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GUARDING THE GASTRECTOMITE
224
Letters
to
the Editor
GUARDING THE GASTRECTOMITE SIR,-There must by now be a large number of middle-aged and elderly people in the population who had a partial gastrectomy or other surgical treatment for peptic ulceration ten, twenty, or even more years ago, and the research findings you have published in the past year or so suggest that, without yet realising the fact, they may well be suffering from lack of iron and from nutritional defects leading to bone disease. What should be done to prevent such troubles, or to check them if they have already appeared ? Must these people wait until they get the sack through feeling always tired from anxmia, or break their leg and find it will not heal because of osteomalacia ? Or could their doctor do some tests on their reserves of the nutrients likely to be affected and prescribe a regimen which will build them up for another twenty years ? Can your experts tell us what nutrients are likely to be affected and whether they could all be supplied together in a grand periodical blunderbuss shot ? E. CLAYTON-JONES. Tonbridge, Kent.
OSTEOMALACIA AFTER GASTRECTOMY SIR,-Your leaderprovides a timely review of the difficulties surrounding the interpretation of the biochemical tests which have been used in the assessment of the frequency of osteomalacia after gastric surgery. Considering the large number of patients with partial gastrectomy who require to be screened2 for metabolic bone disease, one looks forward with much interest to seeing the results of wider application of electrophoretic identification of alkaline-phosphatase 3 and plasma-vitamin-D assays. I should like to draw attention to an additional cause of metabolic bone disease which may lead to confusion. Over the past few years I have seen four patients with osteomalacia who were shown to have renal tubular acidosis. Three had undergone gastric surgery for duodenal ulcer 15-30 years earlier, and the fourth patient had an unoperated duodenal ulcer. These cases will be reported in greater detail elsewhere. It is tempting to think that the combination of these two diseases is not a chance association, and this raises important considerations regarding both the diagnosis and the treatment of post-gastrectomy osteomalacia " in such cases. Published reports provide no help as to gastric acid secretion in renal tubular acidosis. Experience of the present cases seems to suggest that gastric hypersecretion of acid and peptic ulceration are common in renal tubular acidosis, and the place of gastric surgery in such cases may well need to be reviewed. With the recent introduction of the acid load test5 for the diagnosis of the compensated forms of renal tubular acidosis, and the increasing realisation " that the disease is commoner than previously supposed, it should be possible to screen a larger number of patients, both with peptic ulcer and after gastric surgery, to answer these questions.
isoenzymes
"
University Department
of
Materia Medica and Therapeutics. and the Royal Infirmary, Aberdeen.
S. D. MOHAMED.
StR,-One of the main reasons for the wide variation in the reported incidence of osteomalacia after partial gastrectomy is disagreement as to how osteomalacia should be defined. It would be a mistake to accept the finding of isolated bio-
chemical, histological, and radiological changes
as
diagnostic
1. Lancet, 1966. i. 1407 2. Crooks, J. Clark. C G., Amar, S S.. Coull, D C ibid. 1965, ii, 943. 3 Yong, J M. ibid 1966, i, 1132. 4 Tnompson, G R., Neale, G , Watts, J. M., Booth. C. C. ibid. p. 623. 5 Wrong, O. Davies. H E E Q. Jl Med. 1959, 28. 259. 6 Hutn, E. J. Webster. G D . Jr . Elkington, J R Am. J .Med. 1960,
29. 586
of osteomalacia unless they could be shown to be precursors of clinical bone disease. In a study conducted over the past two years,! 210 gastrectomised patients were screened biochemically, radiologically, and clinically with a view to detecting bone disease. A raised alkaline phosphatase was found in 9% of patients, if the upper limit of normal is taken as 13 King-Armstrong units (or 15% if the upper limit of normal is taken as 12 King-Armstrong units). Using a densitometric technique, a significantly lower mean calcium concentration in bone was found among gastrectomised patients than among controls. A relationship was found between a raised alkaline phosphatase and an increase in the area of osteoid tissue present on bone biopsy; but, in most cases, the amount of osteoid was much too small to justify a diagnosis of osteomalacia. Although these biochemical, radiological, and histological changes are presumably manifestations of metabolic changes in bone there was no relationship between these changes and symptoms suggestive of bone disease. With one possible exception, no evidence was found to indicate that the abnormalities were evidence of progressive bone disease. For these reasons we feel that, although abnormalities can be detected in a high proportion of gastrectomised patients, progressive bone disease giving rise to symptoms is rare, and it does not constitute a serious problem. King George Hospital, P. M. HIGGINS. Ilford, Essex.
MEASURING GASTROINTESTINAL PROTEIN LOSS SIR,-Dr. Andersen and Dr. Jarnum2 have tried to show the presumptive superiority of 59Fe-labelled iron-dextran (59Pe LD.) in measurement of gastrointestinal protein loss. This may have been so in a few patients of these workers who, incidentally, failed to point out if their patients had anaemia or gastrointestinal
bleeding. Patients with protein-losing gastroenteropathy quite commonly have iron-deficiency anxmia, and therefore the overall uptake of 59Fe i.D. by iron-depleted marrow will cause a reduction and further dilution of circulating radioactive iron, so that the amount of protein-bound 59Fe i.D. for excretion into the gut is likely to be neither appreciable nor indicative of true protein loss. In addition, if these patients have gastrointestinal
bleeding, some of the substance incorporated into the red bloodcells may be lost through the haemorrhage, causing further confusion. 5’Cr-labellcd albumin is more physiological, has neither of these two pitfalls, and is therefore more reliable than 59Fe i.D. Department of Gastroenterology, Henry Ford Hospital, Detroit, Michigan, U.S.A.
M. MOGHADAM.
MEASUREMENT OF GASTRIC EMPTYING-RATE SIR,-The description of a new method of measuring the rate at which food leaves the stomach by Mr. Griffiths and his co-workers3 prompts us to draw your attention to wo earlier papers on this subject.4We very much agree that there is need of a more physiological method, since Hunt’ss method entails repeated nasogastric intubation over several davsand radiological methods are difficult to evaluaK
quantitatively. In contrast
co-workers
to
we
the method described by Mr. Griffith and his used a stationary counter and the scanning
1. Higgins, P. M., Pridie, R. B. Br. J. Surg. (in the press). 2. Andersen, S. B., Jarnum, S. Lancet, 1966, i, 1060. 3. Griffith, G. H., Owen, G. M., Kirkman, S., Shields, R. Lancet, 1966. 4.
i, 1244. Bromster, D., Carlberger, G., Lundh, G. Paper read at a meeting of the Swedish Association of Surgeons, Stockholm, Sweden, Nov. 27, 1965
Nord. Med. (in the press). 5. Bromster, D., Carlberger, G., Lundh, G., Wittikko, R. ibid. 6. Hunt, J. N., Spurrell, W. R. J. Physiol., Lond. 1951, 113, 157.
Letters
to
the Editor
GUARDING THE GASTRECTOMITE SIR,-There must by now be a large number of middle-aged and elderly people in the population who had a partial gastrectomy or other surgical treatment for peptic ulceration ten, twenty, or even more years ago, and the research findings you have published in the past year or so suggest that, without yet realising the fact, they may well be suffering from lack of iron and from nutritional defects leading to bone disease. What should be done to prevent such troubles, or to check them if they have already appeared ? Must these people wait until they get the sack through feeling always tired from anxmia, or break their leg and find it will not heal because of osteomalacia ? Or could their doctor do some tests on their reserves of the nutrients likely to be affected and prescribe a regimen which will build them up for another twenty years ? Can your experts tell us what nutrients are likely to be affected and whether they could all be supplied together in a grand periodical blunderbuss shot ? E. CLAYTON-JONES. Tonbridge, Kent.
OSTEOMALACIA AFTER GASTRECTOMY SIR,-Your leaderprovides a timely review of the difficulties surrounding the interpretation of the biochemical tests which have been used in the assessment of the frequency of osteomalacia after gastric surgery. Considering the large number of patients with partial gastrectomy who require to be screened2 for metabolic bone disease, one looks forward with much interest to seeing the results of wider application of electrophoretic identification of alkaline-phosphatase 3 and plasma-vitamin-D assays. I should like to draw attention to an additional cause of metabolic bone disease which may lead to confusion. Over the past few years I have seen four patients with osteomalacia who were shown to have renal tubular acidosis. Three had undergone gastric surgery for duodenal ulcer 15-30 years earlier, and the fourth patient had an unoperated duodenal ulcer. These cases will be reported in greater detail elsewhere. It is tempting to think that the combination of these two diseases is not a chance association, and this raises important considerations regarding both the diagnosis and the treatment of post-gastrectomy osteomalacia " in such cases. Published reports provide no help as to gastric acid secretion in renal tubular acidosis. Experience of the present cases seems to suggest that gastric hypersecretion of acid and peptic ulceration are common in renal tubular acidosis, and the place of gastric surgery in such cases may well need to be reviewed. With the recent introduction of the acid load test5 for the diagnosis of the compensated forms of renal tubular acidosis, and the increasing realisation " that the disease is commoner than previously supposed, it should be possible to screen a larger number of patients, both with peptic ulcer and after gastric surgery, to answer these questions.
isoenzymes
"
University Department
of
Materia Medica and Therapeutics. and the Royal Infirmary, Aberdeen.
S. D. MOHAMED.
StR,-One of the main reasons for the wide variation in the reported incidence of osteomalacia after partial gastrectomy is disagreement as to how osteomalacia should be defined. It would be a mistake to accept the finding of isolated bio-
chemical, histological, and radiological changes
as
diagnostic
1. Lancet, 1966. i. 1407 2. Crooks, J. Clark. C G., Amar, S S.. Coull, D C ibid. 1965, ii, 943. 3 Yong, J M. ibid 1966, i, 1132. 4 Tnompson, G R., Neale, G , Watts, J. M., Booth. C. C. ibid. p. 623. 5 Wrong, O. Davies. H E E Q. Jl Med. 1959, 28. 259. 6 Hutn, E. J. Webster. G D . Jr . Elkington, J R Am. J .Med. 1960,
29. 586
of osteomalacia unless they could be shown to be precursors of clinical bone disease. In a study conducted over the past two years,! 210 gastrectomised patients were screened biochemically, radiologically, and clinically with a view to detecting bone disease. A raised alkaline phosphatase was found in 9% of patients, if the upper limit of normal is taken as 13 King-Armstrong units (or 15% if the upper limit of normal is taken as 12 King-Armstrong units). Using a densitometric technique, a significantly lower mean calcium concentration in bone was found among gastrectomised patients than among controls. A relationship was found between a raised alkaline phosphatase and an increase in the area of osteoid tissue present on bone biopsy; but, in most cases, the amount of osteoid was much too small to justify a diagnosis of osteomalacia. Although these biochemical, radiological, and histological changes are presumably manifestations of metabolic changes in bone there was no relationship between these changes and symptoms suggestive of bone disease. With one possible exception, no evidence was found to indicate that the abnormalities were evidence of progressive bone disease. For these reasons we feel that, although abnormalities can be detected in a high proportion of gastrectomised patients, progressive bone disease giving rise to symptoms is rare, and it does not constitute a serious problem. King George Hospital, P. M. HIGGINS. Ilford, Essex.
MEASURING GASTROINTESTINAL PROTEIN LOSS SIR,-Dr. Andersen and Dr. Jarnum2 have tried to show the presumptive superiority of 59Fe-labelled iron-dextran (59Pe LD.) in measurement of gastrointestinal protein loss. This may have been so in a few patients of these workers who, incidentally, failed to point out if their patients had anaemia or gastrointestinal
bleeding. Patients with protein-losing gastroenteropathy quite commonly have iron-deficiency anxmia, and therefore the overall uptake of 59Fe i.D. by iron-depleted marrow will cause a reduction and further dilution of circulating radioactive iron, so that the amount of protein-bound 59Fe i.D. for excretion into the gut is likely to be neither appreciable nor indicative of true protein loss. In addition, if these patients have gastrointestinal
bleeding, some of the substance incorporated into the red bloodcells may be lost through the haemorrhage, causing further confusion. 5’Cr-labellcd albumin is more physiological, has neither of these two pitfalls, and is therefore more reliable than 59Fe i.D. Department of Gastroenterology, Henry Ford Hospital, Detroit, Michigan, U.S.A.
M. MOGHADAM.
MEASUREMENT OF GASTRIC EMPTYING-RATE SIR,-The description of a new method of measuring the rate at which food leaves the stomach by Mr. Griffiths and his co-workers3 prompts us to draw your attention to wo earlier papers on this subject.4We very much agree that there is need of a more physiological method, since Hunt’ss method entails repeated nasogastric intubation over several davsand radiological methods are difficult to evaluaK
quantitatively. In contrast
co-workers
to
we
the method described by Mr. Griffith and his used a stationary counter and the scanning
1. Higgins, P. M., Pridie, R. B. Br. J. Surg. (in the press). 2. Andersen, S. B., Jarnum, S. Lancet, 1966, i, 1060. 3. Griffith, G. H., Owen, G. M., Kirkman, S., Shields, R. Lancet, 1966. 4.
i, 1244. Bromster, D., Carlberger, G., Lundh, G. Paper read at a meeting of the Swedish Association of Surgeons, Stockholm, Sweden, Nov. 27, 1965
Nord. Med. (in the press). 5. Bromster, D., Carlberger, G., Lundh, G., Wittikko, R. ibid. 6. Hunt, J. N., Spurrell, W. R. J. Physiol., Lond. 1951, 113, 157.