- Email: [email protected]
EFFECT OF SALT RESTRICTION ON HYPERTENSION
801
emphasised the favourable properties of endogenous PGE2 and its analogues in maintaining the gastroduodenal mucosa. In contrast, the role of 6-keto Fla, the stable metabolite of PGI2, is less established in the gastroduodenal mucosa, especially in a situation where there is uncertainty over the level of PGE2. We agree with Goren et al that it is important to identify the significance of the possible interaction between C pylori and prostaglandins, but suggest caution in the interpretation of their
nature and
findings.
Department of Gastroenterology, Royal Infirmary, Glasgow G31 2ER and; MRC Unit for Reproductive Biology, Edinburgh
A. A. R. R. R.
S. TAHA W. MCKINLAY UPADHYAY KELLY I. RUSSELL
1. Taha AS, Boothman
P, McLaughlin S, et al. Effect of Campylobacter pylori (CP) on gastric prostaglandins in patients with gastric ulcers and non-ulcer dyspepsia. Gut 1989; 30: A732. P, Cohen F, Zifroni A,
et al. Prostanoid synthesis by cultured gastric and possible role in the pathogenesis of duodenal ulcer. Scand J Gastroenterol 1983; 18: 1045-49. 3. Rachmilewitz D, Ligumsky M, Fich A, et al. Role of endogenous gastric prostanoids in the pathogenesis and therapy of duodenal ulcer. Gastroenterology 1986; 90: 963-69. 4. Andreone P, Baraldini M, Micaletti E, et al. Influence of cimetidine in low doses (
2. Sharon
duodenal
mucosa:
1437-42.
**Thisletter has been reply follows.-ED.L.
shown to Dr Goren and
colleagues, whose
SIR,-We were interested to learn that Dr Taha and colleagues’ results in
a similar study of the effect of Campylobacter pylori gastric prostaglandins were so different from ours.
on
The reasons for this discrepancy are not clear. The patients we studied all had dyspepsia and the number in each diagnostic category (campylobacter-like organism [CLO]-positive in parentheses) were: duodenal ulcer 7 (6); gastric ulcer 10 (6); gastritis 23 (10); normal 24 (10). None of our patients were taking any medication. The histological techniques for detecting CLOs are those in standard use and our results in this respect are very similar to those reported by other workers.1.2 Our prostaglandin assays were all done in the same batch by a biochemist who was unaware of the diagnoses. All CLO-positive patients were included whether ulcers were present or not, and we do not believe that the number of patients with duodenal ulcer was large enough to affect our overall results. We did not find any particular variation in PG levels according to diagnosis but only according to the presence of CLOs or smoking habits. Gastroenterology Research Unit, Addenbrooke’s Hospital, Cambridge CB2 2QQ 1
2
J. O. HUNTER
Tytgat GNJ, Langenberg ML, Rauws E, et al. Campylobacter-like organisms (CLO) m the human stomach. Gastroenterology 1985; 88: 1620. Graham DY, Klein PD. Campylobacter pylondis gastritis; the past, the present and speculations about the future. Am J Gastroenterol 1987; 82: 283-86.
EFFECT OF SALT RESTRICTION ON HYPERTENSION
SIR,-Dr Graudal and Dr Galloe (July 1, p 41) point out that the Australian dietary salt studyl showed a very small difference in blood pressure between treatment and control groups at 14 weeks. It is generally accepted that a sodium excretion rate below 10 mmol per 24 h will even reverse some cases of malignant hypertension,2 and the main questions in the current controversy are: Is a modest reduction in salt intake an effective treatment for mild hypertension? What is the threshold for the therapeutic effect? Will a
threshold lie for a preventive effect? The data from the Australian study suggest that a group with a mean sodium excretion rate of 90 mmol per 24 h stands close to the threshold for the treatment effect, and that lower sodium excretion rates should be investigated for feasibility and effectiveness. A sub-sample of Australian people can make a far greater reduction in sodium excretion. They choose fresh foods, no-addedsalt bread, and no-added-salt groceries in preference to low-salt and reduced-salt foods, and their sodium excretion rate is often below 60 mmol per 24 h. Even in 1981, when few of these foods were available in Australia, 10 out of 113 people had to be excluded from a triaP because (with no outside help) they had already obtained a baseline sodium excretion rate of under 60 mmol per 24 h. With special instruction, the diet group in that trial achieved an excretion rate (mean of three samples) of 37 mmol per 24 h.3 The study was included in Grobbee and Hofman’s meta-analysis,’ and I should have pointed out an error in their paper at the time of publication. They reported only a non-significant fall in blood pressure, without acknowledging that all subjects had been given medication at entry, and that the diet group had discontinued about half their medication whereas the control group had been able to make very little change. A press cuttings indicates that North Americans can also avoid salt very successfully. A survey based on dietary recall in a sample selected from 20 000 people in the University of Maryland’s Cooperative Extension Service is reported to have shown that about 81% had an estimated daily sodium intake under 50 mmol. My letters requesting more information were not answered, and I hope that at least one person in Baltimore who reads The Lancet will break the silence. If it is true that about 16 000 people in Baltimore have an estimated daily sodium intake of less than 50 mmol, many of them might agree to join a prospective study to record the baseline prevalence of hypertension in the group, continued adherence to the diet, and frequency of hypertension (new cases) with the passage of time. From the Intersalt data6 the predicted frequency would be close to zero.
lower salt intake prevent hypertension? And if so, where does the
Menzies Centre for Population Health Research, 43 Collins Street, Hobart, Tasmania 7000, Australia
TREVOR C. BEARD
1. Australian National Health and Medical Research Council
Dietary Salt Study Management Committee. Fall in blood pressure with modest reduction m dietary salt intake in mild hypertension. Lancet 1989; i: 399-402. 2. Report to the Medical Research Council. The nce diet in the treatment of hypertension. Lancet 1950; ii: 509-13. 3. Beard TC, Cooke HM, Gray WR, Barge R. Randomised controlled trial of a no-added-sodium diet for mild hypertension. Lancet 1982; ii: 455-58. 4. Grobbee DE, Hofman A. Does sodium restriction lower blood pressure? Br Med J 1986; 293: 27-29. Honolulu 5. United Press International. Too little salt in diets can be unhealthy too. Sunday Star-Bulletzn and Advertuer 1988, March 27. 6. Intersalt Cooperative Research Group. Intersalt : an international study of electrolyte excrenon and blood pressure: results for 24 hour urinary sodium and potassium excretion. Br Medy 1988; 297: 319-28.
USE OF APOMORPHINE TO TEST FOR DOPAMINE RESPONSIVENESS IN WILSON’S DISEASE
SiR,—In most patients with the neurological features of Wilson’s disease symptoms improve with chelating agents, but some extrapyramidal deficits remain, which mayl or may not2 respond to levodopa.2 High doses of trihexyphenidyl have been reported to be effective in relieving dystonia3 but there have been few reports of the use of other agents. The diverse neurological manifestations frequently include dystonia, tremor, and bradykinesia, which might be expected to respond to dopaminergic therapy. Apomorphine is a quick acting dopamine agonist that has been used as a quick test for dopamine responsiveness in patients with parkinsonism.’°5 Here we describe its use to assess response to dopaminergic stimulation in Wilson’s disease. 7 patients with Wilson’s disease (table) were assessed before and at regular intervals after being given apomorphine subcutaneously. All patients were pretreated with a peripheral dopamine antagonist, domperidone, to prevent the side-effects of nausea and postural hypotension. The starting dose of apomorphine was 1 mg. Increments of 1 mg were given at intervals of at least 1 h until neurological improvement was noted or patients exhibited the
emphasised the favourable properties of endogenous PGE2 and its analogues in maintaining the gastroduodenal mucosa. In contrast, the role of 6-keto Fla, the stable metabolite of PGI2, is less established in the gastroduodenal mucosa, especially in a situation where there is uncertainty over the level of PGE2. We agree with Goren et al that it is important to identify the significance of the possible interaction between C pylori and prostaglandins, but suggest caution in the interpretation of their
nature and
findings.
Department of Gastroenterology, Royal Infirmary, Glasgow G31 2ER and; MRC Unit for Reproductive Biology, Edinburgh
A. A. R. R. R.
S. TAHA W. MCKINLAY UPADHYAY KELLY I. RUSSELL
1. Taha AS, Boothman
P, McLaughlin S, et al. Effect of Campylobacter pylori (CP) on gastric prostaglandins in patients with gastric ulcers and non-ulcer dyspepsia. Gut 1989; 30: A732. P, Cohen F, Zifroni A,
et al. Prostanoid synthesis by cultured gastric and possible role in the pathogenesis of duodenal ulcer. Scand J Gastroenterol 1983; 18: 1045-49. 3. Rachmilewitz D, Ligumsky M, Fich A, et al. Role of endogenous gastric prostanoids in the pathogenesis and therapy of duodenal ulcer. Gastroenterology 1986; 90: 963-69. 4. Andreone P, Baraldini M, Micaletti E, et al. Influence of cimetidine in low doses (
2. Sharon
duodenal
mucosa:
1437-42.
**Thisletter has been reply follows.-ED.L.
shown to Dr Goren and
colleagues, whose
SIR,-We were interested to learn that Dr Taha and colleagues’ results in
a similar study of the effect of Campylobacter pylori gastric prostaglandins were so different from ours.
on
The reasons for this discrepancy are not clear. The patients we studied all had dyspepsia and the number in each diagnostic category (campylobacter-like organism [CLO]-positive in parentheses) were: duodenal ulcer 7 (6); gastric ulcer 10 (6); gastritis 23 (10); normal 24 (10). None of our patients were taking any medication. The histological techniques for detecting CLOs are those in standard use and our results in this respect are very similar to those reported by other workers.1.2 Our prostaglandin assays were all done in the same batch by a biochemist who was unaware of the diagnoses. All CLO-positive patients were included whether ulcers were present or not, and we do not believe that the number of patients with duodenal ulcer was large enough to affect our overall results. We did not find any particular variation in PG levels according to diagnosis but only according to the presence of CLOs or smoking habits. Gastroenterology Research Unit, Addenbrooke’s Hospital, Cambridge CB2 2QQ 1
2
J. O. HUNTER
Tytgat GNJ, Langenberg ML, Rauws E, et al. Campylobacter-like organisms (CLO) m the human stomach. Gastroenterology 1985; 88: 1620. Graham DY, Klein PD. Campylobacter pylondis gastritis; the past, the present and speculations about the future. Am J Gastroenterol 1987; 82: 283-86.
EFFECT OF SALT RESTRICTION ON HYPERTENSION
SIR,-Dr Graudal and Dr Galloe (July 1, p 41) point out that the Australian dietary salt studyl showed a very small difference in blood pressure between treatment and control groups at 14 weeks. It is generally accepted that a sodium excretion rate below 10 mmol per 24 h will even reverse some cases of malignant hypertension,2 and the main questions in the current controversy are: Is a modest reduction in salt intake an effective treatment for mild hypertension? What is the threshold for the therapeutic effect? Will a
threshold lie for a preventive effect? The data from the Australian study suggest that a group with a mean sodium excretion rate of 90 mmol per 24 h stands close to the threshold for the treatment effect, and that lower sodium excretion rates should be investigated for feasibility and effectiveness. A sub-sample of Australian people can make a far greater reduction in sodium excretion. They choose fresh foods, no-addedsalt bread, and no-added-salt groceries in preference to low-salt and reduced-salt foods, and their sodium excretion rate is often below 60 mmol per 24 h. Even in 1981, when few of these foods were available in Australia, 10 out of 113 people had to be excluded from a triaP because (with no outside help) they had already obtained a baseline sodium excretion rate of under 60 mmol per 24 h. With special instruction, the diet group in that trial achieved an excretion rate (mean of three samples) of 37 mmol per 24 h.3 The study was included in Grobbee and Hofman’s meta-analysis,’ and I should have pointed out an error in their paper at the time of publication. They reported only a non-significant fall in blood pressure, without acknowledging that all subjects had been given medication at entry, and that the diet group had discontinued about half their medication whereas the control group had been able to make very little change. A press cuttings indicates that North Americans can also avoid salt very successfully. A survey based on dietary recall in a sample selected from 20 000 people in the University of Maryland’s Cooperative Extension Service is reported to have shown that about 81% had an estimated daily sodium intake under 50 mmol. My letters requesting more information were not answered, and I hope that at least one person in Baltimore who reads The Lancet will break the silence. If it is true that about 16 000 people in Baltimore have an estimated daily sodium intake of less than 50 mmol, many of them might agree to join a prospective study to record the baseline prevalence of hypertension in the group, continued adherence to the diet, and frequency of hypertension (new cases) with the passage of time. From the Intersalt data6 the predicted frequency would be close to zero.
lower salt intake prevent hypertension? And if so, where does the
Menzies Centre for Population Health Research, 43 Collins Street, Hobart, Tasmania 7000, Australia
TREVOR C. BEARD
1. Australian National Health and Medical Research Council
Dietary Salt Study Management Committee. Fall in blood pressure with modest reduction m dietary salt intake in mild hypertension. Lancet 1989; i: 399-402. 2. Report to the Medical Research Council. The nce diet in the treatment of hypertension. Lancet 1950; ii: 509-13. 3. Beard TC, Cooke HM, Gray WR, Barge R. Randomised controlled trial of a no-added-sodium diet for mild hypertension. Lancet 1982; ii: 455-58. 4. Grobbee DE, Hofman A. Does sodium restriction lower blood pressure? Br Med J 1986; 293: 27-29. Honolulu 5. United Press International. Too little salt in diets can be unhealthy too. Sunday Star-Bulletzn and Advertuer 1988, March 27. 6. Intersalt Cooperative Research Group. Intersalt : an international study of electrolyte excrenon and blood pressure: results for 24 hour urinary sodium and potassium excretion. Br Medy 1988; 297: 319-28.
USE OF APOMORPHINE TO TEST FOR DOPAMINE RESPONSIVENESS IN WILSON’S DISEASE
SiR,—In most patients with the neurological features of Wilson’s disease symptoms improve with chelating agents, but some extrapyramidal deficits remain, which mayl or may not2 respond to levodopa.2 High doses of trihexyphenidyl have been reported to be effective in relieving dystonia3 but there have been few reports of the use of other agents. The diverse neurological manifestations frequently include dystonia, tremor, and bradykinesia, which might be expected to respond to dopaminergic therapy. Apomorphine is a quick acting dopamine agonist that has been used as a quick test for dopamine responsiveness in patients with parkinsonism.’°5 Here we describe its use to assess response to dopaminergic stimulation in Wilson’s disease. 7 patients with Wilson’s disease (table) were assessed before and at regular intervals after being given apomorphine subcutaneously. All patients were pretreated with a peripheral dopamine antagonist, domperidone, to prevent the side-effects of nausea and postural hypotension. The starting dose of apomorphine was 1 mg. Increments of 1 mg were given at intervals of at least 1 h until neurological improvement was noted or patients exhibited the