TUBERCULOSIS IN IMMIGRANTS

TUBERCULOSIS IN IMMIGRANTS

620 tion could be secured with old tuberculin ; but at present this is clearly not practical on a large scale. We can measure hypersensitivity by the ...

177KB Sizes 5 Downloads 111 Views

620 tion could be secured with old tuberculin ; but at present this is clearly not practical on a large scale. We can measure hypersensitivity by the skin reaction in a single human being, but we have as yet no ethical conmethod of measuring individual immunity ; statistical to on cumbersome we have rely sequently estimates of immunity, and we should therefore not confuse ourselves by thinking that immunity and hypersensitivity must have something in common. F’limwell. lvadhurst,

G G. Sussex..

E. E LOXTON. . L nvrm
TUBERCULOSIS IN IMMIGRANTS

Sm,-In his letter of Jan. 29 Dr. James says that " in

populations with high tuberculosis death-rates there is always a high proportion of positive reactors, and a high reactor-rate in children is always associated with a high death-rate in young adults." Lewis do not bear this out.

The data

as

found in

In Lewis there is the town of Stornoway (population 4817) and four rural parishes-Stornoway (7842), Barvas (5019), Lochs (3111), and Uig (2716). The villages comprising the TUBERCULOSIS IN LEWIS

amative, d==dead, t = total. The 5-12 age-group was chosen for comparative purposes, because the after age of 12 the country children come to the Nicolson Institute in the burgh of Stornoway.

parish of Stornoway are situated on either side of Broad Bay at distances of from 21/2 to 14 miles, while all the other parish villages are at least 12 to 35 miles from the town. The more remote the lower the positive reactor-rate but the higher the death-rate (see accompanying table). z

Stornoway, Lewis.

R. STEVENSON DOIG. DOIG

CHEMOTHERAPY OF LEPROSY

SiR,ŇMy experience in Northern Rhodesia prompts to endorse Dr. Jopling’s remarks (Jan. 8). In 1951 I saw something of Dr. Lowe’s outstanding work in Eastern Nigeria and was greatly impressed, but results of treatment here in Rhodesia have not been equal to me

Dr. Lowe’s. Since 1950

some

1006

patients

here have had

sulphone

treatment, and while results on the whole are good there is a " hard core " of cases which show little response. It is difficult to assess results accurately in terms of statistics, as conditions here are primitive and patients frequently abscond during treatment ; but of the initial group of 52

patients we started on diaminodiphenylsulphone (D.D.S.) in 1950, 5, all with severe lepromas, have died, while 20 are still here under our care. For five years these 20 patients have been under close medical supervision and on continuous D.D.s., and 7 of them still show masses of bacilli in their smears with no material change in their clinical condition. 10 lepromatous patients that showed a few bacilli in smears in 1950 have now become persistently negative and the disease appears to be arrested. 3 patients were tuberculoid cases, bacteriologically negative when treatment was commenced. These results do not encourage complacency. - Mu<’*h is the "hard core " of we must attack if the

leprosy is self-limiting and it resistant and contagious cases

disease is to be wiped out. It will be a pity if the mass of sulphones diverts attention from the need for more effective remedies.

use

Chitokoloki

Leprosy Settlement, Balovale,

Northern Rhodesia.

J. T. WORSFOLD.

ADRENALECTOMY FOR HYPERTENSION SiR,-This title of your leading article on Jan. 8, the statement in it that " hypertension is not associated

with increased secretion of ..." and the quotation from Jeffers et al.-" This is an experimental approach which cannot at present be recommended as a treatment for hypertension "-all suggest that hypertension is an entity which will respond to a single therapeutic

procedure.

This attitude is anachronistic. It is a " fossil fancy of a bygone age " when clinicians believed that a single mechanism was responsible for the elevation of the blood-pressure. Today we know that hypertension may be brought about by six or seven distinct mechanisms, each of which must be dealt with differently. To refer to the treatment of hypertension in this way is as unjustifiable as to talk about the treatment of pyrexia or of an increased erythrocyte-sedimentation rate. We are all guilty of this solecism, and one reason may be our realisation that the majority of cases of hypertension fall into the group labelled " essential," where itis likely that a single mechanism is responsible for the increase of the blood-pressure. I presume that this thought lay behind your con. fident assertion : " There is now good evidence that, except in phaeochromocytoma, hypertension is not associated with increased secretion of adrenaline or noradrenaline, and it is the adrenal cortex that plays the more important part in pathogenesis." I find it difficult to accept this view, for I believe that the adrenal cortex has little or nothing to do with the pathogenesis of essential hypertension. On the other hand, I regard the evidence in favour of noradrenaline as particularly strong.! Here I would only emphasise that the fall in blood-pressure which follows destruction and blocking of the sympathetic pathways is best explained by these procedures interfering with the production and/or the secretion of noradrenaline. That the adrenal cortex plays little or no part in the pathogenesis of essential hypertension is indicated by these facts : 1. Cushing’s syndrome (adrenal cortical hyperplasia, adrenal cortical adenoma) is rare. 2. Essential hypertension is common. 3. The stigmata of Cushing’s syndrome are not found in essential hypertension. 4. The cause of the hypertension in Cushing’s syndrome is almost certainly plethora induced by sodium retention. 5. Sodium retention is not a feature of uncomplicated essential hypertension. ° 6. Goldzicher2 states : " Injection of cortical extracts. although raising the blood pressure in adrenal insufficiency, does not alter the blood pressure in normal controls. There is no reason to believe that cortical hormone is directly responsible for an increase in the arterial toilus, for the re-establishment of the normal blood volume explains the reaction of the adi’enalectomised animal." 7. McMichael3 states : " efforts to demonstrate increased excretion of suprarenal cortical substances in the urine of£ hypertensives " [presumably essential hypertensives] ’’ have not yet succeeded." ,

Goldblatt’s observation that hypertension induced experimentally by constriction of one renal artery could be abolished by adrenalectomy has little bearing on the solution of our problem. All it proves is that hypertension produced by one mechanism (renal hypertension) can Menof, P. Lancet, 1954, ii, 996 ; Ibid, Jan. 22, 1955, p. 204, Goldzicher, M. A. The Endocrine Glands. New York, 1939, 3, McMichael, J. Brit. med, J. 1952,i, 933. 1. 2.