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EXERCISE-TOLERANCE TESTS
1068 4’9 million. During treatment the patient had again led a normally active life; he moved about the city alone and had started using buses.
EXERCISE-TOLERANCE TESTS
was now
Having to date lost a total of 5
st. with only 12 weeks of he is now in active treatment, his second 6 weeks’ interval on a free diet. That he is not regaining weight confirm our experience that when human chorionic gonadotrophin in small daily doses is added to a severe reducing diet, the patient feels no hunger and does not easily regain weighl when returned to a normal diet. I entirely agree with Dr. Berlyne’s interpretation of the cardiorespiratory syndrome occurring in extremely obese patients as alveolar hypoventilation due to the mechanism: listed in his interesting article. Salvator Mundi International Rome.
Hospital,
A. T. W. SIMEONS,
SIR Dr. Master (Nov. 8) has raised the question of exercise tests based on electrocardiographic changes. His contributions in this field are, of course, well known. I omitted reference to this type of test’ from my article (Aug. 23) because, as at present used, it is primarily a qualitative diagnostic test for ischaemic heart-disease, not a quantitative test which measures a patient’s working
capacity. I feel sure that Dr. Master does not object to my giving his original heart-rate test priority in the section devoted to heart-rate tests, although I readily agree that despite the claims made for it in 1929 and 1935 it is now mainly nf istorical interest.
Department of Medicine, University of Edinburgh
E. A. HARRIS.
A CORONARY PARADOX
SIR,-Your annotation of Nov. 1 refers to the work of Pomerancein demonstrating increased numbers of mast cells in the arteries of cases of coronary thrombosis, and to the work of Sundberg2 who had previously shown a similar state in the veins of patients with venous thrombosis. This is stated to be the precise reverse of the expected results in these investigations, assuming heparin plays a major part in the mechanics of thrombosis.
grounds for the belief that heparin deficiency, impaired heparin activity, may have an important relationship to intravascular clotting. Several workers 3-s have demonstrated increased resistance to the anticoagulant action of heparin in large numbers of patients with recent There
are
reasonable
or
thromboembolic disease. The reduced sensitivity to heparin in these disorders has not previously been adequately explained. A simple explanation is now possible. It has been shown that there is a significantly increased plasma factor-vn activity in cases of thrombosis within 48 hours of the onset of these disorders 7. A further s report shows that serum which is rich in factor-vn activity and factor-vaa extracts prepared by adsorption and elution of serum possess remarkable antagonistic action to the anticoagulant effect of heparin. Resistance to heparin in thromboembolic disease seems likely therefore to result directly from increased factor-vn activity. The relationship to the initiation of clot formation is not well established. Work by Wessler 9 10 who produced rapid intravascular thrombus formation by the infusion of factor vn (s.P.c.A.)-rich solutions, suggests there may be a direct causal role played by factor vn. The effect may, however, be an indirect one resulting from the release of serum products into the circulation. The results of Pomerance and Sundberg may also be
Increased mast-cell explained on the same basis. production may be a direct physiological response to the raised circulating factor-vn level which has neutralised The demonstration by Pomerance natural heparin. that the greatest number of mast cells were in the segments of arteries which were the sites of fresh thrombi, may be taken as further evidence in support of this hypothesis for at these very points in the vascular channels the level of factor-vn activity released from local clot formation may be expected to be greatest. Department of Clinical Pathology, Manchester Royal Infirmary, Manchester. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
L. POLLER
Pomerance, A. J. Path. Bact. 1958, 76, 55. Sundberg, M. Acta path. microbiol. scand. 1955, suppl. no. 107. Ogura, J. J. clin. Invest. 1946, 25, 48. de Takats, G., Marshall, M. M. Surgery, 1952, 31, 13. Rosenthal, R. L., Weaver, J. C. Circulation, 1956, 15, 55. Poller, L. Clin. Sci. 1956, 15, 55. Poller, L. J. clin. Path. 1957, 10, 348. Poller, L. ibid. (to be published). Wessler, S. J. clin. Invest. 1954, 33, 977. Wessler, S. ibid. 1955, 34, 647.
GASTROINTESTINAL HÆMORRHAGE AND SALICYLATES SIR The reports by Dr. Summerskill and Dr. Alvarez (Nov. 1) on the occurrence of gastrointestinal haemorrhage during the administration of salicylates seem to explain many of the puzzling symptoms which develop after coryza, catarrhal fever, or influenza treated with salicylates. Dr. Summerskill and Dr. Alvarez are concerned with the objective sign of occult blood in the stools, and any symptoms of the chemical gastritis would be obscured by the more arresting pains due to the peptic ulcers found in some 50% of these patients. For the past year I have been studying the syndrome created by large and repeated doses of salicylates given " to ward off " colds, febrile catarrhs, and influenza and comparing this syndrome with the natural diseases. Unfortunately, it is difficult to find examples of natural disease and cure because (a) such people do not consult a doctor, and (b) many people try to keep going or avoid troubling the doctor by consuming generous amounts of the tablets and powders advertised and recommended for such conditions. During this period I have observed symptoms of oesophagitis and gastritis following the administration of aspirin compounds, soluble and insoluble, acid or buffered, to patients with coryza, catarrhal fever, and influenza. These are:
(1) Vomiting, mostly in children. (2) Retching of mucus and sour fluid. (3) Accumulation of tenacious mucus in the pharynx overnight. (4) A dry racking cough accompanied by raw, itching, or burning sensations in the centre of the chest. The cough is often in spasms and ends in vomiting. (5) Bruise-like pains or discomfort in the epigastrium or around the costal margins emphasised by coughing. (6) The upper respiratory signs of coryza consisting of sneezing and rhinorrhoea are replaced by complete nasal obstruction and neuralgic pains from congested sinuses. The natural history of these simple virus infections can be reproduced by stopping the aspirin administration in an infection which is not more than about five days old. The patient is put to bed on a very light diet or even a fruit fast, Within twelve hours a fever occurs accompanied by general malaise and headache which lasts from twelve to forty-eight hours. Subsequently there is a sore pharynx and later still nasal obstruction; each phase lasts a day or two and causes little
distress
or
disturbance. Not
one
of the symptoms listed above
appears.
I believe that the states of disease under discussion are defensive reactions of the body when invaded or threatened by viruses, and are therefore beneficial. Aspirin compounds have a cortisone-type action and will check and disrupt this beneficial fever and malaise. When this occurs, what happens to the virus which was probably swarming in the blood during the febrile period so rudely upset by aspirin? It is no longer on the endothelial membrane of the upper respiratory tract
EXERCISE-TOLERANCE TESTS
was now
Having to date lost a total of 5
st. with only 12 weeks of he is now in active treatment, his second 6 weeks’ interval on a free diet. That he is not regaining weight confirm our experience that when human chorionic gonadotrophin in small daily doses is added to a severe reducing diet, the patient feels no hunger and does not easily regain weighl when returned to a normal diet. I entirely agree with Dr. Berlyne’s interpretation of the cardiorespiratory syndrome occurring in extremely obese patients as alveolar hypoventilation due to the mechanism: listed in his interesting article. Salvator Mundi International Rome.
Hospital,
A. T. W. SIMEONS,
SIR Dr. Master (Nov. 8) has raised the question of exercise tests based on electrocardiographic changes. His contributions in this field are, of course, well known. I omitted reference to this type of test’ from my article (Aug. 23) because, as at present used, it is primarily a qualitative diagnostic test for ischaemic heart-disease, not a quantitative test which measures a patient’s working
capacity. I feel sure that Dr. Master does not object to my giving his original heart-rate test priority in the section devoted to heart-rate tests, although I readily agree that despite the claims made for it in 1929 and 1935 it is now mainly nf istorical interest.
Department of Medicine, University of Edinburgh
E. A. HARRIS.
A CORONARY PARADOX
SIR,-Your annotation of Nov. 1 refers to the work of Pomerancein demonstrating increased numbers of mast cells in the arteries of cases of coronary thrombosis, and to the work of Sundberg2 who had previously shown a similar state in the veins of patients with venous thrombosis. This is stated to be the precise reverse of the expected results in these investigations, assuming heparin plays a major part in the mechanics of thrombosis.
grounds for the belief that heparin deficiency, impaired heparin activity, may have an important relationship to intravascular clotting. Several workers 3-s have demonstrated increased resistance to the anticoagulant action of heparin in large numbers of patients with recent There
are
reasonable
or
thromboembolic disease. The reduced sensitivity to heparin in these disorders has not previously been adequately explained. A simple explanation is now possible. It has been shown that there is a significantly increased plasma factor-vn activity in cases of thrombosis within 48 hours of the onset of these disorders 7. A further s report shows that serum which is rich in factor-vn activity and factor-vaa extracts prepared by adsorption and elution of serum possess remarkable antagonistic action to the anticoagulant effect of heparin. Resistance to heparin in thromboembolic disease seems likely therefore to result directly from increased factor-vn activity. The relationship to the initiation of clot formation is not well established. Work by Wessler 9 10 who produced rapid intravascular thrombus formation by the infusion of factor vn (s.P.c.A.)-rich solutions, suggests there may be a direct causal role played by factor vn. The effect may, however, be an indirect one resulting from the release of serum products into the circulation. The results of Pomerance and Sundberg may also be
Increased mast-cell explained on the same basis. production may be a direct physiological response to the raised circulating factor-vn level which has neutralised The demonstration by Pomerance natural heparin. that the greatest number of mast cells were in the segments of arteries which were the sites of fresh thrombi, may be taken as further evidence in support of this hypothesis for at these very points in the vascular channels the level of factor-vn activity released from local clot formation may be expected to be greatest. Department of Clinical Pathology, Manchester Royal Infirmary, Manchester. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
L. POLLER
Pomerance, A. J. Path. Bact. 1958, 76, 55. Sundberg, M. Acta path. microbiol. scand. 1955, suppl. no. 107. Ogura, J. J. clin. Invest. 1946, 25, 48. de Takats, G., Marshall, M. M. Surgery, 1952, 31, 13. Rosenthal, R. L., Weaver, J. C. Circulation, 1956, 15, 55. Poller, L. Clin. Sci. 1956, 15, 55. Poller, L. J. clin. Path. 1957, 10, 348. Poller, L. ibid. (to be published). Wessler, S. J. clin. Invest. 1954, 33, 977. Wessler, S. ibid. 1955, 34, 647.
GASTROINTESTINAL HÆMORRHAGE AND SALICYLATES SIR The reports by Dr. Summerskill and Dr. Alvarez (Nov. 1) on the occurrence of gastrointestinal haemorrhage during the administration of salicylates seem to explain many of the puzzling symptoms which develop after coryza, catarrhal fever, or influenza treated with salicylates. Dr. Summerskill and Dr. Alvarez are concerned with the objective sign of occult blood in the stools, and any symptoms of the chemical gastritis would be obscured by the more arresting pains due to the peptic ulcers found in some 50% of these patients. For the past year I have been studying the syndrome created by large and repeated doses of salicylates given " to ward off " colds, febrile catarrhs, and influenza and comparing this syndrome with the natural diseases. Unfortunately, it is difficult to find examples of natural disease and cure because (a) such people do not consult a doctor, and (b) many people try to keep going or avoid troubling the doctor by consuming generous amounts of the tablets and powders advertised and recommended for such conditions. During this period I have observed symptoms of oesophagitis and gastritis following the administration of aspirin compounds, soluble and insoluble, acid or buffered, to patients with coryza, catarrhal fever, and influenza. These are:
(1) Vomiting, mostly in children. (2) Retching of mucus and sour fluid. (3) Accumulation of tenacious mucus in the pharynx overnight. (4) A dry racking cough accompanied by raw, itching, or burning sensations in the centre of the chest. The cough is often in spasms and ends in vomiting. (5) Bruise-like pains or discomfort in the epigastrium or around the costal margins emphasised by coughing. (6) The upper respiratory signs of coryza consisting of sneezing and rhinorrhoea are replaced by complete nasal obstruction and neuralgic pains from congested sinuses. The natural history of these simple virus infections can be reproduced by stopping the aspirin administration in an infection which is not more than about five days old. The patient is put to bed on a very light diet or even a fruit fast, Within twelve hours a fever occurs accompanied by general malaise and headache which lasts from twelve to forty-eight hours. Subsequently there is a sore pharynx and later still nasal obstruction; each phase lasts a day or two and causes little
distress
or
disturbance. Not
one
of the symptoms listed above
appears.
I believe that the states of disease under discussion are defensive reactions of the body when invaded or threatened by viruses, and are therefore beneficial. Aspirin compounds have a cortisone-type action and will check and disrupt this beneficial fever and malaise. When this occurs, what happens to the virus which was probably swarming in the blood during the febrile period so rudely upset by aspirin? It is no longer on the endothelial membrane of the upper respiratory tract