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PITUITARY-ADRENAL FUNCTION AFTER TOPICAL STEROIDS
1209 HYPOLIPIDÆMIA IN ANÆMIA
SIR,-The observation of Dr. Rifkind and Morna Gale (Sept. 23, p. 640) that the level of plasma-lipids is depressed in
patients with anaemia has led them to suggest that this condition may be implicated in the epidemiology of ischxmic heartdisease. Since their paper will inevitably excite the speculation that differences in haemoglobin levels may contribute to variations in lipid concentration in the plasma of healthy men, we record here the results of our analyses. Over 900 samples of plasma from men without clinical abnormalities (many obtained with the collaboration of Prof. J. N. Morris and his1 colleagues) have been analysed by wellestablished methods. From our estimates of haemoglobin, cholesterol, and lipoprotein distribution we computed the correlation coefficient (r) between the level of hxmoglobin and that of the SfO-12, Sfl2-20, Sr20-100, and SflOO-400 lipoprotein classes,2 and between the haemoglobin level and the cholesterol content of the oc andlipoprotein fractions obtained by the Cohn method.3 r was statistically significant (P<0’01) for all variables except haemoglobin v. Sfl2-20 level, for which r= 0 036 for 916 pairs of observations. In the remaining observations the evidence is summarised by the following statistical data (in which the cholesterol and lipoprotein concentrations are measured in mg. per 100 ml. plasma and the haemoglobin in gm. per 100 ml. blood):
These equations make it clear that a fall in haemoglobin level is associated with a slight tendency for the p-lipoproteins to decline, and the ex-lipoproteins to rise. However, it is also evident from the low values of r that the dispersion of the observations is very great, and it is only in a large number of subjects that a significant trend can be found. For example, the standard deviation of «-lipoprotein cholesterol amounts to il6-7 mg. per 100 ml. about a mean of 46 mg. per 100 ml., while for (3-cholesterol the values are 196:47 mg. per 100 ml. It follows therefore that the relation observed by Dr. Rifkind and Morna Gale in anaemia due to disease (which we can confirm in pernicious anaemia) is far less conspicuous in men with " normal" haemoglobin levels. Nonetheless, although the plasma-lipid level of a single healthy subject cannot be reliably related to his haemoblogin level, men with a low haemoglobin will, as a group, have a lower average plasma-lipid concentration that those in whom the haemoglobin is high. G. L. MILLS PATRICIA A. WILKINSON. Courtauld Institute of Biochemistry. Bland-Sutton Institute of Pathology, Middlesex Hospital Medical School, J. W. STEWART. London, W.1.
PITUITARY-ADRENAL FUNCTION AFTER TOPICAL STEROIDS SiR,_The article by Professor James and his colleagues (Nov. 18, p. 1059) reminds me of a child I saw about three years ago, who presented with papillcedema for which no cause could be found. The papillcedema subsided after stopping her long-term steroid-ointment therapy, which she had
been receiving for widespread
severe eczema.
The patient has since made satisfactory progress with complete clearing of the papilloedema and without further
topical steroid therapy. General
Kettering, 1.
Hospital, Northants.
Dodds, C., Mills,
HYPERALDOSTERONISM AND HYPERTENSION
SiR,-The letter by Dr. Lauwers (Oct. 21, p. 889) prompts write. We, too, were intrigued by Conn’s assertion of increased incidence of " tumours " of the adrenal cortex, causing not only hypertension but diabetes mellitus,l even in the presence of normokalxmia. We surveyed the adrenals in 150 unselected necropsies in our hospitals to determine whether adenomas, cortical nodules, and so-called fasciculata islands (Conn’s nodules) were present more often in hypertensives than in normotensives.2 We did not find any increase of fasciculata islands in hypertensives; in fact, fasciculata islands and cortical nodules were practically ubiquitous, on careful serial screening of normotensives and hypertensives. While adenomas were rather more common in hypertension, they were also quite common in normotensives; thus there seems to be no foundation for statements alleging their " culpability". Potassium levels were not found to be correlated with either adrenal tumours or diabetes. Furthermore, we have good reason to believe that adrenalectomy (including removal of an innocent, normal gland) will " cure " many an essential hypertensive. Obviously, we do not advocate anything of the sort. MARDOQUEO I. SALOMON VICTOR TCHERTKOFF. New York Medical College.
us to
HYDATID DISEASE IN AUSTRALIA AND ICELAND SIR,-Your correspondent from Australia writing in Round the World (July 22, p. 205) is quite right to cast doubt on notifications as an accurate index of human hydatid disease. Tasmania is one of the Australian States in which the disease is notifiable, yet a special survey last year revealed 28 hospital cases confirmed by surgery of which only 7 had been notified. In Tasmania the disease is still highly endemic among livestock. A survey by Howkins in 1965 showed that 30% of mature sheep and 3-8% of lambs going through the main slaughterhouses were infected with Echinococcus granulosus. As Dr. Fitzpatrick (Oct. 28, p. 942) indicates, your correspondent should be able to find teaching material in Victoria without much trouble if he can visit a cooperative establishment at a time when mature sheep are being killed. When I visited Iceland in August, 1967, Dr. P. A. Palsson confirmed that E. granulosus had been eradicated, but never at any time in their campaign was any attempt made to destroy " all farm dogs ". Every farmer has one or two dogs and some have more. The statement by the late Niels Dungal3 that farm killing was banned has also turned out to be misleading. Dungal4 restated the position himself. What was prohibited after 1920 was farm killing for meat intended for sale, thus ending what Dungal called mass slaughtering on individual farms. In 1967 I met farmers who are still killing their own sheep, and Iceland 1966, published by the Central Bank of Iceland, estimates that as late as 1964 about 9% of all sheep slaughtered in Iceland were still being killed on farms. Any reduction in farm killing must help to control the disease, but this is clearly not the crucial factor in eradication that we thought it was. One factor in the disappearance of hydatid disease in Iceland which could be added to Dungal’s list is that fresh sheep’s viscera are available as dog food only during the autumn killing season, which lasts only about seven weeks. The sheep products available throughout the rest of the year are either smoked, salted, or deep-frozen, so they are free from viable protoscolices. This makes the educational problem easier in Iceland than in Australia and New Zealand, because there the Conn, J. W., Cohen, E. L., Rovner, D. R. J. Am. med. Ass. Nesbit, R. M. 1965, 193, 200. Conn, J. W. New Engl. J. Med. 1965, 273, 1135. Conn, J. W., Rovner, D. R., Cohen, E. L., Nesbit, R. M. J. Am. med. Ass. 1966, 195, 21. 2. Salomon, M. T., Tchertkoff, V., Kim, H. S., Garret, M. D., Chabon, A. de. Vasc. Dis. 1967, 4, 191. 3. Dungal, N. N.Z. J. Med. 1957, 56, 212. 4. Dungal, N. Extracts from Seventh International Congress of Hydatid Disease. Rome, 1960. 1.
R. WIGGLESWORTH.
G. L. Lancet, 1959, i, 1160. Dacie, J. V., Lewis, S. M. Practical Hæmatology; p. 36. London, 1963. 2. deLalla, O. F., Gofman, J. W. in Methods of Biochemical Analysis (edited by D. Glick); vol. I, p. 459. New York, 1954. 3. Cohn, E. J., et al. J. Am. chem. Soc. 1950, 72, 465.
SIR,-The observation of Dr. Rifkind and Morna Gale (Sept. 23, p. 640) that the level of plasma-lipids is depressed in
patients with anaemia has led them to suggest that this condition may be implicated in the epidemiology of ischxmic heartdisease. Since their paper will inevitably excite the speculation that differences in haemoglobin levels may contribute to variations in lipid concentration in the plasma of healthy men, we record here the results of our analyses. Over 900 samples of plasma from men without clinical abnormalities (many obtained with the collaboration of Prof. J. N. Morris and his1 colleagues) have been analysed by wellestablished methods. From our estimates of haemoglobin, cholesterol, and lipoprotein distribution we computed the correlation coefficient (r) between the level of hxmoglobin and that of the SfO-12, Sfl2-20, Sr20-100, and SflOO-400 lipoprotein classes,2 and between the haemoglobin level and the cholesterol content of the oc andlipoprotein fractions obtained by the Cohn method.3 r was statistically significant (P<0’01) for all variables except haemoglobin v. Sfl2-20 level, for which r= 0 036 for 916 pairs of observations. In the remaining observations the evidence is summarised by the following statistical data (in which the cholesterol and lipoprotein concentrations are measured in mg. per 100 ml. plasma and the haemoglobin in gm. per 100 ml. blood):
These equations make it clear that a fall in haemoglobin level is associated with a slight tendency for the p-lipoproteins to decline, and the ex-lipoproteins to rise. However, it is also evident from the low values of r that the dispersion of the observations is very great, and it is only in a large number of subjects that a significant trend can be found. For example, the standard deviation of «-lipoprotein cholesterol amounts to il6-7 mg. per 100 ml. about a mean of 46 mg. per 100 ml., while for (3-cholesterol the values are 196:47 mg. per 100 ml. It follows therefore that the relation observed by Dr. Rifkind and Morna Gale in anaemia due to disease (which we can confirm in pernicious anaemia) is far less conspicuous in men with " normal" haemoglobin levels. Nonetheless, although the plasma-lipid level of a single healthy subject cannot be reliably related to his haemoblogin level, men with a low haemoglobin will, as a group, have a lower average plasma-lipid concentration that those in whom the haemoglobin is high. G. L. MILLS PATRICIA A. WILKINSON. Courtauld Institute of Biochemistry. Bland-Sutton Institute of Pathology, Middlesex Hospital Medical School, J. W. STEWART. London, W.1.
PITUITARY-ADRENAL FUNCTION AFTER TOPICAL STEROIDS SiR,_The article by Professor James and his colleagues (Nov. 18, p. 1059) reminds me of a child I saw about three years ago, who presented with papillcedema for which no cause could be found. The papillcedema subsided after stopping her long-term steroid-ointment therapy, which she had
been receiving for widespread
severe eczema.
The patient has since made satisfactory progress with complete clearing of the papilloedema and without further
topical steroid therapy. General
Kettering, 1.
Hospital, Northants.
Dodds, C., Mills,
HYPERALDOSTERONISM AND HYPERTENSION
SiR,-The letter by Dr. Lauwers (Oct. 21, p. 889) prompts write. We, too, were intrigued by Conn’s assertion of increased incidence of " tumours " of the adrenal cortex, causing not only hypertension but diabetes mellitus,l even in the presence of normokalxmia. We surveyed the adrenals in 150 unselected necropsies in our hospitals to determine whether adenomas, cortical nodules, and so-called fasciculata islands (Conn’s nodules) were present more often in hypertensives than in normotensives.2 We did not find any increase of fasciculata islands in hypertensives; in fact, fasciculata islands and cortical nodules were practically ubiquitous, on careful serial screening of normotensives and hypertensives. While adenomas were rather more common in hypertension, they were also quite common in normotensives; thus there seems to be no foundation for statements alleging their " culpability". Potassium levels were not found to be correlated with either adrenal tumours or diabetes. Furthermore, we have good reason to believe that adrenalectomy (including removal of an innocent, normal gland) will " cure " many an essential hypertensive. Obviously, we do not advocate anything of the sort. MARDOQUEO I. SALOMON VICTOR TCHERTKOFF. New York Medical College.
us to
HYDATID DISEASE IN AUSTRALIA AND ICELAND SIR,-Your correspondent from Australia writing in Round the World (July 22, p. 205) is quite right to cast doubt on notifications as an accurate index of human hydatid disease. Tasmania is one of the Australian States in which the disease is notifiable, yet a special survey last year revealed 28 hospital cases confirmed by surgery of which only 7 had been notified. In Tasmania the disease is still highly endemic among livestock. A survey by Howkins in 1965 showed that 30% of mature sheep and 3-8% of lambs going through the main slaughterhouses were infected with Echinococcus granulosus. As Dr. Fitzpatrick (Oct. 28, p. 942) indicates, your correspondent should be able to find teaching material in Victoria without much trouble if he can visit a cooperative establishment at a time when mature sheep are being killed. When I visited Iceland in August, 1967, Dr. P. A. Palsson confirmed that E. granulosus had been eradicated, but never at any time in their campaign was any attempt made to destroy " all farm dogs ". Every farmer has one or two dogs and some have more. The statement by the late Niels Dungal3 that farm killing was banned has also turned out to be misleading. Dungal4 restated the position himself. What was prohibited after 1920 was farm killing for meat intended for sale, thus ending what Dungal called mass slaughtering on individual farms. In 1967 I met farmers who are still killing their own sheep, and Iceland 1966, published by the Central Bank of Iceland, estimates that as late as 1964 about 9% of all sheep slaughtered in Iceland were still being killed on farms. Any reduction in farm killing must help to control the disease, but this is clearly not the crucial factor in eradication that we thought it was. One factor in the disappearance of hydatid disease in Iceland which could be added to Dungal’s list is that fresh sheep’s viscera are available as dog food only during the autumn killing season, which lasts only about seven weeks. The sheep products available throughout the rest of the year are either smoked, salted, or deep-frozen, so they are free from viable protoscolices. This makes the educational problem easier in Iceland than in Australia and New Zealand, because there the Conn, J. W., Cohen, E. L., Rovner, D. R. J. Am. med. Ass. Nesbit, R. M. 1965, 193, 200. Conn, J. W. New Engl. J. Med. 1965, 273, 1135. Conn, J. W., Rovner, D. R., Cohen, E. L., Nesbit, R. M. J. Am. med. Ass. 1966, 195, 21. 2. Salomon, M. T., Tchertkoff, V., Kim, H. S., Garret, M. D., Chabon, A. de. Vasc. Dis. 1967, 4, 191. 3. Dungal, N. N.Z. J. Med. 1957, 56, 212. 4. Dungal, N. Extracts from Seventh International Congress of Hydatid Disease. Rome, 1960. 1.
R. WIGGLESWORTH.
G. L. Lancet, 1959, i, 1160. Dacie, J. V., Lewis, S. M. Practical Hæmatology; p. 36. London, 1963. 2. deLalla, O. F., Gofman, J. W. in Methods of Biochemical Analysis (edited by D. Glick); vol. I, p. 459. New York, 1954. 3. Cohn, E. J., et al. J. Am. chem. Soc. 1950, 72, 465.