1356 LEADING CAUSES OF MORTALITY RATES IN SCOTLAND AND CORRESPONDING RATES IN SWEDEN: MALES AGED
*The
missing ranks
in Sweden
are
attributed
to
other
45-54
mortahty condi-
tions:
(45-54). The rank order of the ten leading causes of mortality in Scotland and the corresponding rankings of causes Sweden reveal interesting differences (see table). Mortality from cancer of the lung ranks second in Scotland but fifth in Sweden. Bronchitis ranks fourth in Scotland and fourteenth in Sweden. The second leading cause of mortality in Sweden is suicide (ninth in Scotland). Although Edinburgh men drink more, cirrhosis of the liver is commoner in Sweden where it occupies third place in ranking. Perhaps the national trends in drinking habits are different from those in the capital cities. In respect of the other variables (smoking and blood-pressure) the results from the random samples of men resident in the capital cities seem to validate the national mortality-rates for the associated diseases I.H.D., lung cancer, c.v.D. and bronchitis. Smoking causes much ill-health in every community. The results from the Edinburgh/Stockholm study highlight the relative unimportance of bronchitis and lung cancer in Stockholm where men smoke less heavily. In contrast the high mortality-rates in Sweden for men aged 45-54 from suicides (45.4 vs. 13.7 in Scotland) and accidental poisonings (9-5 5 vs. 1.0) are disturbing and need further investigation.
in
Department of Medical Statistics, Welsh National School of Medicine, Cardiff CF4 4XN
T. KHOSLA
H. CAMPBELL
PROSTACYCLIN PRODUCTION BY VASCULAR SMOOTH-MUSCLE CELLS
SIR,-The work of S. Moncada, J. R. Vane, and their colleagues has shown that the endothelium is the main source of prostacyclin. This led to the suggestion that the key event in early platelet formationl2 and atherogenesis’ was non-intact endothelial surface coverage, resulting in reduced prostaglandin (p.G.)Iz production. Investigations of the prostacyclin-pro1. Moncada, S., 2. Bunting, S.,
Vane, J. R., Whittle, B. J. R. J. Physiol. 1977, 273, 20. Gryglewski, J. R., Moncada, S., Vane, J. R. Prostaglandins, 1976, 12, 897.
3. Herman, A.
G., Moncada, S., Vane, J. R Naunyns Arch.
1977, 227, 162.
int.
ducing ability of vascular endothelial and smooth-muscle cells in vascular tissue and in culture have proved contradictory. However, Maclntyre et al.4 have lately reported that prostacyclin (P.G.Iz), a bicyclic prostaglandin derived from the prostaglandin endoperoxides, is generated by endothelial cells in culture5.6 but not by cultured fibroblasts5 or smooth-muscle cells.5 Preincubation of cells in angiotensin 11 and bradykinin did not alter the availability Of P. G. 1’.44 We have investigated ten samples of human arterial tissue morpho-
(1975)
Pharmak.
logically controlled by light microscopy and by transmission and scanning electronmicroscopy before and after bioassay for P.G.I2. Arterial tissue with or without endothelial lining, intimal preparations, specimens from endarterectomies, and medial tissue were incubated at 22°C for 3 min in "tris" HCI buffer (0-05 mol/l, pH 7.5) without mechanical injury (to avoid enhanced prostacyclin activity). Tissue samples were also incubated in ketoprofen, a cyclo-oxygenase inhibitor (200 g/ml), angiotensin 11 (20 g/ml), kallikrem (10 umts/ml), and vasopressin (25 f.l-g/ml). By differential centrifugation of anticoagulated (3-8% sodium citrate, 10/1 v/v) whole human blood and rat blood, platelet-rich plasma (P.R.P.) and platelet-poor plasma (P.P.P.) were prepared. Platelet aggregation was done in a platelet aggregometer (Born) with 0.7 ml samples of P.R.P. and continuous recording (’Omniscribe’). Platelet aggregation was induced by A.D.P. in a final concentration of 1-2 mol/ml P.R.P. at 37°C and stirring at 1000 U/min. We used a P.G.E, titration curve and prostacyclin was expressed in ng per mg wet tissue per min. We assumed that P.G.I2 is thirty times more active as a platelet-aggregation inhibiting compound than P.G.I,. Controls were run with P.G.I2. Human arteries contained much more P.G.I2 activity than did the other tissues examined. Incubation of vascular tissue in P.R.P. directly enhanced the production of prostacyclin in all samples studied. After endothelial desquamation-i.e., storage for some minutes in cooled buffer (OOC) or active mechanical stripping-important p.G.Iz activity was found in the vessel wall. Similar results were obtained with intimal and medial preparations and specimens from endarterectomies. In all specimens activity fell from the inner to the outer part of the vessel wall. The total activity of human vascular tissue was small, but there was significant P.G.Iz production by smoothmuscle cells. The platelet-aggregation-inhibiting substance liberated by all vascular tissues studied was identified as prostacyclin by its short half-life, heat instability (destroyed by boiling for a short time), activity despite long-term freezing of both supernatant and tissue in buffer or liquid nitrogen, and pH instability.
Prostacyclin production was prevented by ketoprofen and significantly enhanced by the incubation of vascular tissue in angiotensin n, kallikrein, and vasopressin. Our results confirm that most of the prostacyclin generated by vascular tissue comes from the endothelium .7- 10 However, in contrast to some other reports, we found that smooth-muscle cells can also produce n.G.I2. These results accord with findings in rat’O and rabbit8 arterial tissue. Prostacyclin is reported to have dose-dependent relaxingZ,5,7, and moderate contractile effect" on smooth-muscle cells is found, but it is found more over cells with unimportant contractile potency8-1O,12.13 than over media-contractile smooth muscle
cells. 14 Studies of prostacyclin activity and mode of action in human vascular tissue must be combined with morphological inspection if we are to elucidate the functional significance of 4. Maclntyre, D. E., Pearson, J. D., Gordon, J. L. Nature, 1978, 271, 549 5. Moncada, S., Higgs, E. A., Vane, J. R. Lancet, 1977, i, 18. 6. Weksler, B. B., Marcus, A. J., Jaffe, E. A. Proc. nat. Acad. Sci. U.S.A, 1977,
74, 3922. 7. Moncada, S., Gryglewski, R., Bunting, S., Vane, J. R. Nature, 1976, 263, 663. 8. Moncada, S., Herman, A. G., Higgs, E. A., Vane, J. R. Thromb. Res. 1977,
11, 323. Silberbauer, K., Sinzinger, H., Winter, M., Feigl, W., Ring, F. Experientia (in the press). 10. Hornstra, G., Haddeman, E., Don, J. A. Circulation Res. (in the press). 11. Dustig, G. J., Moncada, S., Vane, J. R. Eur. J Pharmac. 1977, 45, 301. 12. Sinzinger, H., Silberbauer, K., Winter, M. Vasa (in the press). 13. Sinzinger, H., Silberbauer, K., Wagner, O., Winter, M Atherogenese (in the 9.
press). 14. Ross, R., Glomset,
J. A. Science, 1973, 180, 1332.
1357
prostacyclin-producing cells and their role in arterial-cell contractility and the prevention of mural platelet thrombus formation. Austrian Association for Morphological and Functional Research in Atherosclerosis, A-1090 Vienna, Austria
K. SILBERBAUER H. SINZINGER M. WINTER
IS TRICHINELLA PSEUDOSPIRALIS LIKELY TO BE A HUMAN PATHOGEN?
study was partly supported by grant 05-334-2, Center for DisControl, U.S. Public Health Service, and was done in Bilthoven.
This ease
will be presented in part by W. Kociecka and F. van the IV International Congress of Parasitologists in Warsaw, and will be published in detail elsewhere. These
findings
Knapen
at
Clinic of Parasitic Poznan, Poland
Diseases,
Z. S. PAWLOWSKI
Laboratory for Pathology, Rijksinstituut voor de Volksgezondheid,
E.
Bilthoven, Netherlands
J. RUITENBERG
SIR,- Trichinella pseudospiralis is
a new species of nemaby B. L. Garkavi in 1972 in the raccoon (Procyon lotor) in Dagestan, North Caucasus. In morphology T. pseudospiralis adults and larvw resemble T. spiralis. The important difference is that T. pseudospiralis muscle larvae are not encapsulated, and this makes it more difficult to recognise than the coiled and encapsulated T. spiralis larvee. Therefore, natural infections of T. pseudospiralis might not be rare in small wild predators, rodents, and birds. Trichinella-like parasites have been described in Bandicota bengalensis, the Indian plague rat, around Bombay’ and Bubo virginianis, the American eagle-owl, in Iowa.2 Laboratory animals (mouse, rat, Syrian hamster, guineapig, rabbit), domestic animals (pig, cat), and birds (owl, starling, chickens) are susceptible to experimental infections.3-7 For comparative studies T. pseudospiralis has been introduced to helminth laboratories throughout the
tode found
BIRD-FANCIER’S LUNG AND CŒLIAC DISEASE
SiR,—The clinical and immunopathological association between bird-fancier’s lung (B.F.L.) and coeliac disease (c.D.) are provocative.n2 Faux et aJ.2 have reported that 35% of patients with C.D. had precipitins against avian antigens and they postulated that ingestion of eggs was the source of sensitisation in c.D. They speculated further than "Once established, B.F.L. may be followed by ’egg eater’s lung’, which could be particularly aggressive if the patient had coincident c.D.". They coexist morphologically: jejunal villous atrophy with true gluten-
world. Human infection with T. pseudospiralis has not been reported, but the possibility of infection from natural or laboratory hosts cannot be excluded. The susceptibility of animals to T. pseudospiralis is different,’ so it is important to know whether this nematode is pathogenic to man. To answer this question, experimental studies on the dynamics of infection, clinical, course and pathology of T. pseudospiralisinfection were performed in 1976/77 jointly in Poznan and Bilthoven. Monkeys (Macacus fasciolaris) were used since they develop symptoms of trichinellosis as in man.8 The conclusions from the experiments in monkeys are:
(1) Intestinal infection by T. pseudospiralis is intensive but shorter than for T. spiralis, whereas muscle invasion is much less intensive but
prolonged. (2) The type of clinical symptoms is similar in T. pseudospiralis and T. spiralis infection: periorbital oedema, fever, reduced muscle activity, eosinophilia, and leukoytosis have been observed. At the same infective dose in T. pseudospiralis infection symptoms appear later on, are less pronounced, and disappear earlier. (3) Antibodies to T. spiralis and T. pseudospiralis were detected equally well by both immunofluorescence and ELISA tests with T. spiralis antigens. (4) In light and electron microscopy studies the T. spiralis infected animals showed classical capsular formation around the invaded transformed muscle fibres, whereas in the T. pseudospiralis infected animals invaded muscle fibres were less transformed and surrounded by a "pseudocapsule". Our experiments in monkeys suggest that any T. pseudospiralis infection in man might be as dangerous as is classical T. spiralis infection. Pigs can be infected experimentally’ so man may become infected by consumption of raw or inadequately processed pork. We would stress that the traditional slaughterhouse control method for pigs (i.e., trichinoscopy) will not identify T. pseudospiralis. Theoretically, serological methods could overcome this problem. Niphadkar, S. M. Curr. Sci. 1973, 42, 135. Zimmerman, W. J., and others J. Parasit, 1962, 48, 429. 3. Garkavi, B. L. Veterinariya, 1973, 9, 64 (in Russian). 4. Garkavi, B. L. Proc. III int. Congr. Parasit. (Munich) 1974, p. 661. 5. Garkavi, B. L. Parasitologiya, 1974, 8, 489 (in Russian). 6. Garkavi, B. L. ibid. 1976, 10, 154.
Indirect immunofluorescence
using
B.F.L.
serum
and anti within
IgG/fluorescein-isothiocyanate, displaying reactivity the crypts of pigeon intestine (x200).
sensitive enteropathy was noted in five of nine patients with B.F.L.33 We have a hypothesis which could explain the association and unify the immunopathogenesis of concurrent B.F.L. and C.D. We found, using a sensitive immunofluorescent technique, that patients with B.F.L. have antibodies which react with the intestinal mucosal cells of birds (figure). Could the anti-intestinal antibodies, or other hypersensitivity mechanisms which develop to bird gut mucosa of the patient with B.F.L., crossreact with intestine, eliciting C.D.? The cross-reacting anti-bird gut antibodies do not appear in all patients with B.F.L. Autoimmunity5 and c.D.6 occur in persons predisposed by certain HLA groups. Thus
c.D.
and, possibly,
B.F.L. occur on an
ecogenetic
basis: environmental exposure to pigeon droppings or other antigens in a genetically predisposed person could result in the disorders.
1. 2.
7. 8.
Miroshnitchenko, L. S. in 2nd All-Union Conference on Trichinellosis Vilnius, 1976, p. 86 (in Russian). Kociecka, W., and others III int. Conf. Trichinellosis (edited by C. W. Kim); p. 123. New York, 1974.
1. Editorial. Lancet, 1978, i, 917. 2. Faux, J. A., Hendrick, D. J., Anand, B. S. Clin. Allergy, 1978, 8, 101. 3. Berrill, W. T., Fitzpatrick, P. F., Macleod, W. M., Eade, O. E., Hyde, I., Wright, R. Lancet, 1975, ii, 1006. 4. Yang, J. P. S., Purtilo, D. T. Clin. Immun. Immunopath. 1975, 4, 46. 5. Purtilo, D. T., Yunis, E. J, et al. New Engl. J. Med. 1977, 297, 400. 6. Stokes, P. L., Ferguson, R., Holmes, G. K. T., Cooke, W. T. Q. Jl Med.
1976, 45, 567.
*The
missing ranks
in Sweden
are
attributed
to
other
45-54
mortahty condi-
tions:
(45-54). The rank order of the ten leading causes of mortality in Scotland and the corresponding rankings of causes Sweden reveal interesting differences (see table). Mortality from cancer of the lung ranks second in Scotland but fifth in Sweden. Bronchitis ranks fourth in Scotland and fourteenth in Sweden. The second leading cause of mortality in Sweden is suicide (ninth in Scotland). Although Edinburgh men drink more, cirrhosis of the liver is commoner in Sweden where it occupies third place in ranking. Perhaps the national trends in drinking habits are different from those in the capital cities. In respect of the other variables (smoking and blood-pressure) the results from the random samples of men resident in the capital cities seem to validate the national mortality-rates for the associated diseases I.H.D., lung cancer, c.v.D. and bronchitis. Smoking causes much ill-health in every community. The results from the Edinburgh/Stockholm study highlight the relative unimportance of bronchitis and lung cancer in Stockholm where men smoke less heavily. In contrast the high mortality-rates in Sweden for men aged 45-54 from suicides (45.4 vs. 13.7 in Scotland) and accidental poisonings (9-5 5 vs. 1.0) are disturbing and need further investigation.
in
Department of Medical Statistics, Welsh National School of Medicine, Cardiff CF4 4XN
T. KHOSLA
H. CAMPBELL
PROSTACYCLIN PRODUCTION BY VASCULAR SMOOTH-MUSCLE CELLS
SIR,-The work of S. Moncada, J. R. Vane, and their colleagues has shown that the endothelium is the main source of prostacyclin. This led to the suggestion that the key event in early platelet formationl2 and atherogenesis’ was non-intact endothelial surface coverage, resulting in reduced prostaglandin (p.G.)Iz production. Investigations of the prostacyclin-pro1. Moncada, S., 2. Bunting, S.,
Vane, J. R., Whittle, B. J. R. J. Physiol. 1977, 273, 20. Gryglewski, J. R., Moncada, S., Vane, J. R. Prostaglandins, 1976, 12, 897.
3. Herman, A.
G., Moncada, S., Vane, J. R Naunyns Arch.
1977, 227, 162.
int.
ducing ability of vascular endothelial and smooth-muscle cells in vascular tissue and in culture have proved contradictory. However, Maclntyre et al.4 have lately reported that prostacyclin (P.G.Iz), a bicyclic prostaglandin derived from the prostaglandin endoperoxides, is generated by endothelial cells in culture5.6 but not by cultured fibroblasts5 or smooth-muscle cells.5 Preincubation of cells in angiotensin 11 and bradykinin did not alter the availability Of P. G. 1’.44 We have investigated ten samples of human arterial tissue morpho-
(1975)
Pharmak.
logically controlled by light microscopy and by transmission and scanning electronmicroscopy before and after bioassay for P.G.I2. Arterial tissue with or without endothelial lining, intimal preparations, specimens from endarterectomies, and medial tissue were incubated at 22°C for 3 min in "tris" HCI buffer (0-05 mol/l, pH 7.5) without mechanical injury (to avoid enhanced prostacyclin activity). Tissue samples were also incubated in ketoprofen, a cyclo-oxygenase inhibitor (200 g/ml), angiotensin 11 (20 g/ml), kallikrem (10 umts/ml), and vasopressin (25 f.l-g/ml). By differential centrifugation of anticoagulated (3-8% sodium citrate, 10/1 v/v) whole human blood and rat blood, platelet-rich plasma (P.R.P.) and platelet-poor plasma (P.P.P.) were prepared. Platelet aggregation was done in a platelet aggregometer (Born) with 0.7 ml samples of P.R.P. and continuous recording (’Omniscribe’). Platelet aggregation was induced by A.D.P. in a final concentration of 1-2 mol/ml P.R.P. at 37°C and stirring at 1000 U/min. We used a P.G.E, titration curve and prostacyclin was expressed in ng per mg wet tissue per min. We assumed that P.G.I2 is thirty times more active as a platelet-aggregation inhibiting compound than P.G.I,. Controls were run with P.G.I2. Human arteries contained much more P.G.I2 activity than did the other tissues examined. Incubation of vascular tissue in P.R.P. directly enhanced the production of prostacyclin in all samples studied. After endothelial desquamation-i.e., storage for some minutes in cooled buffer (OOC) or active mechanical stripping-important p.G.Iz activity was found in the vessel wall. Similar results were obtained with intimal and medial preparations and specimens from endarterectomies. In all specimens activity fell from the inner to the outer part of the vessel wall. The total activity of human vascular tissue was small, but there was significant P.G.Iz production by smoothmuscle cells. The platelet-aggregation-inhibiting substance liberated by all vascular tissues studied was identified as prostacyclin by its short half-life, heat instability (destroyed by boiling for a short time), activity despite long-term freezing of both supernatant and tissue in buffer or liquid nitrogen, and pH instability.
Prostacyclin production was prevented by ketoprofen and significantly enhanced by the incubation of vascular tissue in angiotensin n, kallikrein, and vasopressin. Our results confirm that most of the prostacyclin generated by vascular tissue comes from the endothelium .7- 10 However, in contrast to some other reports, we found that smooth-muscle cells can also produce n.G.I2. These results accord with findings in rat’O and rabbit8 arterial tissue. Prostacyclin is reported to have dose-dependent relaxingZ,5,7, and moderate contractile effect" on smooth-muscle cells is found, but it is found more over cells with unimportant contractile potency8-1O,12.13 than over media-contractile smooth muscle
cells. 14 Studies of prostacyclin activity and mode of action in human vascular tissue must be combined with morphological inspection if we are to elucidate the functional significance of 4. Maclntyre, D. E., Pearson, J. D., Gordon, J. L. Nature, 1978, 271, 549 5. Moncada, S., Higgs, E. A., Vane, J. R. Lancet, 1977, i, 18. 6. Weksler, B. B., Marcus, A. J., Jaffe, E. A. Proc. nat. Acad. Sci. U.S.A, 1977,
74, 3922. 7. Moncada, S., Gryglewski, R., Bunting, S., Vane, J. R. Nature, 1976, 263, 663. 8. Moncada, S., Herman, A. G., Higgs, E. A., Vane, J. R. Thromb. Res. 1977,
11, 323. Silberbauer, K., Sinzinger, H., Winter, M., Feigl, W., Ring, F. Experientia (in the press). 10. Hornstra, G., Haddeman, E., Don, J. A. Circulation Res. (in the press). 11. Dustig, G. J., Moncada, S., Vane, J. R. Eur. J Pharmac. 1977, 45, 301. 12. Sinzinger, H., Silberbauer, K., Winter, M. Vasa (in the press). 13. Sinzinger, H., Silberbauer, K., Wagner, O., Winter, M Atherogenese (in the 9.
press). 14. Ross, R., Glomset,
J. A. Science, 1973, 180, 1332.
1357
prostacyclin-producing cells and their role in arterial-cell contractility and the prevention of mural platelet thrombus formation. Austrian Association for Morphological and Functional Research in Atherosclerosis, A-1090 Vienna, Austria
K. SILBERBAUER H. SINZINGER M. WINTER
IS TRICHINELLA PSEUDOSPIRALIS LIKELY TO BE A HUMAN PATHOGEN?
study was partly supported by grant 05-334-2, Center for DisControl, U.S. Public Health Service, and was done in Bilthoven.
This ease
will be presented in part by W. Kociecka and F. van the IV International Congress of Parasitologists in Warsaw, and will be published in detail elsewhere. These
findings
Knapen
at
Clinic of Parasitic Poznan, Poland
Diseases,
Z. S. PAWLOWSKI
Laboratory for Pathology, Rijksinstituut voor de Volksgezondheid,
E.
Bilthoven, Netherlands
J. RUITENBERG
SIR,- Trichinella pseudospiralis is
a new species of nemaby B. L. Garkavi in 1972 in the raccoon (Procyon lotor) in Dagestan, North Caucasus. In morphology T. pseudospiralis adults and larvw resemble T. spiralis. The important difference is that T. pseudospiralis muscle larvae are not encapsulated, and this makes it more difficult to recognise than the coiled and encapsulated T. spiralis larvee. Therefore, natural infections of T. pseudospiralis might not be rare in small wild predators, rodents, and birds. Trichinella-like parasites have been described in Bandicota bengalensis, the Indian plague rat, around Bombay’ and Bubo virginianis, the American eagle-owl, in Iowa.2 Laboratory animals (mouse, rat, Syrian hamster, guineapig, rabbit), domestic animals (pig, cat), and birds (owl, starling, chickens) are susceptible to experimental infections.3-7 For comparative studies T. pseudospiralis has been introduced to helminth laboratories throughout the
tode found
BIRD-FANCIER’S LUNG AND CŒLIAC DISEASE
SiR,—The clinical and immunopathological association between bird-fancier’s lung (B.F.L.) and coeliac disease (c.D.) are provocative.n2 Faux et aJ.2 have reported that 35% of patients with C.D. had precipitins against avian antigens and they postulated that ingestion of eggs was the source of sensitisation in c.D. They speculated further than "Once established, B.F.L. may be followed by ’egg eater’s lung’, which could be particularly aggressive if the patient had coincident c.D.". They coexist morphologically: jejunal villous atrophy with true gluten-
world. Human infection with T. pseudospiralis has not been reported, but the possibility of infection from natural or laboratory hosts cannot be excluded. The susceptibility of animals to T. pseudospiralis is different,’ so it is important to know whether this nematode is pathogenic to man. To answer this question, experimental studies on the dynamics of infection, clinical, course and pathology of T. pseudospiralisinfection were performed in 1976/77 jointly in Poznan and Bilthoven. Monkeys (Macacus fasciolaris) were used since they develop symptoms of trichinellosis as in man.8 The conclusions from the experiments in monkeys are:
(1) Intestinal infection by T. pseudospiralis is intensive but shorter than for T. spiralis, whereas muscle invasion is much less intensive but
prolonged. (2) The type of clinical symptoms is similar in T. pseudospiralis and T. spiralis infection: periorbital oedema, fever, reduced muscle activity, eosinophilia, and leukoytosis have been observed. At the same infective dose in T. pseudospiralis infection symptoms appear later on, are less pronounced, and disappear earlier. (3) Antibodies to T. spiralis and T. pseudospiralis were detected equally well by both immunofluorescence and ELISA tests with T. spiralis antigens. (4) In light and electron microscopy studies the T. spiralis infected animals showed classical capsular formation around the invaded transformed muscle fibres, whereas in the T. pseudospiralis infected animals invaded muscle fibres were less transformed and surrounded by a "pseudocapsule". Our experiments in monkeys suggest that any T. pseudospiralis infection in man might be as dangerous as is classical T. spiralis infection. Pigs can be infected experimentally’ so man may become infected by consumption of raw or inadequately processed pork. We would stress that the traditional slaughterhouse control method for pigs (i.e., trichinoscopy) will not identify T. pseudospiralis. Theoretically, serological methods could overcome this problem. Niphadkar, S. M. Curr. Sci. 1973, 42, 135. Zimmerman, W. J., and others J. Parasit, 1962, 48, 429. 3. Garkavi, B. L. Veterinariya, 1973, 9, 64 (in Russian). 4. Garkavi, B. L. Proc. III int. Congr. Parasit. (Munich) 1974, p. 661. 5. Garkavi, B. L. Parasitologiya, 1974, 8, 489 (in Russian). 6. Garkavi, B. L. ibid. 1976, 10, 154.
Indirect immunofluorescence
using
B.F.L.
serum
and anti within
IgG/fluorescein-isothiocyanate, displaying reactivity the crypts of pigeon intestine (x200).
sensitive enteropathy was noted in five of nine patients with B.F.L.33 We have a hypothesis which could explain the association and unify the immunopathogenesis of concurrent B.F.L. and C.D. We found, using a sensitive immunofluorescent technique, that patients with B.F.L. have antibodies which react with the intestinal mucosal cells of birds (figure). Could the anti-intestinal antibodies, or other hypersensitivity mechanisms which develop to bird gut mucosa of the patient with B.F.L., crossreact with intestine, eliciting C.D.? The cross-reacting anti-bird gut antibodies do not appear in all patients with B.F.L. Autoimmunity5 and c.D.6 occur in persons predisposed by certain HLA groups. Thus
c.D.
and, possibly,
B.F.L. occur on an
ecogenetic
basis: environmental exposure to pigeon droppings or other antigens in a genetically predisposed person could result in the disorders.
1. 2.
7. 8.
Miroshnitchenko, L. S. in 2nd All-Union Conference on Trichinellosis Vilnius, 1976, p. 86 (in Russian). Kociecka, W., and others III int. Conf. Trichinellosis (edited by C. W. Kim); p. 123. New York, 1974.
1. Editorial. Lancet, 1978, i, 917. 2. Faux, J. A., Hendrick, D. J., Anand, B. S. Clin. Allergy, 1978, 8, 101. 3. Berrill, W. T., Fitzpatrick, P. F., Macleod, W. M., Eade, O. E., Hyde, I., Wright, R. Lancet, 1975, ii, 1006. 4. Yang, J. P. S., Purtilo, D. T. Clin. Immun. Immunopath. 1975, 4, 46. 5. Purtilo, D. T., Yunis, E. J, et al. New Engl. J. Med. 1977, 297, 400. 6. Stokes, P. L., Ferguson, R., Holmes, G. K. T., Cooke, W. T. Q. Jl Med.
1976, 45, 567.
