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ECHOVIRUSES AND CARDITIS
1395 Amantadine was given in a dosage of 100 mg. twice daily. On the fourth day of amantadine treatment, the daily dose of L-dopa was decreased by 0-5 g. Two further reductions of 05 g. per day were prescribed on the seventh and tenth days if there was no deterioration. One patient, with a background of psychoneurosis, complained of nausea and dizziness in the first few days and was withdrawn from the trial. Four patients worsened to some degree with the first 0-5 g. reduction of L-dopa and resumed the previous dose while continuing amantadine. Two of these, however, reported disappearance of transient weakness in the afternoon-a symptom they had usually had before starting amantadine. The remaining two patients tolerated a substantial reduction of the L-dopa dose-from 4 to 3 g. and from 3 to 1.5 g. daily respectively-without any clinical change. These patients have been observed for more than one month on the new regimen, and a carry-over effect of the previous dose of L-dopa can be ruled out. Thus, amantadine had a clear additive effect with L-dopa in two out of six patients. The effect was more obvious than that obtainable with conventional antiparkinson drugs such as diphenhydramine (which had been tried previously in the same patients with very dubious results). I am grateful to Dr. E. Robotti, of Istituto De Angeli, Milan, for the supply of L-dopa and amantadine and for helpful suggestions and discussion.
University Clinic for
GIUSEPPE SCOTTI.
ECHOVIRUSES AND CARDITIS SIR,-Dr. Rainford and Dr. Lewes (May 23, p. 1114) are strictly correct in that the paper by Dr. von Oldershausen1 does not specify isolation of echovirus 9 from the asepticmeningitis cases with electrocardiographic changes. Nevertheless, von Oldershausen was describing clinical aspects of cases seen during the large echovirus-9 epidemic which affected the whole of Europe in 1956, as mentioned by Dr. Lyle (May 23, p. 1118) and recorded by many others, including myself and other speakers, at a symposium on virus meningo-encephalitis.2 Speaking at that symposium, von Oldershausen discussed the diagnostic significance of virus isolation, and referred to virological evidence of echovirus 9 in his patients, most of whom had neurological illnesses.3 Although the available evidence is admittedly incomplete, the probability is at least very high that von Oldershausen’s patients with electrocardiographic changes had echovirus-9 infection. Glasgow University Department of Infectious Diseases, Ruchill Hospital, Glasgow N.W.
NORMAN R. GRIST.
EXTRAFAUCIAL DIPHTHERIA
SIR,-As Dr. Urquhart says (June 20, p. 1341), extrafaucial diphtheria was not uncommon in the Western Desert in the 1939-45 war. It was possible to isolate growths from suitable cases-usually Corynebacterium diphtheria mitis. In 1942, I did a necropsy on a soldier whose tight prepuce had been slit
forward station. The prepuce had become infected, and he had died shortly after admission to a general hospital. I isolated C. diphtheriae from the infected prepuce, but not from the other sores on his body. I have no memory of the further investigations of this culture, but I do recollect that one of the medical officers who had at
developed
a
diphtheritic infection of his
Group Pathology Laboratory, Warwick.
ALLEN PRIOR
SIR,-From my own experience as pathologist to the Hospital on the Suez Canal in 1942, I can confirm the statements of Dr. Urquhart about the large number 42 General
of
diphtheritic paralysis, many of which originated At one clinical meeting, cases of paralysis of accommodation, pharynx, wrist-drop, and foot-drop cases
of
in desert
sores.
all shown. These took about two months to recover, serious cause of loss of manpower. The sores originated where the shirt rubbed the back of the neck, where the shorts rubbed the back of the knee, and where the boots rubbed above the ankle. These abrasions were aggravated by the sand. The serous ooze was inoculated with C. diphtheria from the throats of the man and his comrades. In Iran and the North-West frontier of India (now Pakistan) the same hot, dry, and sandy conditions obtain. Swansea Hospital, H. C. M. WALTON. Swansea, SA1 4DA. were
and
were a
PLASMA-INSULIN IN DIABETES on this subject (June 6, p. 1211) is of considerable interest. It seems, however, pertinent to highlight the important fact that plasma-insulin concentrations do not demonstrate directly the actual output of insulin from the pancreas.1 Insulin concentration in plasma is a function of several factors, and the role of liver is by no means unimportant. 20-50% of the insulin coming out of the pancreas into the portal vein is degraded during its passage through the liver.2 This degradation depends on the enzyme glutathione-insulin transhydrogenase, which promotes the cleavage of disulphide bonds of insulin 3,4 by catalysing sulphydryl-disulphide interchange.5 This leads to the breakdown of insulin into its component A and B chains. There is strong evidence that an increased amount of B chain tagged to albumin (synalbumin positive) is present in the plasma of diabetics as well as individuals constituted as diabetics.8 Synalbumin concentration does vary in response to changes in the blood-glucose.’ A normal or subnormal increase in plasma-insulin in response to a glucose load is therefore consistent with either a decreased insulin output from the pancreas or an increased removal in the liver, resulting in a concomitant increase in the concentration of B chainalbumin in the circulation. A disproportionate increase in the amount of free A chain in the plasma of diabetics 8,and potential diabetics9 tends to favour this hypothesis. Pfeiffer et al.1O cannulated the portal vein through the umbilical vein in newborn infants and studied changes in the insulin-like activity (LL.A.) in response to an intravenously administered glucose load. It was shown that I.L.A. in the portal-vein plasma was significantly higher in infants born of diabetic or prediabetic mothers. These findings of reactive hyperinsulinism are consistent with the histopathological observation of extreme hyperplasia of the islets of
SiR,-Your leader
Nervous and Mental Diseases
Milan, Italy.
examined him
forefinger.
a
1. von Oldershausen, H. F. Dt. med. Wschr. 1957, 82, 442. 2. Virus Meningo-encephalitis. Ciba Fdn Symp. London, 1961. 3. von Oldershausen, H. F., Gruetzner, L., Friedebold, G. Klin. Wschr. 1960, 38, 923.
Langerhans in prediabetics.11 1. 2. 3. 4. 5. 6.
7. 8. 9. 10. 11.
Cerasi, E., Luft, R. Israel J. med. Sci. 1970, 6, 284. Samols, E., Ryder, J. J. clin. Invest. 1961. 40, 2092. Tomizawa, H. H., Varandani, P. T. J. biol. Chem. 1965, 240, 3191. Katzen, H. M., Stetten, D., Jr. Diabetes, 1962, 11, 271. Varandani, P. T. Biochim. biophys. Acta 1966, 118, 198. Vallance-Owen, J. in Modern Trends in Endocrinology (edited by H. Gardner-Hill); p. 152. London, 1967. Jervell, J., Vallance-Owen, J. Lancet, 1967, i, 1253. Meek, J. C., Doffing, K. M., Bolinger, R. E. Diabetes, 1968, 17, 61. Varandani, P. T. ibid. p. 547. Pfeiffer, E. F. in Diabetes (edited by J. Östman); p. 277. Amsterdam, 1969. Gepts, W. ibid. p. 273.
University Clinic for
GIUSEPPE SCOTTI.
ECHOVIRUSES AND CARDITIS SIR,-Dr. Rainford and Dr. Lewes (May 23, p. 1114) are strictly correct in that the paper by Dr. von Oldershausen1 does not specify isolation of echovirus 9 from the asepticmeningitis cases with electrocardiographic changes. Nevertheless, von Oldershausen was describing clinical aspects of cases seen during the large echovirus-9 epidemic which affected the whole of Europe in 1956, as mentioned by Dr. Lyle (May 23, p. 1118) and recorded by many others, including myself and other speakers, at a symposium on virus meningo-encephalitis.2 Speaking at that symposium, von Oldershausen discussed the diagnostic significance of virus isolation, and referred to virological evidence of echovirus 9 in his patients, most of whom had neurological illnesses.3 Although the available evidence is admittedly incomplete, the probability is at least very high that von Oldershausen’s patients with electrocardiographic changes had echovirus-9 infection. Glasgow University Department of Infectious Diseases, Ruchill Hospital, Glasgow N.W.
NORMAN R. GRIST.
EXTRAFAUCIAL DIPHTHERIA
SIR,-As Dr. Urquhart says (June 20, p. 1341), extrafaucial diphtheria was not uncommon in the Western Desert in the 1939-45 war. It was possible to isolate growths from suitable cases-usually Corynebacterium diphtheria mitis. In 1942, I did a necropsy on a soldier whose tight prepuce had been slit
forward station. The prepuce had become infected, and he had died shortly after admission to a general hospital. I isolated C. diphtheriae from the infected prepuce, but not from the other sores on his body. I have no memory of the further investigations of this culture, but I do recollect that one of the medical officers who had at
developed
a
diphtheritic infection of his
Group Pathology Laboratory, Warwick.
ALLEN PRIOR
SIR,-From my own experience as pathologist to the Hospital on the Suez Canal in 1942, I can confirm the statements of Dr. Urquhart about the large number 42 General
of
diphtheritic paralysis, many of which originated At one clinical meeting, cases of paralysis of accommodation, pharynx, wrist-drop, and foot-drop cases
of
in desert
sores.
all shown. These took about two months to recover, serious cause of loss of manpower. The sores originated where the shirt rubbed the back of the neck, where the shorts rubbed the back of the knee, and where the boots rubbed above the ankle. These abrasions were aggravated by the sand. The serous ooze was inoculated with C. diphtheria from the throats of the man and his comrades. In Iran and the North-West frontier of India (now Pakistan) the same hot, dry, and sandy conditions obtain. Swansea Hospital, H. C. M. WALTON. Swansea, SA1 4DA. were
and
were a
PLASMA-INSULIN IN DIABETES on this subject (June 6, p. 1211) is of considerable interest. It seems, however, pertinent to highlight the important fact that plasma-insulin concentrations do not demonstrate directly the actual output of insulin from the pancreas.1 Insulin concentration in plasma is a function of several factors, and the role of liver is by no means unimportant. 20-50% of the insulin coming out of the pancreas into the portal vein is degraded during its passage through the liver.2 This degradation depends on the enzyme glutathione-insulin transhydrogenase, which promotes the cleavage of disulphide bonds of insulin 3,4 by catalysing sulphydryl-disulphide interchange.5 This leads to the breakdown of insulin into its component A and B chains. There is strong evidence that an increased amount of B chain tagged to albumin (synalbumin positive) is present in the plasma of diabetics as well as individuals constituted as diabetics.8 Synalbumin concentration does vary in response to changes in the blood-glucose.’ A normal or subnormal increase in plasma-insulin in response to a glucose load is therefore consistent with either a decreased insulin output from the pancreas or an increased removal in the liver, resulting in a concomitant increase in the concentration of B chainalbumin in the circulation. A disproportionate increase in the amount of free A chain in the plasma of diabetics 8,and potential diabetics9 tends to favour this hypothesis. Pfeiffer et al.1O cannulated the portal vein through the umbilical vein in newborn infants and studied changes in the insulin-like activity (LL.A.) in response to an intravenously administered glucose load. It was shown that I.L.A. in the portal-vein plasma was significantly higher in infants born of diabetic or prediabetic mothers. These findings of reactive hyperinsulinism are consistent with the histopathological observation of extreme hyperplasia of the islets of
SiR,-Your leader
Nervous and Mental Diseases
Milan, Italy.
examined him
forefinger.
a
1. von Oldershausen, H. F. Dt. med. Wschr. 1957, 82, 442. 2. Virus Meningo-encephalitis. Ciba Fdn Symp. London, 1961. 3. von Oldershausen, H. F., Gruetzner, L., Friedebold, G. Klin. Wschr. 1960, 38, 923.
Langerhans in prediabetics.11 1. 2. 3. 4. 5. 6.
7. 8. 9. 10. 11.
Cerasi, E., Luft, R. Israel J. med. Sci. 1970, 6, 284. Samols, E., Ryder, J. J. clin. Invest. 1961. 40, 2092. Tomizawa, H. H., Varandani, P. T. J. biol. Chem. 1965, 240, 3191. Katzen, H. M., Stetten, D., Jr. Diabetes, 1962, 11, 271. Varandani, P. T. Biochim. biophys. Acta 1966, 118, 198. Vallance-Owen, J. in Modern Trends in Endocrinology (edited by H. Gardner-Hill); p. 152. London, 1967. Jervell, J., Vallance-Owen, J. Lancet, 1967, i, 1253. Meek, J. C., Doffing, K. M., Bolinger, R. E. Diabetes, 1968, 17, 61. Varandani, P. T. ibid. p. 547. Pfeiffer, E. F. in Diabetes (edited by J. Östman); p. 277. Amsterdam, 1969. Gepts, W. ibid. p. 273.