NUTRITION AT GREAT HEIGHTS

NUTRITION AT GREAT HEIGHTS

698 PREVENTION OF POISONING SIR,-Isupport Dr. Goulding’s plea for strip packs (last week, p. 636). Since aspirin can be obtained without difficulty fr...

318KB Sizes 4 Downloads 54 Views

698 PREVENTION OF POISONING SIR,-Isupport Dr. Goulding’s plea for strip packs (last week, p. 636). Since aspirin can be obtained without difficulty from pharmacies and general shops it is easy to obtain supplies up to any number. Acts of deliberate self-poisoning are often impulsive. Difficulty in taking the drug may allow the mood to pass. I had one female patient who was found sitting in a chair weeping. Her lap was full of wrapped ’Aspro ’ tablets and around her were torn packings-she had given up after undoing 15. Strip packing will not deter the determined psychotic, but it could cut the number of young " inadequates " admitted. Certainly it would cut the number of children poisoned with aspirin-34 out of the 110 children admitted with poisoning last year had taken aspirin. There could be a case for extending strip packing to other dangerous drugs. A further 25 children were poisoned with other tablets, mainly antidepressants and hypnotics. In addition, is it not time that aspirin and allied substances should be barred from shops other than pharmacies, and that there counter-hands should be warned of their dangers and told not to sell them to children ? General Hospital, W. A. NICHOLSON. Hartlepool, Co. Durham.

morning of the 1st day 12-5 units was also injected intravenously. Treatment was well tolerated in all cases, and no side-effects were observed. Average plasma-hydrocortisone levels (mg. per 100 ml.), measured on an opton spectrofluorimeter, rose strikingly, as follows: 11’4 ±0-8 before, 315-191hour after, and 36-44:3-1 2 hours after the intravenous injections. The number of eosinophils in the circulating blood decreased considerably. Urinary output of total 17-ketosteroids, total 17K-hydroxycorticosteroids, and Bloodpregnanetriol increased significantly (see table). pressure, blood-sugar, serum cholesterol, sodium, potassium, and chloride, urinary sodium, chloride, and creatinine output, and endogenous creatinine clearance did not change strikingly. Urinary potassium excretion rose: the 3-day average (meq. per 24 hours) was 38-6-1-9 before, and 48-2±3-4 during, the administration of S.H.C. The substance was also administered to 3 patients who were hyperergic to other corticotrophin products, but hypersensitivity was not found. The details of this

study will be reported in Acta MedicaHungarica.

I Department of Medicine, University Medical School, Szeged, Hungary.

K. KOVÁCS F. A. LÁSZLÓ F. DURSZT I. SZIJJ

I. FAREDIN I. TÓTH L. CZAKÓ A. BIRO M. JULESZ.

EFFECTS OF SYNTHETIC HUMAN

CORTICOTROPHIN al.l synthesised human corticotrophin having the same aminoacid sequence as found by Lee et al. The biological activity of this polypeptide has been studied in our laboratory and the preliminary results are reported here. Biological activity was first examined in rats by the method of Lipscomb and Nelson.3 Synthetic human a-corticotrophin (S.H.C.) was administered in various amounts intravenously to rats hypophysectomised a few hours earlier and the plasmacorticosteroid level was measured on an ’Opton ’ spectrofluorimeter. The activity of S.H.C. was expressed in units by comparing its effect with that of highly purified corticotrophin (Organon). s.H.c. caused a striking ascorbic-acid depletion in the adrenals of hypophysectomised rats. It considerably decreased the number of eosinophils in the circulating blood of intact rats and induced adrenal enlargement and thymic atrophy. Since the thyroids, ovaries, and uterus did not show any change the substance possessed no thyrotrophic or gonadotrophic activity. The rats tolerated it well: body-weight did not decrease, there were no toxic reactions, and microscopically no abnormalities were seen in their organs. It caused transitory hypoglycxmia in intact and in adrenalectomised mice, but no decrease of blood-sugar level could be demonstrated in alloxandiabetic mice. This extra-adrenal effect, occurring also after the administration of other corticotrophin products, is explicable by insulin release.4** The effect of s.H.c. has also been studied in ten patients (five males, five females, average age 27 years) with no endocrine or other organic diseases. 12-5 units was administered intra8 hours for 3 consecutive days, and on the muscularly every

SIR,-In

1. 2. 3. 4.

1967

Bajusz

et

Bajusz, S., Medzihradszky, K., Paulay, Z., Lang, Zs. Acta chim. hung. 1967, 52, 335. Lee, T. H., Lerner, A. B., Buettner-Janusch, V. J. biol. Chem. 1961, 236, 2970. Lipscomb, H. S., Nelson, D. H. Endocrinology, 1962, 71, 13.

THE NICOTINE HABIT SIR,-I was interested to read Dr. Grant’s response (last week, p. 644) to your annotation (March 16, p. 579). Plasma11-hydroxycorticosteroids are antagonistic to the actions but not to the production of insulin, and so their rise after heavy smoking could well explain my finding of hyperinsulinism1 in such individuals. University Department of Nutrition, Queen Elizabeth College, London W.8.

NUTRITION AT GREAT HEIGHTS SIR,-In a recent study of the nutrition and health of the Indian herdsmen who live in the mountains around the desert of Atacama at a height of 4000-4500 metres above sea-level, I found no signs of hypovitaminosis, although their intake of vitamins A and D was insignificant, and of vitamin C about 1 mg. daily. These people obtain three-quarters of their caloric requirements from dried corn brought from the lowlands and a quarter from meat (mostly dried in the sun) and offal from their herds of llamas, goats, and sheep. They do not use milk or milk products. Fruit and vegetables are unknown. Some of the ten family groups, whose nutrition was studied for a year, suffered periodically from hunger. The children showed signs of retarded physical evolution and hypomineralisation of their bones, especially of the chest, which was often deformed as a result of the mother’s custom of tightly " binding the chest of newborns in order to avoid deviations of the vertebral column ". This hypomineralisation of the bones was probably not due to deficiency of vitamin D-the intense ultraviolet irradiation from the permanent sunshine at this altitude is sufficient to explain the absence of typical rachitic symptoms. The softness of the bones during growth was due

Lebovitz, H. E. Excerpta med. Int. Congr. Ser. 1965, 83, 1231.

EFFECT OF S.H.C. ON URINARY OUTPUT OF TOTAL

1.

17-KETOSTEROIDS,

(mg.

PER

STEPHEN SZANTO.

TOTAL

24 HOURS,

Szanto, S. Br. med. J. 1967, iii,

17
±S.E.)

178.

AND PREGNANETRIOL

699 " low-calcium rickets ", for their diet contained only 75 mg. of calcium daily. Keratosis pilaris, which most textbooks consider a typical sign of vitamin-A deficiency, was seen in almost all children between four and fourteen years of age; but I treated a group of them with high doses of vitamin A for three weeks without any effect. This well-known dermatological feature is found in all children over all the world who are living under bad hygienic conditions, and it is probably not due to deficiency of vitamin A. Further, I never saw " Bitot’s spots ". I did not test for nyctalopia, but from my experience of living for years amongst these Indians, I am sure that their night vision is excellent. Years ago I studied Eskimos similarly, and thought that their very good night vision was due to their high intake of vitamin A (50,000 i.u. daily). I now believe that visual acuity in darkness depends also on racial and individual factors. It seems to be better developed in dark-complexioned people than in Caucasians, perhaps owing to their greater choroidal pigmentation. Despite their low vitamin-C consumption, scurvy was unknown. The Arctic reports, which are rich in accounts of scurvy, show that this malady usually occurs in men who live on a diet poor in proteins. I never proved a single case of The scurvy in Eskimos who lived on their natural diet.1 Indian herdsmen’s 95 g. of protein daily may be sufficient to protect them against scurvy. The deficient atmospheric content of oxygen at this altitude (12% against 21% at sea-level) partly explained the high infant mortality (300 per thousand live births) and the retardation of body growth. For the same reason large animals, such as horses, cows, and pigs, cannot live and reproduce themselves at heights over 4000 metres. Oxygen, too, is of course a very important nutritional factor.

to

Hospital de Niños, Salta, Argentina.

ARNE HOEYGAARD.

IONIC HORMONAL PRECURSOR HYPOTHESIS SIR,-Following our observations that certain inorganic cobalt compounds such as cobaltous chloride 2 and sodium cobaltinitrite 3-5 possess anti-tumorigenic and anti-inflammatory activities, induce cleft palates, and strikingly inhibit cleft palates produced by cortisone 6 in mice, we suggest that cobalt ions not only mimic the peripheral actions of cortisone under special circumstances, but also act in a similar if not identical manner. This " ionic hormonal precursor hypothesis " postulates that the forebears of certain hormones were specific cations and anions which were obtained by primitive organisms from their aquatic environment. With increased cellular specialisation and, in some cases, when evolution or transition from aquatic to terrestrial environments occurred, ionic availability became severely restricted. To compensate, the organism was forced either to incorporate the ion in a more complicated and efficient substance (iodine in thyroxine), or to synthesise a different compound (cortisone, posterior pituitary) whose actions could be enhanced by the presence of the original ion (cobaltand magnesium," respectively, in these compounds). The attraction that certain specialised tissues show for ions (cobalt in adrenal tissue,9 iodine in thyroid 10) may indicate a vestige of the early capability of the developing organism to entrap these ions from the sea. Thus, to confirm this hypothesis one would anticipate a more dramatic ionic 1. Hoeygaard, A. Studies on the Nutrition and Physiopathology of Eskimoes. Oslo, 1941. 2. 3. 4. 5. 6. 7. 8. 9.

Kasirsky, G., Gautieri, R. F., Mann, D. E., Jr. J. pharm. Sci. 1965, 54, 491. Orzechowski, R. F., Gautieri, R. F., Mann, D. E., Jr. ibid. 1964, 53, 388. Thompson, R. S., Gautieri, R. F., Mann, D. E., Jr. ibid. 1965, 54, 595. Mancini, R. T., Gautieri, R. F., Mann, D. E., Jr. ibid. 1964, 53, 385. Kasirsky, G., Gautieri, R. F., Mann, D. E., Jr. ibid. 1967, 56, 1330. Fisher, J. W. J. Pharmac. exp. Ther. 1961, 132, 232. Chan, W. Y., Kelley, N. ibid. 1967, 156, 150. Braude, R., Free, A. A., Page, J. E., Smith, E. L. Br. J. Nutr. 1949, 3, 289.

10.

Mann, W., Leblond, C. P., Warren, S. L. J. biol. Chem. 1942, 142,

905.

response in foetal tissues than in those of the adult. This has

been noted in the interaction of cobalt in mice. Department of Pharmacology, Temple University, Philadelphia 40, Pennsylvania.

compounds and cortisone DAVID E. MANN, Jr. RONALD F. GAUTIERI GILBERT KASIRSKY.

A NEW MUCOPOLYSACCHARIDOSIS? SIR,-Various workers 12 have suggested that progressive myoclonus epilepsy with Lafora inclusion bodies could be a glycoprotein-acid-mucopolysaccharide dystrophy. In our study of a patient with Lafora inclusion bodies by cortical and liver biopsy,3 we observed an increase of mucopolysaccharides, and by electrophoresis and ’Dowex ’-column fractionation we also found an abnormally high quantity of heparitin sulphate. The father and the brother of our patient showed the same increase of urinary mucopolysaccharides as the patient herself. Since, in a similar case, Janeway et al. detected an increase of urinary mucopolysaccharides which later became normal, we were inclined to think that our findings might be fortuitous. However, we have found the same features in two other patients, who are first cousins. Both are children of consanguineous parents and have a slowly progressive form of

myoclonus epilepsy. Could this syndrome be a new inborn error of metabolismmucopolysaccharidosis with a predominantly motor clinical expression ? The syndrome may include other reported casesfor instance, those in which the clinical expression is characterised by extrapyramidal symptoms, with inclusion Lafora bodies.5 Institut Universitaire de Génétique Médicale, Laboratoire du Service de Chirurgie de l’Hôpital Cantonal, Geneva, Switzerland.

E. RALLO F. INFANTE.

ESCALATOR INJURIES seen seven serious injuries to children as a result of escalator accidents in the past five years at this hospital. Four of these were seen in a fairly short period of time.6 Of these seven injuries, six were traumatic amputations of portions of one or both hands; the seventh was a buttock injury sustained by a child who was sitting on the escalator. All these injuries resulted from a portion of the body being caught between the treads of the step and the comb-plate, the teeth of which interdigitate with the treads of the escalator steps at the top and bottom of the escalator. The injuries are dirty wounds with various degrees of softtissue and skeletal damage, similar to those seen in industrial accidents. As in other types of severely contaminated wounds, reconstruction of the damaged limb may have to be staged. The newer types of escalators have narrower tolerances between moving and stationary parts, making it more difficult for a foot, finger, or part of the clothing to be caught. However, many of the escalators still in use fall below what would be minimum safety standards. This is certainly an area in which preventive medicine on the part of local government, stimulated by the interest of doctors such as Mr. Kates (Feb. 17, p. 365) and Mr. Reid (March 2, p. 473), would prevent some tragic accidents to children.

SIR,-We have

St. Vincent’s Hospital and Medical Center of New New York 10011.

York,

ANTHONY SHAW VINCENT J. FONTANA.

Seitelberger, F., Jacob, H., Peiffer, J., Colmant, H. J. Fortschr. Neurol. Psychiat. 1964, 32, 7. 2. Schwarz, G., Yanoff, M. Archs Neurol., Chicago, 1965, 12, 2. 3. Rallo, E., Martin, F., Infante, F., Beaumanoir, A., Klein, D. Unpublished. 4. Janeway, R., Ravens, J. R., Pearce, L. A., Odor, D. L., Suzuki, K. Archs Neurol., Chicago, 1967, 16, 6. 5. Vanderhaegen, J. J., Manil, J., Franken, L., Cappel, R. Acta neuropath. 1967, 9, 45. 6. Cahill, M. J., Shaw, A., Fontana, V. J. New Engl. J. Med. 1964, 271, 1.

1310.