MANIFESTATIONS OF ENDEMIC FLUOROSIS

MANIFESTATIONS OF ENDEMIC FLUOROSIS

610 In all these instances excessive intake produces-or is said to produce-changes which are related to the known action of the factor concerned as i...

224KB Sizes 32 Downloads 187 Views

610

In all these instances excessive intake produces-or is said to produce-changes which are related to the known action of the factor concerned as indicated by the effects This was first shown with hyperseen in deficiency. vitaminosis D, which gave rise to an increase in the blood level ofphosphate and calcium with consequent calcification.4 Excess of nicotinic acid affects the skin and occasionally the gastrointestinal tract, and excess of vitamin Bi is reported to affect the nerves. A novel aspect of hypervitaminosis, however, has recently been studied by Loewenthal of BaBle.8 He suggests that large amounts of ascorbic acid, which are excreted by the kidney, might produce changes in the urine conducive to the formation of urinary calculi. Loewenthal ingested 1 or 2 g. of the vitamin daily for five weeks and carried out several types of investigation-some rather unusual-on the urine before and during this, period. The effect of the vitamin was to produce an increase in the titratable acidity of the urine, an increase in the turbidity and a change in the gold-sol reaction (a test usually applied to the C.S.F.). He does not profess to be able to explain the exact nature of these last two changes but interprets them simply as indicating an alteration in the " protective colloids " of the urine. This, together with the increased acidity, are assumed to imply a greater tendency to the formation of urinary a great calculi. These tentative conclusions will deal of confirmation and elaboration. But even if true, they will certainly not deter us from the appropriate and adequate treatment of suspected deficiency of vitamin C. The daily requirements of the vitamin are probably about 50 mg. and even a case of severe scurvy will be cured by the administration of 1 g. daily for a week or two. Doses such as those taken by Loewenthal are thus rarely if ever required. Moreover, the fact that unnecessarily large overdoses of vitamin D produce toxic symptoms has not interfered with the cure or prevention of rickets by the intelligent use of this substance. The danger of hypervitaminosis in ordinary conditions of therapy or prophylaxis is often exaggerated, but its existence may at least serve the useful purpose of directing attention to the quantitative aspect of vitamin dosage. There is a tendency to order a convenient preparation without thinking of the amount of the vitamin really desired. The possibility of overdosage, and incidentally a great deal of waste of precious nutritional material, will be avoided when vitamins are prescribed in units or milligrammes or in human " daily shares " and not as so many capsules or tablets.

require

MANIFESTATIONS OF -

ENDEMIC

FLUOROSIS

SURVEYS in Americaand in

England 10 have shown that in children the mottled enamel of mild endemic fluorosis is associated with a greater than average resistance to dental caring, and that the toxic action of fluorine tends to affect those whose general nutrition is poor. In other parts of the body fluorine may exert an indirect action. Young and his colleagues 11 pointed out that in the aetiology of endemic goitre the absolute iodine content of the water and soil is not the only factor and that something else determines the availability of the iodine to meet human and animal needs. In at least one area of this country, among people living under conditions of low iodine intake Wilson 10 has established a relationship between the distribution of goitre, of fluorine in rock and of mottled enamel. In the locomotor system fluorosis especially attacks tissues rich in calcium. Roholm 12 described the pathological calcification of tendons,, ligaments and fasciae, and the formation of osteophytes among cryolite workers absorbing large 8. Loewenthal, M. Schweiz. med. Wschr. 9. Dean, H. T., Jay, P., Arnold, F. A. Jun.

1941, 71, 761.

and Elvove, E. Publ.

Rep. Wash. 1941, 56, 761. 10. Wilson, D. C. Lancet, 1941, 1, 211, 375. 11. Spec. Rep Ser. med. Res. Coun. Lond. No. 217, 1936. 12. Roholm, K. Fluorine Intoxication, London, 1937.

Hlth

amounts of fluorine.

In endemic human fluorosis bone

changes were first detected by Shortt and others 13 among communities in South India, and subsequently Pundit and his colleagues,14 by comparative dietary surveys among these same people, showed that the incidence of bone deformity bore a definite relation to the economic and nutritional state of the communities concerned,

indicating again that the toxicity of fluorine is made more evident by a "poor" diet. Recently Ockerse 15 in South Africa has described bone changes among villagers in the Pretoria district using borehole water containing over 11 parts per million of fluorine. Clinical symptoms include stiffness of the spine in the lumbar, thoracic and cervical regions, and pain and stiffness around the joints of the arms and legs and lumbar regions. The radio-

advanced case show ossification with increas. of bone and calcification of the lumbar and thoracic vertebrae and attachments ; osteophytic outgrowths and periosteal deposits are also present along the radius and ulna and around the elbow-joint and margins of the ribs. The clinical picture is similar to that of the most severe cases in South India. Fluorine, then, has a claim to be one of the trace elements necessary for nutri. tion, but its intake must be carefully limited and balanced with adequate iodine and the other factors influencing ossification. Unfortunately we have a long way to go before we can decide what the optimum intake of fluorine is and can ensure that everyone gets it. grams of

an

ing density

STETHOSCOPES OLD AND NEW day in 1816 when Laennec took a quire of paper, rolled it up to form a tube and applied it to the chest of a corpulent young woman, the art of auscultation has been developed to a fine degree. Although " immediate " auscultation seems to have been practised by Hippocrates and Harvey, medical men were slow to appreciate the significance of the heart sounds. Indeed Parisanus (1663), a physician of Venice, rejected Harvey’s observations with the words " Nor we, poor deafs, nor any other doctor in Venice can hear them, but happy is he who can hear them in London." The great Corvisart, nearly two hundred years later, referring to the heart sounds, wrote " I have never had an opportunity, I repeat it, of ascertaining the unquestionably rare observations ; I have barely heard these strokes by applying my Both statements, in ear close to the patient’s chest." their obtuseness, recall Sir James Mackenzie’s words on another aspect of cardiac examination. " Indeed I am doubtful," he wrote in 1920, " if an X-ray examination of the heart has ever thrown the slightest light on any cardiac condition." From the roll of paper to the perforated wooden cylinder was Laennec’s next step, while Piorry’s modifications and his addition of ear piece and chest piece in 1828 resulted in what is essentially the monaural stethoscope of recent times. Williams probably described the first binaural model about 1843 while Cammann replaced the lead tubes by flexible ones in 1855. Thus, briefly, was evolved the modern binaural stethoscope. The chest piece in all these models was funnel or trumpet shaped. In the phonendoscope, invented by Bianchi in 1894, a diaphragm chest piece with a rigid membrane was first used. The combined bell and diaphragm chest piece of the latest models seem satisfactorily to cover the acoustic ranges necessary for clinical examination of the heart and lungs. In a recent study of the laws governing auscultation Rappaport and Sprague 16 of Boston point out that the bell chest piece when applied to the patient’s chest functions in reality as a diaphragm chest piece.. The skin enclosed by the lip of the bell acts as a diaphragm, while the subcutaneous

SiNCE that

13. Shortt, H. E., McRobert, G. R., Barnard, T. W. and Nayar, A. S. M. Ind. J. med. Res. 1937, 25, 553. 14. Pundit, C. G., Raghavachari, T. N. S., Subba Rao, D. and Krishnamurti, V. Ibid, 1940, 28, 559. 15. Ockerse, T. S. Afr. med. J. 1941, 15, 261. 16. Rappaport, M. B. and Sprague, H. B. Amer. Heart J.1941, 21, 257.