- Email: [email protected]
POTASSIUM, GLUCOSE, AND INSULIN IN MYOCARDIAL INFARCTION
277 vascular changes in early diabetes are most likely not limited to the conjunctiva and the glomerulus, and the capillary permeability of other vascular beds ought to be investigated. Medical Department F, Glostrup Hospital, and
Department of Medicine, Aalborg Municipal Hospital, Denmark.
J. DITZEL M. SCHWARTZ.
POTASSIUM, GLUCOSE, AND INSULIN IN MYOCARDIAL INFARCTION SIR,-Dr. Mittra is to be congratulated on an excellent paper1 and on his excellent results. However, he gives little credit to the originator of this treatment, which is known in North America as the " G.I.K." treatment, and which was started by Dr. D. Sodi-Pollares of Mexico City, to whom Dr. Mittra gives full credit in his first article2 on this treatment in myocardial infarction. I have had a large experience of this treatment and I agree with Dr. Mittra that there is a significant difference between treated and untreated control groups, as regards mortality and as regards those that recover from heart block in a shorter time with treatment. I feel that, rather than call the treatment " P.G.I." therapy, it should be called " G.I.K." therapy, standing for glucose, insulin, and kalium. Hillbrow, B. A. BRADLOW. Johannesburg.
small benign polypoid lesions in the distal colon, which were removed transabdominally. Hypertension, hypertensive retinopathy, and early renal failure were also noted. The patient refused further investigation or therapy and left hospital. He was next seen in October, 1963, complaining of failing vision. The patient now had grade 3 (Keith-Wagner) hypertensive retinopathy, blood-urea-nitrogen level of 95 mg. per 100 ml., cardiomegaly, and left-ventricular-strain pattern on the electrocardiogram, and his blood-pressure (B.P.) was 170;130 mm. Hg. Despite therapy with hydrallazine, chlorpromazine, guanethidine, reserpine, and digoxin, he improved little and he died of urxmia on Oct. 31, 1964. Necropsy showed " no specific changes in the brain ", and " arteritis deformans " in the vascular renal tissues. The kidneys resembled those of " chronic pyelonephritis ".
COLD-CLIMATE SIGN
Acute intermittent porphyria is diagnosed chemically by noting an increase in urinary excretion of porphyrin precursors, aminolaevulic acid (A.L.A.) and porphobilinogen. False positive and negative tests of porphobilinogen in the urine have been recorded.45 A.L.A. is now found to be increased in the urine of patients with acute porphyria and present in about 70% of persons with latent porphyriaof the Swedish intermittent type, so that latent cases can be more easily detected. Hypertension has been reported as accompanying attacks of acute intermittent porphyria but interval B.P. readings apparreturn to normal. This patient showed progressive ently " malignant " hypertension due to chronic pyelonephritis, probably unrelated to his porphyria. Department of Internal Medicine, The Spence Clinic, 910 Ridgway Street, Fort William, Ontario, Canada. J. R. AUGUSTINE.
SiR,—In this day of specialised laboratory work, it seems well to remember the importance of allowing the patient to relate his story in careful detail. On May 25, 1954, a 48-year-old prospector was transferred here from Little Long Lac Hospital to the care of the late Dr. P. McK. Spence. He had had episodes of mid-abdominal pain with constipation, anorexia, and nervousness, in 1932, 1936, and 1940, each lasting about eight to ten days, and usually requiring analgesics or sedatives; the last episode had necessitated his admission to hospital. In 1951 he was in hospital for ten days because of severe abdominal pain, and had His upper an epileptic seizure two days after admission. gastrointestinal tract and his central nervous system were well investigated, but no diagnosis was made. A minor episode of abdominal pain occurred in 1953 while the patient was prospecting in the bush, but passed spontaneously after five days. The illness prompting his admission here had begun on May 2, 1954, with constipation, nervousness, and anorexia, followed in two days by severe mid-abdominal pain radiating to the mid-back area and constant in character. The referring " physician had noted the urine to be bloody " but no red cells had been seen in the sediment. The patient said that he often passed " dirty and dark " urine. Dr. Spence’s notes at that time aptly describe the " cold-climate sign ". The patient said, " that when he would void into the snow on prospecting trips, it would be a different colour to his mates, and that when it would freeze, it would turn a dark reddish colour by nighttime when they returned down the trail ". He was noted to be hypertensive (170/120 mm. Hg), and a Watson-Schwartz test3 was positive for urinary porphobilinogen. Two sisters had died in middle age of " menstrual pains " and appendicitis after many years of attacks of abdominal pain. Neither his Swedish parents nor six other siblings were known to have had abdominal complaints or central-nervous-system symptoms. In March, 1962, the patient, who had been under my care since 1959, was admitted to hospital because of a severe episode of abdominal pain and anxiety. This was well controlled with chlorpromazine, intravenous fluids, and prednisone. He was bleeding per rectum, and barium enema disclosed two "
1. Mittra, B. Lancet, 1966, ii, 1438. 2. Mittra, B. ibid. 1965, ii, 607. 3. Watson, C. J., Schwartz, S. Proc. Soc.
ASSESSMENT OF BODY-IRON STORES SIR,-I was interested to read the article by Dr. Smith and others (Jan. 21, p. 133). My experience has been that the result of the differential ferrioxamine test (Fv value) will certainly reflect the reaccumulation of iron stores over several months after cessation of venesection therapy for heemochromatosis, but that this value only parallels the rebound of the serum-iron. Furthermore despite administration of pancreatic extract in the form of ’Pancrex V Forte ’, 4 tablets four times a day, two patients here have already relapsed within 6 months of cessation of venesection. Thus for one patient the values were as follows:
University Department of Clinical Hæmatology, The Royal Infirmary, Manchester 13.
METHYLMALONICACIDURIA AND PERNICIOUS ANÆMIA of our SIR,-The object original communicationwas to demonstrate that methylmalonic acid could not be responsible for the neurological manifestations of pernicious ansemia, and this is unaffected whether methylmalonyl CoA isomerase or racemase is defective in methylmalonicaciduria, an account of which is now in the press.8 The possibility that this new syndrome was due to a deficiency of methylmalonyl CoA racemase, as Dr. White (Jan. 14, p. 110) suggests, had been 4. 5.
1941, 47, 393.
Ludwig, G. D. J. clin. Invest. 1958, 37, Kaelbling, R., Craig, J. B., Pasamanick,
914. B. Archs gen.
Psychiat. 1961, 5,
494.
6. 7.
8. exp. Biol. Med.
E. N. WARDLE.
Haeger, B. Lancet, 1958, ii, 606. Levin, B., Oberholzer, V. G., Burgess, E. A., Young, W. 1966, ii, 1415. Oberholzer, V. G., Levin, B., Burgess, E. A., Young, W. F. Childh. (in the press).
F.
Lancet,
Archs Dis.
Department of Medicine, Aalborg Municipal Hospital, Denmark.
J. DITZEL M. SCHWARTZ.
POTASSIUM, GLUCOSE, AND INSULIN IN MYOCARDIAL INFARCTION SIR,-Dr. Mittra is to be congratulated on an excellent paper1 and on his excellent results. However, he gives little credit to the originator of this treatment, which is known in North America as the " G.I.K." treatment, and which was started by Dr. D. Sodi-Pollares of Mexico City, to whom Dr. Mittra gives full credit in his first article2 on this treatment in myocardial infarction. I have had a large experience of this treatment and I agree with Dr. Mittra that there is a significant difference between treated and untreated control groups, as regards mortality and as regards those that recover from heart block in a shorter time with treatment. I feel that, rather than call the treatment " P.G.I." therapy, it should be called " G.I.K." therapy, standing for glucose, insulin, and kalium. Hillbrow, B. A. BRADLOW. Johannesburg.
small benign polypoid lesions in the distal colon, which were removed transabdominally. Hypertension, hypertensive retinopathy, and early renal failure were also noted. The patient refused further investigation or therapy and left hospital. He was next seen in October, 1963, complaining of failing vision. The patient now had grade 3 (Keith-Wagner) hypertensive retinopathy, blood-urea-nitrogen level of 95 mg. per 100 ml., cardiomegaly, and left-ventricular-strain pattern on the electrocardiogram, and his blood-pressure (B.P.) was 170;130 mm. Hg. Despite therapy with hydrallazine, chlorpromazine, guanethidine, reserpine, and digoxin, he improved little and he died of urxmia on Oct. 31, 1964. Necropsy showed " no specific changes in the brain ", and " arteritis deformans " in the vascular renal tissues. The kidneys resembled those of " chronic pyelonephritis ".
COLD-CLIMATE SIGN
Acute intermittent porphyria is diagnosed chemically by noting an increase in urinary excretion of porphyrin precursors, aminolaevulic acid (A.L.A.) and porphobilinogen. False positive and negative tests of porphobilinogen in the urine have been recorded.45 A.L.A. is now found to be increased in the urine of patients with acute porphyria and present in about 70% of persons with latent porphyriaof the Swedish intermittent type, so that latent cases can be more easily detected. Hypertension has been reported as accompanying attacks of acute intermittent porphyria but interval B.P. readings apparreturn to normal. This patient showed progressive ently " malignant " hypertension due to chronic pyelonephritis, probably unrelated to his porphyria. Department of Internal Medicine, The Spence Clinic, 910 Ridgway Street, Fort William, Ontario, Canada. J. R. AUGUSTINE.
SiR,—In this day of specialised laboratory work, it seems well to remember the importance of allowing the patient to relate his story in careful detail. On May 25, 1954, a 48-year-old prospector was transferred here from Little Long Lac Hospital to the care of the late Dr. P. McK. Spence. He had had episodes of mid-abdominal pain with constipation, anorexia, and nervousness, in 1932, 1936, and 1940, each lasting about eight to ten days, and usually requiring analgesics or sedatives; the last episode had necessitated his admission to hospital. In 1951 he was in hospital for ten days because of severe abdominal pain, and had His upper an epileptic seizure two days after admission. gastrointestinal tract and his central nervous system were well investigated, but no diagnosis was made. A minor episode of abdominal pain occurred in 1953 while the patient was prospecting in the bush, but passed spontaneously after five days. The illness prompting his admission here had begun on May 2, 1954, with constipation, nervousness, and anorexia, followed in two days by severe mid-abdominal pain radiating to the mid-back area and constant in character. The referring " physician had noted the urine to be bloody " but no red cells had been seen in the sediment. The patient said that he often passed " dirty and dark " urine. Dr. Spence’s notes at that time aptly describe the " cold-climate sign ". The patient said, " that when he would void into the snow on prospecting trips, it would be a different colour to his mates, and that when it would freeze, it would turn a dark reddish colour by nighttime when they returned down the trail ". He was noted to be hypertensive (170/120 mm. Hg), and a Watson-Schwartz test3 was positive for urinary porphobilinogen. Two sisters had died in middle age of " menstrual pains " and appendicitis after many years of attacks of abdominal pain. Neither his Swedish parents nor six other siblings were known to have had abdominal complaints or central-nervous-system symptoms. In March, 1962, the patient, who had been under my care since 1959, was admitted to hospital because of a severe episode of abdominal pain and anxiety. This was well controlled with chlorpromazine, intravenous fluids, and prednisone. He was bleeding per rectum, and barium enema disclosed two "
1. Mittra, B. Lancet, 1966, ii, 1438. 2. Mittra, B. ibid. 1965, ii, 607. 3. Watson, C. J., Schwartz, S. Proc. Soc.
ASSESSMENT OF BODY-IRON STORES SIR,-I was interested to read the article by Dr. Smith and others (Jan. 21, p. 133). My experience has been that the result of the differential ferrioxamine test (Fv value) will certainly reflect the reaccumulation of iron stores over several months after cessation of venesection therapy for heemochromatosis, but that this value only parallels the rebound of the serum-iron. Furthermore despite administration of pancreatic extract in the form of ’Pancrex V Forte ’, 4 tablets four times a day, two patients here have already relapsed within 6 months of cessation of venesection. Thus for one patient the values were as follows:
University Department of Clinical Hæmatology, The Royal Infirmary, Manchester 13.
METHYLMALONICACIDURIA AND PERNICIOUS ANÆMIA of our SIR,-The object original communicationwas to demonstrate that methylmalonic acid could not be responsible for the neurological manifestations of pernicious ansemia, and this is unaffected whether methylmalonyl CoA isomerase or racemase is defective in methylmalonicaciduria, an account of which is now in the press.8 The possibility that this new syndrome was due to a deficiency of methylmalonyl CoA racemase, as Dr. White (Jan. 14, p. 110) suggests, had been 4. 5.
1941, 47, 393.
Ludwig, G. D. J. clin. Invest. 1958, 37, Kaelbling, R., Craig, J. B., Pasamanick,
914. B. Archs gen.
Psychiat. 1961, 5,
494.
6. 7.
8. exp. Biol. Med.
E. N. WARDLE.
Haeger, B. Lancet, 1958, ii, 606. Levin, B., Oberholzer, V. G., Burgess, E. A., Young, W. 1966, ii, 1415. Oberholzer, V. G., Levin, B., Burgess, E. A., Young, W. F. Childh. (in the press).
F.
Lancet,
Archs Dis.