JohnHunter and Prof. Bryan McSwiney have arrived at Kingston,Jamaica, as representatives of the University of Londonto consider plans for setting up a medical school as part ofthe proposed University of the West Indies. The new uni-versity would be associated with the University of London,and several of the West Indian governments have alreadyaccepted in principle the proposals for its establishment in

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