- Email: [email protected]
ECHOVIRUSES AND CARDITIS
520 calculated as 0-00090-0005. The incidence of the anomaly is equal to four affected in one million births, and the frequency of heterozygotes is 450 times the frequency of affected. Our data agree with the hypothesis that all the (Brazilian) cases of acheiropodia are due to one original mutation of the gene. This working hypothesis implies an exceedingly low mutation-rate for the gene, and could explain why, to date, the anomaly has been detected only in Brazil. The penetrance of the gene is complete and its expressivity varies little (the major variability consists of the presence of fingers in the upper stumps of some individuals, as shown in fig. 3). In its homozygous state, the gene is under strong selection pressure (s=0-83). In the analysis of the genetic load, it has been calculated that a=8x 10-7, B = 9 x 10-4, and B/A= 1,102, thus confirming that acheiropodia behaves according to the mutational load. The mutation-rate of the gene has been calculated as 3-3 x 10-6. Attention should also be called to the importance of acheiropodia in the area of genetic counselling. Geneticists often seek an example of an anomaly which, though highly mutilating, does not necessarily imply total incapacity. As Henry Viscardi, Jr. says, there are no incapable individuals, but only individuals with different capacities for different kinds of work. Acheiropodia is a living example of this assertion. I am grateful to Prof. Newton E. Morton and Dr. Eliane Azevedo, of Hawaii University, for performing the segregation analysis. 3 of the sibships were ascertained by Dr. Sergio Toledo and Prof. Newton Freire-Maia, and I thank them for allowing me
their data. A number of the affected families were investigated while I was a research student at the Laboratorio de Genetica Humana de Universidade do Parana. I am grateful to Professor FreireMaia, head of the laboratory, and his associates for their help.
to use
Departamento de Genética, Faculdade de Ciências Médicas e Biológicas, Botucatú, Est. São Paulo, Brazil.
ADEMAR FREIRE-MAIA.
AUTOANTIBODIES IN PATIENTS WITH THYROTOXICOSIS IN AN ENDEMIC GOITRE AREA AFTER IODATION OF BREAD SIR,-Dr. Connolly and his colleagues (p. 500 report a twofold increase in incidence of thyrotoxicosis in Tasmania after the iodation of bread for prophylaxis against endemic goitre. We tested patients in this study for autoantibodies to thyroid epithelial and gastric parietal cells by the indirect immunofluorescence test using human toxic thyroid gland and rat gastric mucosa as sources of antigen. The incidence of positive reactions compared with that in sporadic Graves’ disease in patients in the State of Victoria is as follows:
event, the iodation of bread. Thus there is the inference of more than one cause of thyrotoxicosis: an autoimmune cause, exemplified by Graves’ disease and mediated by long-acting thyroid stimulator, and nonautoimmune causes exemplified here by the 7odba sedow of the Tasmanian patients. extraneous
Clinical Research Unit, Royal Melbourne Hospital, and Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050. Australia.
ECHOVIRUSES AND CARDITIS
SIR,-We were most interested in the paper on this subject by Dr. Bell and Professor Grist (Feb. 14, p. 326). Having seen a number of cases of pericarditis with proven viral infection at Bedford Hospital, we now routinely perform electrocardiograms (E.C.G.) on all patients with suspected viral infections, even if there are no cardiac symptoms or signs. We find that myocarditis, indicated by changes in the E.C.G., is far commoner than is generally believed. All our patients were young, so coronary-artery disease, as a cause of the electrocardiographic abnormalities, is extremely unlikely. The cardiographic changes were mainly over the right-ventricular surface leads and septal leads-ptedominantly ST depression (often with " coving ") and T-wave inversion. The E.C.G. usually reverted to normal within the first seven days of the illness, but occasionally changes persisted for weeks or months. We have found myocarditis associated with virologically proven infection with echo-9,echo-30, and influenza A2. Interestingly, we have two cases in which Mycoplasma pneumonia was the infecting organism. We believe that the association of M. pneumoniae with myocarditis has not previously been reported. In contrast to Dr. Bell and Professor Grist, we found one case with undoubted electrocardiographic evidence of myocarditis among six cases of virologically proven echo-9 infection. We are surprised that these workers should state: " The relationship [of echoviral infection] to cardiac disease was less definite, but does not exclude the possibility of an occasional causal role. No case of cardiac disease or pleurodynia was found to be associated with any of the 208 echo-9 virus infections ..." Dr. Bell and Professor Grist do not specify what they mean by " cardiac disease ", and mention electrocardiographic changes in only two of their reported cases (case 1 with pericarditis and echo-6 infection, and case 7 with acute rheumatism and echo-19 infection). We assume that by " cardiac disease " they mean cardiac symptoms or physical signs such as pericarditis, but not symptomless electrocardiographic evidence of myocarditis. The E.c.G. is generally regarded as the most sensitive test in common use for detecting myocardial injury or damage. We believe that had Dr. Bell and Professor Grist carried out routine E.c.G.s on their patients irrespective of cardiac symptoms or physical signs, they would have demonstrated " myocardial injury or damage-i.e., cardiac disease "-in a substantial proportion of their 833 cases of echovirus infection, instead of a mere 5 cases. The significance of sub-clinical myocarditis " will be discussed in detail when our full findings are published. We believe that we have been able to correlate important clinical findings with electrocardiographic evidence of viral myocarditis, and that institution of bed rest in the early stages of viral illnesses, in patients with evidence of myocarditis, may help reduce morbidity and mortality. DAVID LEWES Bedford General Hospital, DAVID J. RAINFORD. Bedford. "
*
Significantly greater
at
P<0’001.
There are two, possibly interrelated, explanations for the significantly lower incidence of thyrogastric autoantibodies (P < 0.001) in the thyrotoxic patients from Tasmania. Many had toxic nodular goitre rather than Graves’ disease, and the disease in many presumably was precipitated by an "
1.
Whittingham, S., Irwin, J., Mackay, Aust. Ann. Med. 1969, 18, 130.
I.
"
R., Marsh, S., Cowling, D. C.
S. WHITTINGHAM I. R. MACKAY.
their data. A number of the affected families were investigated while I was a research student at the Laboratorio de Genetica Humana de Universidade do Parana. I am grateful to Professor FreireMaia, head of the laboratory, and his associates for their help.
to use
Departamento de Genética, Faculdade de Ciências Médicas e Biológicas, Botucatú, Est. São Paulo, Brazil.
ADEMAR FREIRE-MAIA.
AUTOANTIBODIES IN PATIENTS WITH THYROTOXICOSIS IN AN ENDEMIC GOITRE AREA AFTER IODATION OF BREAD SIR,-Dr. Connolly and his colleagues (p. 500 report a twofold increase in incidence of thyrotoxicosis in Tasmania after the iodation of bread for prophylaxis against endemic goitre. We tested patients in this study for autoantibodies to thyroid epithelial and gastric parietal cells by the indirect immunofluorescence test using human toxic thyroid gland and rat gastric mucosa as sources of antigen. The incidence of positive reactions compared with that in sporadic Graves’ disease in patients in the State of Victoria is as follows:
event, the iodation of bread. Thus there is the inference of more than one cause of thyrotoxicosis: an autoimmune cause, exemplified by Graves’ disease and mediated by long-acting thyroid stimulator, and nonautoimmune causes exemplified here by the 7odba sedow of the Tasmanian patients. extraneous
Clinical Research Unit, Royal Melbourne Hospital, and Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050. Australia.
ECHOVIRUSES AND CARDITIS
SIR,-We were most interested in the paper on this subject by Dr. Bell and Professor Grist (Feb. 14, p. 326). Having seen a number of cases of pericarditis with proven viral infection at Bedford Hospital, we now routinely perform electrocardiograms (E.C.G.) on all patients with suspected viral infections, even if there are no cardiac symptoms or signs. We find that myocarditis, indicated by changes in the E.C.G., is far commoner than is generally believed. All our patients were young, so coronary-artery disease, as a cause of the electrocardiographic abnormalities, is extremely unlikely. The cardiographic changes were mainly over the right-ventricular surface leads and septal leads-ptedominantly ST depression (often with " coving ") and T-wave inversion. The E.C.G. usually reverted to normal within the first seven days of the illness, but occasionally changes persisted for weeks or months. We have found myocarditis associated with virologically proven infection with echo-9,echo-30, and influenza A2. Interestingly, we have two cases in which Mycoplasma pneumonia was the infecting organism. We believe that the association of M. pneumoniae with myocarditis has not previously been reported. In contrast to Dr. Bell and Professor Grist, we found one case with undoubted electrocardiographic evidence of myocarditis among six cases of virologically proven echo-9 infection. We are surprised that these workers should state: " The relationship [of echoviral infection] to cardiac disease was less definite, but does not exclude the possibility of an occasional causal role. No case of cardiac disease or pleurodynia was found to be associated with any of the 208 echo-9 virus infections ..." Dr. Bell and Professor Grist do not specify what they mean by " cardiac disease ", and mention electrocardiographic changes in only two of their reported cases (case 1 with pericarditis and echo-6 infection, and case 7 with acute rheumatism and echo-19 infection). We assume that by " cardiac disease " they mean cardiac symptoms or physical signs such as pericarditis, but not symptomless electrocardiographic evidence of myocarditis. The E.c.G. is generally regarded as the most sensitive test in common use for detecting myocardial injury or damage. We believe that had Dr. Bell and Professor Grist carried out routine E.c.G.s on their patients irrespective of cardiac symptoms or physical signs, they would have demonstrated " myocardial injury or damage-i.e., cardiac disease "-in a substantial proportion of their 833 cases of echovirus infection, instead of a mere 5 cases. The significance of sub-clinical myocarditis " will be discussed in detail when our full findings are published. We believe that we have been able to correlate important clinical findings with electrocardiographic evidence of viral myocarditis, and that institution of bed rest in the early stages of viral illnesses, in patients with evidence of myocarditis, may help reduce morbidity and mortality. DAVID LEWES Bedford General Hospital, DAVID J. RAINFORD. Bedford. "
*
Significantly greater
at
P<0’001.
There are two, possibly interrelated, explanations for the significantly lower incidence of thyrogastric autoantibodies (P < 0.001) in the thyrotoxic patients from Tasmania. Many had toxic nodular goitre rather than Graves’ disease, and the disease in many presumably was precipitated by an "
1.
Whittingham, S., Irwin, J., Mackay, Aust. Ann. Med. 1969, 18, 130.
I.
"
R., Marsh, S., Cowling, D. C.
S. WHITTINGHAM I. R. MACKAY.