618 SAFETY OF
LIQUID-PROTEIN DIETS
SIR,-We were interested to read your editorial’ on liquidprotein diets and ventricular tachycardia. We have reported the successful use of a liquid-protein diet in the management of obesity.2-4 The principal ingredient is milk protein which is of much higher biological value than the hydrolysates used in the "last chance" diet. Essential minerals, fatty acids, and vitamins are contained in the formulation, thus removing the worry of compliance with medically administered supplements. Most of the patients we studied took the diet for 1-3 months. Serial electrocardiograms showed only asymptomatic T-wave inversion in one patient (out of fifty) after 6 weeks, and this reverted to normal 1 month after resumption of a normal diet; Q-T intervals were unchanged. Serum electrolytes remained normal and hypokalaemia was not observed, in contrast to the hypokalsemia implicated in the deaths reported in the United States.5 One hypertensive patient on propranolol 160 mg twice a day developed asymptomatic hypotension which necessitated a dosage reduction to 40 mg twice a day. Caution must therefore be observed with concomitant hypotensive medication in obese patients on formula diets. While we agree that, even with this formulation, problems may arise if the diet is used for longer periods or in patients with pre-existing ischsmic heart-disease, we have found it a safe, useful therapeutic manoeuvre in obesity resistant to conventional management. I. MCLEAN BAIRD E. R. LITTLEWOOD West Middlesex Hospital, A. N. HOWARD Isleworth, Middlesex TW7 6AF
SUBMUCOSAL ŒSOPHAGEAL VARICES
SIR,-On the basis of Miskowiak’s hypothesis6 on the role of the lower oesophageal sphincter in the aetiology of submucosal oesophageal varices, Mr Johnson and Dr Murray-Lyon (Jan. 20, p. 155) have stated that the capricious results of injection sclerotherapy could be explained by the site of injection in relation to the lower cesophageal sphincter. They postulate better results with injections low in the oesophagus. This view has been challenged by Mr Kirkham (Feb. 10, p. 334). Our data support the view of Johnson and Murray-Lyon. Assessment at 25 months in a prospective controlled clinical trial, designed
to
compare
PHENYLKETONURIA
SIR,-Atypical phenylketonuria (P.K.U.) is thoroughly investigated at only a few research-oriented centres. Your editorial (Feb. 10) on new varieties of P.K.U. should encourage more general interest and it is therefore important that the limitations of present methods of investigation are appreciated. The in-vivo measurement of hepatic phenylalanine-hydroxylase activity is especially controversial. The work of Curtius and co-workers’ to which you refer is technically elegant and the results are in qualitative agreement with expectations, but the human body is a highly compartmented system and tracer experiments are seldom as simple as they appear. In this method, deuterated phenylalanine is given orally and deuterated tyrosine appearing in the plasma is measured. Hepatic and plasma tyrosine pools are not in equilibrium, however, and in normal subjects only a small proportion of the labelled tyrosine produced in the liver after a phenylalanine load is released into the circulation, most being oxidised by the homogentisate pathway.2 The fraction released is not necessarily constant for different rates of tyrosine production (i.e., different rates of phenylalanine hydroxylation) and the fraction of labelled tyrosine incorporated in protein is affected by tyrosine pool size. Thus a consistent linear relationship between labelled tyrosine in the plasma and hepatic phenylalanine hydroxylase activity cannot be assumed and has yet to be established. The method
of Kaufman and co-workers, based on the production of labelled water on hydroxylation of labelled phenylalanine, is less liable to compartmentation problems but probably requires the use of tritium for application to man.3 In view of these difficulties, it is perhaps fortunate that formal estimation of the phenylalanine hydroxylation-rate in vivo, whether by tracer methods or by conventional methods such as intravenous phenylalanine loading or balance studies, is of little value in assessing the atypical phenylketonuric. The clinician who wishes to know whether his new "mild" case has a partial deficiency of phenylalanine hydroxylase itself and merely requires slight restriction of phenylalanine intake, or whether the phenylalanine intolerance indicates a potentially more serious condition, will have to rely on in-vitro enzyme studies and analysis of pteridines in body fluids. M.R.C. Unit for Metabolic Studies
Psychiatry, Middlewood Hospital, Sheffield S6 1TP
in
R.
J. POLLITT
repeated injection sclerotherapy
with conventional medical management, has shown that it was possible to eradicate oesophageal varices in all survivors in the repeated injection sclerotherapy group. Furthermore, no patient in this group had a recurrent variceal bleed once the varices had been eradicated. The technique used included the injection of ethanolamine oleate via a rigid cesophagoscope under general anaesthesia, with the injections being performed only in the lower cesophagus,’ and therefore in the region of the lower
oesophageal sphincter. of Surgery and Medical Research, Council Liver Research Group,
Department
University of Cape Town, Observatory 7925, Cape Town, South Africa Department of Surgery, King’s College Hospital, London SE5
INVESTIGATION OF ATYPICAL
CAMPYLOBACTER ENTERITIS IN A FOOD FACTORY
SIR,-In this food-producing company strict regulations
employees with gastrointestinal disturbances or poswith patients affected with such illnesses. They to be stool tested, followed up, and cleared before they return to normal working. So long as stool specimens are positive employees stay away from work on normal pay. Specimens
apply sible have
to
contact
examined by two laboratories, one internal and one external. When an employee has an episode of gastrointestinal disturbance he is seen in the medical department, where a detailed questionnaire is completed. During 1978 we detected in this way 9 cases of Campylobacter enteritis, 8 confirmed by the external laboratory and 6 by our own laboratory. The company employs 1900 people so 9 cases in one year (compared with 2 cases of Salmonella) indicated that this organism is significant in clinical gastroenteritis. In the first few weeks of this year 3 more cases have been identified.
are
JOHN TERBLANCHE D. KAHN P. BORNMAN
J. M. A. NORTHOVER
1. Lancet, 1978,ii,976 2. Baird, I. McL., Parsons, R. L., Howard, A. N. Metabolism, 1974, 23, 645. 3. Howard, A. N., Baird, I. McL Int. J. Obesity, 1977, 1, 63. 4. Baird, I. McL., Howard, A. N. ibid. 1977, 1, 271. 5. See J. Am med. Ass. 1977, 238, 2680. 6. Miskowiak, J. Lancet, 1978,i,1284 7. Terblanche, J., Northover, J. M. A., Bornman, P., Kahn, D., Silber, W., Barbezat, G. O., Sellars, S., Campbell, J A H., Saunders, S. J. Surg. Gynec Obstet. (in the press).
Curtius, H. C. Zagalak, M. J., Baerlocher, K, Schaub, J., Leimbacher, W., Redweik, U. Helv. pœdiat. Acta, 1977, 32, 461. 2. Fell, V., Hoskins, J.A., Pollitt, R. J. Clin, chim. Acta, 1978, 83, 259. 3. Kaufman, S., and others New Engl. J. Med. 1978, 299, 673.
1.
619
Clinically
characterised by abdominal pain and diarrhoea, usually severe, lasting 2-10 days (6 days on average). Of the 9 patients 6 had animals at home. 4 patients had a history of severe gastrointestinal upset. Clearance of stools tooka long time-28-5 days (range 18-39) in tests done in our own laboratory and 25-5 (18-33) in tests done outside-indicating the need for prolonged monitoring. This is particularly important, in view of the fact that the complete life cycle of Campylobacter in man has not been established as it has for Salmonella infection. the illness
was
Medical Department, General Foods Ltd,
ALAN
Banbury, Oxon
transferable enzymes found in N. gonorrhaeae and H. in-
fluenzce. Laboratory of Bacteriology, Institute of Tropical Medicine, B2000 Antwerp, Belgium, and Department of Microbiology, University of Washington, Seattle, Washington 98195, U.S.A. Hôpital de Joliniont, Haine-Saint-Paul, Belgium
JONES
PETER PIOT MARILYN ROBERTS
GASTON NINANE
SYNOVIAL INFLAMMATION IN
SHIGELLA
INFECTION
mechanism
&bgr;-LACTAMASE PRODUCTION IN COMMENSAL NEISSERIACEÆ
SIR,-Siiice the emergence of p-lactamase-producing strains of Neisseria gonorrhaeae in 1976,’ there has been much concern that other Neisseriaceae, particularly N. meningitidis, which is closely related to the gonococcus, might acquire in vivo the R-plasmid encoding the TEM type p-lactamase which has been isolated from penicilliri-resistant N. gonorrhaeae and ampicillinresistant Hcemophilus influenzae. &bgr;-Iactamase-producing Branhamella catarrhalis isolates have been reported.2-4 Their enzyme is not of the TEM-type found in gonococci; and seeins to be unique on isoelectric focusing pattern and substrate profile.5,6 Using an agarose gel electrophoresis method’ we could not find a plasmid in any of eight isolates tested. We have isolated two &bgr;-lactamase-producing strains of N. perflava from the throat of healthy people in Belgium. The strains were recovered iri the same (Jolimont) over a period of 10 months during a surveillance programme on ,3-lactamase-’producing bacteria. The strains were gram-negative diplococci with yellowish and smooth colonies; no growth at room temperature; oxidase and catalase positive, D.N.A.se, o-nitrophenyl-p-D-galactopyranoside, and H2S negative; acid produced from glucose, maltose, and sucrose, but not from ldctose ; prototrophic on Catlin’s defined medium. &bgr;-Iactamaseproduction was shown with the chromogenic cephalosporin test.8 The minimum inhibitory concentration (M.l.c.) of benzylpenicillin for both organisms was 16 mg/1 in an agar dilution system with an inoculum of 104 colony-forming units. (Sensitive strains of N. perflava have m.i.c.s of less than 0.06 nig/I.) There was a marked inoculum effect on M.t.c. determinaiions. The isolates were resistant to oxacillin and sensitive to cephalothin (disc method). Plasmids were not found by agarose-gel electrophoresis.’ The enzyme is under investigation. We think that surveillance of 3-lactamase production in "commensal" Neisseriaceae (besides N. gonorrhaeae and N. meningitidis) is important because these may constitute a potential source of j3-lactamase transferable to other more pathogenic bacteria, including meningococci, coexisting in the upper respiratory tract. A 4.4x 106 dalton plasmid coding for 11-lactamase production in N. gonorrhaeae has been transferred to N. flava in vitro.9 However, in the two strains reported here, the 3-lactamase is different from the plasmid mediated and
of synovial inflamSIR,-Little is known of the mation in patients with Shigella infection.1,2 (P.G.E) has been established as a mediator of inflam’ination.1;4 Addition of Shigella endotoxin to cultured human synovial fibroblasts (derived from synovial tissue of patients undergoing
Prostaglandin t
laboratory
1. World Health Organisation Wkly epidem. Rec. 1976, 51, 293. 2. Ninane, G., Joly, J., Piot, P., Kraytman, M. Lancet, 1977, ii, 149. 3 Malmvall, B. E., Brorsson, J. E., Johnson, J. J. antimicrob. Chemother.
1977, 3, 374. 4. Percival, A., Corkill, J. E., Rowlands, J., Sykes, R. B. Lancet, ii, 1175. 5. Sykes, R. B., Percival, A. in Immunobiology of Neisseria gonorrhœœ (edited by Brooks et al.), p. 68, A.S.M., Washington, D.C., 1978. 6. Buu Hoi-Dang Van, A., Brive-Le Bouguenec, C., Barthelemy, M., Labia, R. Ann.Microbiol. 1978, 129B, 397. 7.Elwell, L. P., Roberts, M., Mayer, L. W., Falkow, S. Antimicrob. Ag. Chemother. 1977, 11, 528. 8. O’Callaghan, C. H., Morris, A., Kirby, S. M., Shingler, A. H. ibid. 1972,
i,283. 9. Eisenstein, B. I.,
Sox, T., Biswas, G., Blackman, E., Sparling, P. 1977, 195, 998.
F. Science,
Dose-resporise curve of stimulation of P.G.E and hyaiW6xo,&
acid
production in cultured human synovial fibroblasts by Shigella endotoxin.
P.G.É concentration in medium determined by radioimmunoassay and hyaluronic acid by a carbazol colour reaction, Vertical bars represent S.E.M.
menisectoniy) induced a dose-related increase in ,prQtaglandin
hyaluronic acid production by synovial fibroblast cul(figure). We have found a relationship between p.G.E and hyaluronic acid prodtiction by synovial fibroblast:>.5 We suggest that Shigella endotoxin may trigger a p;G.Emediated synovial inflammation and pathological acciimulation of joint fluid in patients with Shigella infections. E and tures
Arthritis Research Unit, Department of Physical Medicine and Rheumatology, Ichilov Hospital Medical Center and Sackler School of Medicine, Tel Aviv, Israel, and Department of Hormone Research, Weizmann Institute of Science, Rehovot
1. 2.
Noer, H. R. J. Am. med. Ass. 1966, 198, 693. Calin, A., and others. Ann. intern. Med. 1976, 84, 564. 3. DiRosa, M., and others. J. Path. 1971, 104, 15. 4. Floman, Y., and others. Clin. Orthop. 1977, 125, 214. 5. Yaron, M., and others. Arths. Rheum. 1978, 21, 694.
MICHAEL YARON
ILANA YARON URIEL ZOR
LIQUID-PROTEIN DIETS
SIR,-We were interested to read your editorial’ on liquidprotein diets and ventricular tachycardia. We have reported the successful use of a liquid-protein diet in the management of obesity.2-4 The principal ingredient is milk protein which is of much higher biological value than the hydrolysates used in the "last chance" diet. Essential minerals, fatty acids, and vitamins are contained in the formulation, thus removing the worry of compliance with medically administered supplements. Most of the patients we studied took the diet for 1-3 months. Serial electrocardiograms showed only asymptomatic T-wave inversion in one patient (out of fifty) after 6 weeks, and this reverted to normal 1 month after resumption of a normal diet; Q-T intervals were unchanged. Serum electrolytes remained normal and hypokalaemia was not observed, in contrast to the hypokalsemia implicated in the deaths reported in the United States.5 One hypertensive patient on propranolol 160 mg twice a day developed asymptomatic hypotension which necessitated a dosage reduction to 40 mg twice a day. Caution must therefore be observed with concomitant hypotensive medication in obese patients on formula diets. While we agree that, even with this formulation, problems may arise if the diet is used for longer periods or in patients with pre-existing ischsmic heart-disease, we have found it a safe, useful therapeutic manoeuvre in obesity resistant to conventional management. I. MCLEAN BAIRD E. R. LITTLEWOOD West Middlesex Hospital, A. N. HOWARD Isleworth, Middlesex TW7 6AF
SUBMUCOSAL ŒSOPHAGEAL VARICES
SIR,-On the basis of Miskowiak’s hypothesis6 on the role of the lower oesophageal sphincter in the aetiology of submucosal oesophageal varices, Mr Johnson and Dr Murray-Lyon (Jan. 20, p. 155) have stated that the capricious results of injection sclerotherapy could be explained by the site of injection in relation to the lower cesophageal sphincter. They postulate better results with injections low in the oesophagus. This view has been challenged by Mr Kirkham (Feb. 10, p. 334). Our data support the view of Johnson and Murray-Lyon. Assessment at 25 months in a prospective controlled clinical trial, designed
to
compare
PHENYLKETONURIA
SIR,-Atypical phenylketonuria (P.K.U.) is thoroughly investigated at only a few research-oriented centres. Your editorial (Feb. 10) on new varieties of P.K.U. should encourage more general interest and it is therefore important that the limitations of present methods of investigation are appreciated. The in-vivo measurement of hepatic phenylalanine-hydroxylase activity is especially controversial. The work of Curtius and co-workers’ to which you refer is technically elegant and the results are in qualitative agreement with expectations, but the human body is a highly compartmented system and tracer experiments are seldom as simple as they appear. In this method, deuterated phenylalanine is given orally and deuterated tyrosine appearing in the plasma is measured. Hepatic and plasma tyrosine pools are not in equilibrium, however, and in normal subjects only a small proportion of the labelled tyrosine produced in the liver after a phenylalanine load is released into the circulation, most being oxidised by the homogentisate pathway.2 The fraction released is not necessarily constant for different rates of tyrosine production (i.e., different rates of phenylalanine hydroxylation) and the fraction of labelled tyrosine incorporated in protein is affected by tyrosine pool size. Thus a consistent linear relationship between labelled tyrosine in the plasma and hepatic phenylalanine hydroxylase activity cannot be assumed and has yet to be established. The method
of Kaufman and co-workers, based on the production of labelled water on hydroxylation of labelled phenylalanine, is less liable to compartmentation problems but probably requires the use of tritium for application to man.3 In view of these difficulties, it is perhaps fortunate that formal estimation of the phenylalanine hydroxylation-rate in vivo, whether by tracer methods or by conventional methods such as intravenous phenylalanine loading or balance studies, is of little value in assessing the atypical phenylketonuric. The clinician who wishes to know whether his new "mild" case has a partial deficiency of phenylalanine hydroxylase itself and merely requires slight restriction of phenylalanine intake, or whether the phenylalanine intolerance indicates a potentially more serious condition, will have to rely on in-vitro enzyme studies and analysis of pteridines in body fluids. M.R.C. Unit for Metabolic Studies
Psychiatry, Middlewood Hospital, Sheffield S6 1TP
in
R.
J. POLLITT
repeated injection sclerotherapy
with conventional medical management, has shown that it was possible to eradicate oesophageal varices in all survivors in the repeated injection sclerotherapy group. Furthermore, no patient in this group had a recurrent variceal bleed once the varices had been eradicated. The technique used included the injection of ethanolamine oleate via a rigid cesophagoscope under general anaesthesia, with the injections being performed only in the lower cesophagus,’ and therefore in the region of the lower
oesophageal sphincter. of Surgery and Medical Research, Council Liver Research Group,
Department
University of Cape Town, Observatory 7925, Cape Town, South Africa Department of Surgery, King’s College Hospital, London SE5
INVESTIGATION OF ATYPICAL
CAMPYLOBACTER ENTERITIS IN A FOOD FACTORY
SIR,-In this food-producing company strict regulations
employees with gastrointestinal disturbances or poswith patients affected with such illnesses. They to be stool tested, followed up, and cleared before they return to normal working. So long as stool specimens are positive employees stay away from work on normal pay. Specimens
apply sible have
to
contact
examined by two laboratories, one internal and one external. When an employee has an episode of gastrointestinal disturbance he is seen in the medical department, where a detailed questionnaire is completed. During 1978 we detected in this way 9 cases of Campylobacter enteritis, 8 confirmed by the external laboratory and 6 by our own laboratory. The company employs 1900 people so 9 cases in one year (compared with 2 cases of Salmonella) indicated that this organism is significant in clinical gastroenteritis. In the first few weeks of this year 3 more cases have been identified.
are
JOHN TERBLANCHE D. KAHN P. BORNMAN
J. M. A. NORTHOVER
1. Lancet, 1978,ii,976 2. Baird, I. McL., Parsons, R. L., Howard, A. N. Metabolism, 1974, 23, 645. 3. Howard, A. N., Baird, I. McL Int. J. Obesity, 1977, 1, 63. 4. Baird, I. McL., Howard, A. N. ibid. 1977, 1, 271. 5. See J. Am med. Ass. 1977, 238, 2680. 6. Miskowiak, J. Lancet, 1978,i,1284 7. Terblanche, J., Northover, J. M. A., Bornman, P., Kahn, D., Silber, W., Barbezat, G. O., Sellars, S., Campbell, J A H., Saunders, S. J. Surg. Gynec Obstet. (in the press).
Curtius, H. C. Zagalak, M. J., Baerlocher, K, Schaub, J., Leimbacher, W., Redweik, U. Helv. pœdiat. Acta, 1977, 32, 461. 2. Fell, V., Hoskins, J.A., Pollitt, R. J. Clin, chim. Acta, 1978, 83, 259. 3. Kaufman, S., and others New Engl. J. Med. 1978, 299, 673.
1.
619
Clinically
characterised by abdominal pain and diarrhoea, usually severe, lasting 2-10 days (6 days on average). Of the 9 patients 6 had animals at home. 4 patients had a history of severe gastrointestinal upset. Clearance of stools tooka long time-28-5 days (range 18-39) in tests done in our own laboratory and 25-5 (18-33) in tests done outside-indicating the need for prolonged monitoring. This is particularly important, in view of the fact that the complete life cycle of Campylobacter in man has not been established as it has for Salmonella infection. the illness
was
Medical Department, General Foods Ltd,
ALAN
Banbury, Oxon
transferable enzymes found in N. gonorrhaeae and H. in-
fluenzce. Laboratory of Bacteriology, Institute of Tropical Medicine, B2000 Antwerp, Belgium, and Department of Microbiology, University of Washington, Seattle, Washington 98195, U.S.A. Hôpital de Joliniont, Haine-Saint-Paul, Belgium
JONES
PETER PIOT MARILYN ROBERTS
GASTON NINANE
SYNOVIAL INFLAMMATION IN
SHIGELLA
INFECTION
mechanism
&bgr;-LACTAMASE PRODUCTION IN COMMENSAL NEISSERIACEÆ
SIR,-Siiice the emergence of p-lactamase-producing strains of Neisseria gonorrhaeae in 1976,’ there has been much concern that other Neisseriaceae, particularly N. meningitidis, which is closely related to the gonococcus, might acquire in vivo the R-plasmid encoding the TEM type p-lactamase which has been isolated from penicilliri-resistant N. gonorrhaeae and ampicillinresistant Hcemophilus influenzae. &bgr;-Iactamase-producing Branhamella catarrhalis isolates have been reported.2-4 Their enzyme is not of the TEM-type found in gonococci; and seeins to be unique on isoelectric focusing pattern and substrate profile.5,6 Using an agarose gel electrophoresis method’ we could not find a plasmid in any of eight isolates tested. We have isolated two &bgr;-lactamase-producing strains of N. perflava from the throat of healthy people in Belgium. The strains were recovered iri the same (Jolimont) over a period of 10 months during a surveillance programme on ,3-lactamase-’producing bacteria. The strains were gram-negative diplococci with yellowish and smooth colonies; no growth at room temperature; oxidase and catalase positive, D.N.A.se, o-nitrophenyl-p-D-galactopyranoside, and H2S negative; acid produced from glucose, maltose, and sucrose, but not from ldctose ; prototrophic on Catlin’s defined medium. &bgr;-Iactamaseproduction was shown with the chromogenic cephalosporin test.8 The minimum inhibitory concentration (M.l.c.) of benzylpenicillin for both organisms was 16 mg/1 in an agar dilution system with an inoculum of 104 colony-forming units. (Sensitive strains of N. perflava have m.i.c.s of less than 0.06 nig/I.) There was a marked inoculum effect on M.t.c. determinaiions. The isolates were resistant to oxacillin and sensitive to cephalothin (disc method). Plasmids were not found by agarose-gel electrophoresis.’ The enzyme is under investigation. We think that surveillance of 3-lactamase production in "commensal" Neisseriaceae (besides N. gonorrhaeae and N. meningitidis) is important because these may constitute a potential source of j3-lactamase transferable to other more pathogenic bacteria, including meningococci, coexisting in the upper respiratory tract. A 4.4x 106 dalton plasmid coding for 11-lactamase production in N. gonorrhaeae has been transferred to N. flava in vitro.9 However, in the two strains reported here, the 3-lactamase is different from the plasmid mediated and
of synovial inflamSIR,-Little is known of the mation in patients with Shigella infection.1,2 (P.G.E) has been established as a mediator of inflam’ination.1;4 Addition of Shigella endotoxin to cultured human synovial fibroblasts (derived from synovial tissue of patients undergoing
Prostaglandin t
laboratory
1. World Health Organisation Wkly epidem. Rec. 1976, 51, 293. 2. Ninane, G., Joly, J., Piot, P., Kraytman, M. Lancet, 1977, ii, 149. 3 Malmvall, B. E., Brorsson, J. E., Johnson, J. J. antimicrob. Chemother.
1977, 3, 374. 4. Percival, A., Corkill, J. E., Rowlands, J., Sykes, R. B. Lancet, ii, 1175. 5. Sykes, R. B., Percival, A. in Immunobiology of Neisseria gonorrhœœ (edited by Brooks et al.), p. 68, A.S.M., Washington, D.C., 1978. 6. Buu Hoi-Dang Van, A., Brive-Le Bouguenec, C., Barthelemy, M., Labia, R. Ann.Microbiol. 1978, 129B, 397. 7.Elwell, L. P., Roberts, M., Mayer, L. W., Falkow, S. Antimicrob. Ag. Chemother. 1977, 11, 528. 8. O’Callaghan, C. H., Morris, A., Kirby, S. M., Shingler, A. H. ibid. 1972,
i,283. 9. Eisenstein, B. I.,
Sox, T., Biswas, G., Blackman, E., Sparling, P. 1977, 195, 998.
F. Science,
Dose-resporise curve of stimulation of P.G.E and hyaiW6xo,&
acid
production in cultured human synovial fibroblasts by Shigella endotoxin.
P.G.É concentration in medium determined by radioimmunoassay and hyaluronic acid by a carbazol colour reaction, Vertical bars represent S.E.M.
menisectoniy) induced a dose-related increase in ,prQtaglandin
hyaluronic acid production by synovial fibroblast cul(figure). We have found a relationship between p.G.E and hyaluronic acid prodtiction by synovial fibroblast:>.5 We suggest that Shigella endotoxin may trigger a p;G.Emediated synovial inflammation and pathological acciimulation of joint fluid in patients with Shigella infections. E and tures
Arthritis Research Unit, Department of Physical Medicine and Rheumatology, Ichilov Hospital Medical Center and Sackler School of Medicine, Tel Aviv, Israel, and Department of Hormone Research, Weizmann Institute of Science, Rehovot
1. 2.
Noer, H. R. J. Am. med. Ass. 1966, 198, 693. Calin, A., and others. Ann. intern. Med. 1976, 84, 564. 3. DiRosa, M., and others. J. Path. 1971, 104, 15. 4. Floman, Y., and others. Clin. Orthop. 1977, 125, 214. 5. Yaron, M., and others. Arths. Rheum. 1978, 21, 694.
MICHAEL YARON
ILANA YARON URIEL ZOR
