205 immunisation was not more readily obtained, despite greater interval (six months) between the two injections. Centre Edouard Rist,
a
S. DELONS D. KLEINKNECHT A. M. COUROUCE
Hôpital de Montreuil, 93105 Montreuil, and Centre National de Transfusion Sanguine, Pans, France.
LABORATORY-ACQUIRED HEPATITIS B SiR,—Dr Seder and his colleagues have recorded their significant and objective confirmation that splashes and aerosols from handling blood-samples can contaminate the working area with HBsAg and therefore potentially with hepatitis-B virus (Dec. 27, p. 1316). It is less clear how they relate this to "non-parenteral" exposure of workers to infection since there are many possibilities of inapparent parenteral infection as well as of enteral infection in these circumstances. My objections to the confusing and ambiguous neologism "non-parenteral" are on record.’ In discussions at the 15th European Symposium on Poliomyelitis and Other Virus Diseases, in Vienna in September, 1975, it was agreed that this term was unsatisfactory and should not be used. Can
a
Departments of Hæmatology, Obstetrics, and Gynæcology,
University Hospital, Wilhelmina Gasthuis, Amsterdam, The Netherlands.
contrary view be defended?
NORMAN R. GRIST
COAGULATION DISORDERS AFTER HYPERTONIC-SALINE ABORTION
StR,—We were interested in the article by Dr MacKenzie and others (Nov. 29, p. 1066) describing a significant rise in fibrin degradation products (F.D.P.) and factor-vm clotting activity during second-trimester abortion by intra-amniotic prostaglandin E2 alone or in combination with hypertonic glucose or urea.
As we described before,2 thrombin formation may be detected (by the generation of fibrinopeptide A and a positive ETHANOL-GELATION TEST BEFORE AND AFTER INSTILLATION OF
HYPERTONIC SALINE
*loading dose 20 mg followed by 6 mg/h continuously. t Loading dose 20 mg followed by 12 mg/h continuously.
ethanol-gelation test [E.G.T.]) as early as 2 hours after instillation of hypertonic saline. These findings precede the formation Of F.D.P. We also found a consistent decrease in factor-vm clotting activity, with a maximum 6-8 hours after the injection. We believe that the major coagulation events may be detected within 6-8 hours of intra-amniotic instillation of hypertonic solutions, and that these findings are missed in studies starting later. To prevent complications of hypertonic-saline-induced abortion due to disseminated intravascular coagulation, we decided to heparinise our patients. Heparin administration started imGrist, N. R. Lancet, 1974, i, 935. Royen, E. A. van, Treffers, P. E., Cate, J. 13, 166.
TEN CATE ERIC A. VAN ROYEN PIETER E. TREFFERS
JAN W.
DENTAL CARIES AND SUGAR INTAKE
SIR,-Dr McKendrick and others’
University Department of Infectious Diseases, Ruchill Hospital, Glasgow G20 9NB.
1 2
the intervention and was continued for 6 hours. The results were recorded by the E.G.T. (see table). Surprisingly high concentrations of heparin were needed to obtain a negative E.G.T. Concentrations of 0.3 to 0.9 u/ml plasma were measured when heparin was administered in a dose of 12 mg/h. 2 positive E.G.T.s were recorded 4 hours after hypertonic-saline instillation with heparin concentrations of 0-3and 035u respectively. 5 patients were also studied after 24 hr, and at that time no signs of intravascular coagulation could be demonstrated. Platelet function (bleeding-time, platelet-count, platelet-retention in a glass-bead column, platelet aggregation) were also studied in all patients in order to exclude haemorrhage. So far no bleeding problems have been encountered.
mediately before
aver that in our letter the that is not critical factor in dental maintaining sugar caries2 we gave only evidence favourable to our view. This is incorrect. A letter allows of few references, but virtually all points raised by these workers have been discussed elsewhere. Certainly some, but not all, studies on animals indicate sugar to be more cariogenic than other carbohydrate foods. Again, many, but not all, short-term in-vivo and in-vitro observations on oral biochemistry and microbiology in man have yielded the same conclusion. Assuredly too, the Vipeholm and Turku sugar studies have demonstrated that under acute and particular experimental conditions sugar is strongly cariogenic, and that total replacement of sugar inhibits dental decay. Additionally, the study on dentists’ young children at Bristol showed that restriction of soft foods, and regular dental care, led to better teeth. This investigation, however, undertaken 15 years ago, requires confirmation by others, with the provision of more dietary information and D.M.F. (decayed/missing/filled) scores on dentists’ much older children. In gross contrast, however, as indicated in our letter2 are the numerous observations on groups of children under everyday circumstances, with and without access to school tuck-shops, with and without snacks between meals, with and without soft foods at bedtime, &c., which have revealed D.M.F. scores differing by only about 1-2 units. Our own studies on four ethnic groups of adolescents revealed no significant differences in D.M.F. scores between segments accustomed to high and low consumptions of sugar. Added to this information are the results of epidemiological studies such as that made in 1946 at Lewis where children had excellent teeth despite a high intake of sugar. Not least to be considered are the disappointing results of the dental campaigns in which enormous curtailment of sugar and sugar-containing foods has been urged. Inexplicably, scarcely any of the foregoing items of information are mentioned or critically examined in recent reviews on diet and dental caries.4 J. A. Ryle stressed that the study of the unfit should be matched in endeavour by the study of the fit.’ Would it not be highly profitable to divert part of the tremendous effort now being expended on experimental caries studies in order to try to learn more of the dietary and other characteristics of moieties of adult populations who still possess good teeth? This task should be possible even though in Scotland half the population 1. 2. 3.
McKendrick, A. J. W., Roberts, G. S., Duguit, R. Lancet, 1975, ii, 1086. Walker, A. R. P., Cleaton-Jones, P. E. ibid. 1975, ii, 765. Retief, D. P., Cleaton-Jones, P. E., Walker, A. R. P. Br. dent. J. 1975, 138,
4. 5.
Hartles, R. L., Leach, S. A. Br. med. Bull. 1975, 31, 137. Ryle, J. A. Br. med. J. 1943, ii, 633.
463. W.
ten
Scand.
J.
Hœmat.
1974,
a
S. DELONS D. KLEINKNECHT A. M. COUROUCE
Hôpital de Montreuil, 93105 Montreuil, and Centre National de Transfusion Sanguine, Pans, France.
LABORATORY-ACQUIRED HEPATITIS B SiR,—Dr Seder and his colleagues have recorded their significant and objective confirmation that splashes and aerosols from handling blood-samples can contaminate the working area with HBsAg and therefore potentially with hepatitis-B virus (Dec. 27, p. 1316). It is less clear how they relate this to "non-parenteral" exposure of workers to infection since there are many possibilities of inapparent parenteral infection as well as of enteral infection in these circumstances. My objections to the confusing and ambiguous neologism "non-parenteral" are on record.’ In discussions at the 15th European Symposium on Poliomyelitis and Other Virus Diseases, in Vienna in September, 1975, it was agreed that this term was unsatisfactory and should not be used. Can
a
Departments of Hæmatology, Obstetrics, and Gynæcology,
University Hospital, Wilhelmina Gasthuis, Amsterdam, The Netherlands.
contrary view be defended?
NORMAN R. GRIST
COAGULATION DISORDERS AFTER HYPERTONIC-SALINE ABORTION
StR,—We were interested in the article by Dr MacKenzie and others (Nov. 29, p. 1066) describing a significant rise in fibrin degradation products (F.D.P.) and factor-vm clotting activity during second-trimester abortion by intra-amniotic prostaglandin E2 alone or in combination with hypertonic glucose or urea.
As we described before,2 thrombin formation may be detected (by the generation of fibrinopeptide A and a positive ETHANOL-GELATION TEST BEFORE AND AFTER INSTILLATION OF
HYPERTONIC SALINE
*loading dose 20 mg followed by 6 mg/h continuously. t Loading dose 20 mg followed by 12 mg/h continuously.
ethanol-gelation test [E.G.T.]) as early as 2 hours after instillation of hypertonic saline. These findings precede the formation Of F.D.P. We also found a consistent decrease in factor-vm clotting activity, with a maximum 6-8 hours after the injection. We believe that the major coagulation events may be detected within 6-8 hours of intra-amniotic instillation of hypertonic solutions, and that these findings are missed in studies starting later. To prevent complications of hypertonic-saline-induced abortion due to disseminated intravascular coagulation, we decided to heparinise our patients. Heparin administration started imGrist, N. R. Lancet, 1974, i, 935. Royen, E. A. van, Treffers, P. E., Cate, J. 13, 166.
TEN CATE ERIC A. VAN ROYEN PIETER E. TREFFERS
JAN W.
DENTAL CARIES AND SUGAR INTAKE
SIR,-Dr McKendrick and others’
University Department of Infectious Diseases, Ruchill Hospital, Glasgow G20 9NB.
1 2
the intervention and was continued for 6 hours. The results were recorded by the E.G.T. (see table). Surprisingly high concentrations of heparin were needed to obtain a negative E.G.T. Concentrations of 0.3 to 0.9 u/ml plasma were measured when heparin was administered in a dose of 12 mg/h. 2 positive E.G.T.s were recorded 4 hours after hypertonic-saline instillation with heparin concentrations of 0-3and 035u respectively. 5 patients were also studied after 24 hr, and at that time no signs of intravascular coagulation could be demonstrated. Platelet function (bleeding-time, platelet-count, platelet-retention in a glass-bead column, platelet aggregation) were also studied in all patients in order to exclude haemorrhage. So far no bleeding problems have been encountered.
mediately before
aver that in our letter the that is not critical factor in dental maintaining sugar caries2 we gave only evidence favourable to our view. This is incorrect. A letter allows of few references, but virtually all points raised by these workers have been discussed elsewhere. Certainly some, but not all, studies on animals indicate sugar to be more cariogenic than other carbohydrate foods. Again, many, but not all, short-term in-vivo and in-vitro observations on oral biochemistry and microbiology in man have yielded the same conclusion. Assuredly too, the Vipeholm and Turku sugar studies have demonstrated that under acute and particular experimental conditions sugar is strongly cariogenic, and that total replacement of sugar inhibits dental decay. Additionally, the study on dentists’ young children at Bristol showed that restriction of soft foods, and regular dental care, led to better teeth. This investigation, however, undertaken 15 years ago, requires confirmation by others, with the provision of more dietary information and D.M.F. (decayed/missing/filled) scores on dentists’ much older children. In gross contrast, however, as indicated in our letter2 are the numerous observations on groups of children under everyday circumstances, with and without access to school tuck-shops, with and without snacks between meals, with and without soft foods at bedtime, &c., which have revealed D.M.F. scores differing by only about 1-2 units. Our own studies on four ethnic groups of adolescents revealed no significant differences in D.M.F. scores between segments accustomed to high and low consumptions of sugar. Added to this information are the results of epidemiological studies such as that made in 1946 at Lewis where children had excellent teeth despite a high intake of sugar. Not least to be considered are the disappointing results of the dental campaigns in which enormous curtailment of sugar and sugar-containing foods has been urged. Inexplicably, scarcely any of the foregoing items of information are mentioned or critically examined in recent reviews on diet and dental caries.4 J. A. Ryle stressed that the study of the unfit should be matched in endeavour by the study of the fit.’ Would it not be highly profitable to divert part of the tremendous effort now being expended on experimental caries studies in order to try to learn more of the dietary and other characteristics of moieties of adult populations who still possess good teeth? This task should be possible even though in Scotland half the population 1. 2. 3.
McKendrick, A. J. W., Roberts, G. S., Duguit, R. Lancet, 1975, ii, 1086. Walker, A. R. P., Cleaton-Jones, P. E. ibid. 1975, ii, 765. Retief, D. P., Cleaton-Jones, P. E., Walker, A. R. P. Br. dent. J. 1975, 138,
4. 5.
Hartles, R. L., Leach, S. A. Br. med. Bull. 1975, 31, 137. Ryle, J. A. Br. med. J. 1943, ii, 633.
463. W.
ten
Scand.
J.
Hœmat.
1974,
