1084

syringe manufacturers, pharmaceutical industry, and diabetic patients. The coordinator and the committee will enlist the support and patience of professional groups and diabetics, and will also draw on the considerable experience of colleagues in other countries who have already introduced U-100 insulin. C. HARDWICK, Chairman

British Diabetic Association, 10 Queen Anne Street, London W1M 0BD

A. BLOOM, Chairman, Medical and Scientific Section H. KEEN, Chairman, Medical Advisory Committee P. J. WATKINS, Secretary, Medical Advisory Committee

POSTMENOPAUSAL OSTEOPOROSIS

SiR,-The observation by Dr Manelogas and colleagues p. 597)-that the only significant differences to be oophorectomised women who had lost bone rapidly higher urinary free cortisol excretion and a paradoxi-

(Sept. 22, found in was a

cally diminished cortisol response to corticotropin-is a major step toward an explanation of postmenopausal osteoporosis. I do wonder, however, if these findings in oophorectomised be extended to women who have had a normal menopause. The ovary, certainly in the early years after menopause, may continue to produce steroid-precursors. Normal menopause is therefore likely to be associated with hormone profiles significantly different from those described by Manelogas et al. It would be interesting to see the results of similar studies in postmenopausal women with intact ovaries, subdivided into those with very fast and those with very slow bone loss.

before any significant soft tissue change could have occurred. The sleep attacks persisted in two other individuals despite considerable regression of their clinical acromegaly. Guilleminault and van den Hoed now hold that "valid diagnosis of patients with daytime sleepiness requires systematic polygraphic monitoring including monitoring of cardiac and respiratory variables". Sleep laboratories are notoriously expensive, and in conditions of financial stringency we feel that skilled clinical assessment (including, of course, questioning of the spouse, wherever possible) still has a role to play in the attribution of diurnal somnolence to sleep apnoea. The same probably applies to the many cases of hypertension, cor pulmonale, cardiac arrhythmia, morning headache, and abnormal daytime behaviour now being investigated "polygraphically" (as possible cases of sleep apnoea) in laboratories throughout the U.S.A. It seems likely that excessive daytime sleep in acromegalic patients has a variety of causes, including sleep apnoea. It would seem to us unwise, however, to attribute all paroxysmal diurnal sleep in acromegalics to this mechanism. In our opinion other causes both exist-and have to be excluded-before all sleepy acromegalics are automatically submitted to tra-

cheostomy.

women can

postmenopausal

Department of Reproductive Biology, Case Western Reserve University, Cleveland, Ohio 44106, U.S.A.

WULF H. UTIAN

SIR,-We welcome the interest shown by Dr Rees and Dr

Ayres (Sept. 8, p. 524) and by Dr Guilleminault and Dr van den Hoed (Oct. 6, p. 750) in our preliminary communication of Aug. 18 on the association of narcolepsy and acromegaly. Guilleminault and van den Hoed assert that the "daytime somnolence of acromegalics is clearly associated with the obstructive sleep apnoea syndrome". They imply that our patients were drowsy by day because they slept poorly at night, and that they slept poorly by night because their acromegaly obstructed their upper respiratory passages. We are familiar with intermittent or permanent airwayss obstruction as a possible complication of acromegaly. Our department has indeed recently reported on one aspect of this.’ We are also familiar with sleep apnoea as a cause of diurnal somnolence. But as Guilleminault himself once pointed out,’ this is a condition which it should be possible to recognise clinically. In his own words, "the spouse or other bed partner is the best source of current information and appropriate questioning always results in a vivid description of the loud snoring and unusual nocturnal respiratory pattern". Other clinical components of the sleep apnoea syndrome may include abnormal sleep behaviour (violent movements, somnambulism, and others) and repeated morning headache or "grogginess". Our patients slept normally and felt well in the mornings. Following their daytime "naps" they awoke feeling refreshed, whereas patients with sleep apncea often feel drowsy after diurnal sleep. Moreover, in three of our patients the diurnal somnolence resolved within a few days of implantation with yttrium-90, J, McKelvie P, Joplin GF. Reversal of laryngeal obstruction following of acromegaly. J Laryngol Otol 1979; 93: 403-04. Guilleminault C, Tilkian A, Dement WC. The sleep apnoea syndromes. Ann treatment

2.

RevMed 1976: 465-84.

London W12

A. J. BARNES

G. F. JOPLIN C. PALLIS

FATAL ASTHMA

SIR,-Professor Stolley and Rita Schinnar, in their letter of

(p. 897), try to use your Aug. 18 editorial to reopen a six-year gap, on the surprising increase in asthma deaths in the U.K. during 1966-67. They still believe the cause to have been the "toxic" overuse of the beta-agonist isoprenaline aerosol, the overuse of which results, however, in tolerance not toxicity. Their other arguments have been answered in my letter of Sept. 7, 1972, in the American Review of Respiratory Diseases and also in a discussion of the so-called toxic properties of aerosol propellants and of the widely varying relations between isoprenaline use and asthma mortality in Australia, the U.S.A., West Germany, France, Italy, Sweden, and Japan, set out in my book Guide to Bronchial Asthma (1975). The conclusion from all these data can only be that the rise and fall of asthma mortality has a multifactorial Etiology which is only partly known. Isoprenaline cannot be an important cause because it has been replaced worldwide by other aerosols with different properties, but asthma mortality does

Oct. 27

discussion, after

ACROMEGALY AND NARCOLEPSY

1. Cassar

Department of Medicine, Royal Postgraduate Medical School,

not

seem to

have declined.

9 Park Crescent, London N3 2NL

H. HERXHEIMER

MAGNESIUM AND SUDDEN DEATH FROM HEART DISEASE

SiR,-From their data on the ion content of heart muscle from patients in Burnley and Hull Dr B. and Dr J. Chipperfield (Oct. 6, p. 709) suggest that deviation of the potassium/ sodium ratio from 2-8—3-0 may be associated with increased risk of sudden death in ischaemic heart disease (IHD). They cite Dr M. S. Seelig’s observation that the Western diet is deficient in magnesium, and her suggestion that the lower magnesium content of soft water could be important in increasing IHD sudden deaths and that it might possibly underlie the high incidence of cardiovascular disease in soft-water areas. The implications are not clear-is hypomagnesxmia, low cellular magnesium levels, or actual myocardial deficiency of magnesium the important factor? Why should such a deficiency affect men more seriously than women, when the men and women studied had consumed the same diet? Could the

Postmenopausal osteoporosis.

1084 syringe manufacturers, pharmaceutical industry, and diabetic patients. The coordinator and the committee will enlist the support and patience of...
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