219
Physical examination was unremarkable except for signs of respiratory distress. The postnatal course was complicated by mild R.D.S. that resolved within 24 h, a sepsis work-up for possible amnionitis, and frequent apnoeic spells treated with theophylline. Laboratory data included negative blood, C.S.F., and urine cultures, haemoglobin 12.4 g/dl, haematocrit 37.4%, reticulocyte-count 10.3%, and 340 000 platelets/pd. Cord-blood IgM was 15 mg/dl. A Venereal Disease Research Laboratory test was non-reactive. Blood type was 0+ and direct Coombs was negative. The absolute w.B.c. count in the first two weeks is shown in the figure. The differential count revealed a predominance of neutrophils and neutrophil precursors, including myelocytes, metamyelocytes, and blast forms. This left shift persisted until the 1 lth day of life. mild
The normal W.B.C. count for a neonate ranges from 9000 to 000/pl with a predominance of neutrophils. The number of neutrophils and neutrophil precursors decreases from 12 to 72 h of age and then remains relatively constant through the first month of life.’ By one week of age the W.B.C. count normally ranges from 5000 to 20 000/1. Between one and four weeks of age the lymphocyte becomes the predominant leucocyte. This patient had a marked deviation from the normal W.B.C. count pattern suggestive of a leukxmoid reaction. Several causes of leukaemoid reaction were investigated in this infant. Infectious processes were ruled out; there was mild anaemia at birth but no evidence of acute blood-loss or haemolysis ; congenital leukaemia was considered but normal platelet and raised reticulocyte counts make this unlikely; V.D.R.L. was negative in both maternal and cord blood. Although unlikely, one possible aetiology for this leukaemoid reaction may have been a hypoxic insult due to perinatal asphyxia, R.D.S., or apnaeic episodes; however, prolonged periods of subnormal oxygen status were not recorded. With other causes of leukaemoid reaction discarded, the prenatal administration of betamethasone has to be considered. Activity of betamethasone has been detected in cord blood as early as one hour after maternal therapy.2 Corticosteroid administration may increase the W.B.C. count by decreasing leucocyte outflow from vessels and by increasing bone-marrow release of neutrophils. The result is not only an increase in 1 w.B.c. but also a shift to the left.’ We are not sure why this leuksemoid reaction occurred but we think that it was related to the prenatal use of betamethasone. Our experience with this drug reflects that of other investigators: unless more serious side-effects are recorded betamethasone remains the treatment of choice for prevention OfR.D.S. 30
Division of Perinatal
Medicine, Department of Pediatrics, Monmouth Medical Center, Long Branch, New Jersey 07740, U.S.A.
DONALD BIELAWSKI I. MARK HIATT THOMAS HEGYI
HYDROGEN-SULPHIDE POISONING
SIR,-I found your warning (Jan. 7, p. 28) on the dangers of hydrogen sulphide excellent, but you state that there is no specific antidote. The toxicity of hydrogen sulphide seems to be due to inhibition of cytochrome oxidase, and in this it resembles cyanide. Smith et al.,3 in experiments on mice, found that the efficacy of nitrite in acute sulphide poisoning was superior to that of oxygen. Nitrite converts some of the haemoglobin to methxmoglobin, and presumably this traps sulphide as sulph-
methsmoglobin. The regimen which we have introduced for the treatment of hydrogen-sulphide poisoning is as follows. The rescuer puts on breathing apparatus and then removes the casualty to the fresh air. The airway is maintained, and, if the casualty is 1. Wetzman, M. Am. J. Dis. Child. 1975, 129, 1183. 2. Anderson, A., and others, Obstet Gynec. 1977, 49, 471. 3. Smith, R. P., Kruszyna, R., Kruszyna, H. Archs envir. Hlth,
1976, 31, 116.
breathing, a capsule of amyl nitrite (which is kept at specific plants) is broken into a cloth and the casualty breathes the vapour. When medical aid is available 10 ml of 3% sodium nitrite is injected intravenously over 2-3 min. If symptoms recur a further 5 ml may be given. We feel it justified, in areas where there is a potential for hydrogen-sulphide poisoning, to keep available capsules of amyl nitrite for use by first-aiders trained in basic life support. Esso Medical Centre, Fawley, Southampton
A. DOWNIE
SO4 1TX
FALSE-POSITIVE IgM ANTI-TOXOPLASMA FLUORESCENT TEST DUE TO RHEUMATOID FACTOR
SIR,-Camargo et al.l detected IgM anti-toxoplasma antiby immunofluorescence (I.F.) in a high percentage of sera containing rheumatoid factor (R.F.). These results, however, were not entirely convincing because treatment of sera with heat-aggregated human gammaglobulin-which was not screened for IgM anti-toxoplasma antibodies2-removed IgM anti-toxoplasma antibodies without modifying the R.F. titres. We have seen an 18-year-old patient with systemic lupus erythematosus who had an anti-toxoplasma IgM titre of 1/800 and a rheumatoid factor titre of 1/320. We found that the IgM bodies
GEL-FILTRATION OF SERUM CONTAINING RHEUMATOID FACTOR AND ANTI-TOXOPLASMA ANTIBODIES
antibodies detectable by LF. were due to R.F. Gel filtration of from this patient on ’Sephadex G200’ under dissociatconditions (pH 4.0) gave three peaks, peakcontaining ing R.F. and IgM without anti-toxoplasma antibodies and peak II containing neither IgM nor R.F. but having anti-toxoplasma activity (see table). Radial immunodiffusion showed that the decrease in protein content during fractionation was negligible. When a fixed concentration of peak i protein was mixed with increasing concentrations of peak II protein IgM anti-toxoplasma I.F. was restored and the titre of IgM LF. increased in parallel with IgG concentration, returning to the activity of whole serum. To confirm the role played by R.F. in this false IgM Of. anti-toxoplasma reaction, we removed R.F. from serum by absorption, either with latex particles coated with IgG or with glutaraldehyde-polymerised IgG. In both cases, despite an insignificant loss of protein, IgM I.F. was abolished by R.F. absorption. R.F. is thus capable of reacting with IgG antibodies bound to the antigen during in-vitro reaction and can subsequently be revealed by the anti-jjt fluorescent antibodies, giving a false-positive reaction in tests for IgM. In further investigations, false reactions were detected in 80% of sera which showed positive latex tests. False-positive IgM antibodies to toxoplasma previously described in patients with juvenile rheumatoid arthritis3 or systemic lupus erythematosus4 may well be due to R.F. R.F. also causes false-positive IgM Of. in some viral and bacterial diseases.s,6 Avoidance of serum
1. Camargo, M.
E., Leser, P. G., Rocca, A.
Rev. Inst. Med. trop. São
Paulo,
1972, 14, 310. 2. Cohen, I. R., Norins, L. C., Julian, A. J. J. Immun. 1967, 98, 143. 3. Cat, I., Marinoni, L. P., Giraldi, D. J., Costa, O. Lancet, 1971, ii, 1156. 4. Araujo, F. G., Barnett, E. V., Gentry, L. O., Remington, J. S. Appl. Microbiol. 1971, 22, 270. 5. Reimer, C. B., Black, C. M., Phillips, D. J., Logan, L. C., Hunter, E. F., Pender, B. J., McGrew, B. E. Ann. N.Y. Acad. Sci. 1975, 254, 77. 6. Robertson, P. W., Kertesz, V., Cloonan, M. J. J. clin. Microbiol. 1977, 6, 174.
220
IgM anti-toxoplasma false reactions is particularly important in pregnancy-in which a diagnosis of evolutive toxoplasmosis may indicate a therapeutic abortion-and in patients with connective tissue diseases in whom toxoplasmosis is particularly severe because they are immunosuppressed and who very frequently have R.F. In these circumstances, sephadex G200 gel filtration under dissociating conditions or R.F. absorption may avoid a falsepositive IgM I.F. anti-toxoplasma reaction. Inserm U 131, Service de Rhumatologie, Hôpital Antoine Béclère, 92141 Clamart, France
IMMUNOREACTIVE CALCITONIN, PROSTAGLANDINS, AND VASOACTIVE INTESTINAL PEPTIDE IN PLASMA OF VIPOMA
PATIENTS
P. YENI P. SEGOND P. MASSIAS
J. PILLOT
HYPERCALCITONINÆMIA IN VIPOMAS
SIR,-Increased circulating immunoreactive calcitonin (ic.T.) which was initially reported in medullary carcinoma of the thyroid,’ has been observed in patients with non-thyroid tumours.2,3 We have found high levels of plasma-ic.T. in three consecutive cases of vipoma (see table), the first of which has been described elsewhere.4 The three patients presented with the usual watery diarrhoea of pancreatic cholera and on laparotomy had an islet-cell carcinoma with hepatic metastases. Immunoreactive prostaglandins E and Fa were raised in the plasma of two cases (see table). Several mechanisms could account for hypercalcitoninaemia in vipoma. It can arise from bone metastases.3 None of our patients had clinical or biological evidence of secondary bonedeposits. These cannot be yet completely ruled out since no skeletal scanning was done and bones were not tested at necropsy in case 2. However, the increase in circulating c.T. in patients with bone metastasis is usually small.3 None of the three patients had clinical or scintiscan evidence of a thyroid tumour and the gland was normal at necropsy in cases 2 and 3. Moreover, medullary thyroid carcinoma has not yet been associated with pancreatic cholera. Stimulation of thyroid c.T. synthesis and release might also produce hypercalcitoninoemia. Hypercalcaemia is observed in nearly half of the patients with pancreatic choleras and could induce a moderate increase in thyroid c.T. production. Our three patients had a normal plasma-calcium. Mild stimulation of thyroid C.T. has been reported in a malignant tumour not associated with hypercalcxmia.6 Glucagon, a peptide structurally and pharmacologically related to the vasoactive intestinal peptide (v.I.P.), releases thyroid C.T. in several animal species7,8 and in some patients with medullary carcinoma of the thyroid.9 However, the persistence of an increased plasma ic.T. level after pancreatic
tumour
patient 2 while the level of v.l.p. in nearly normal, argues against such a mech-
resection in
plasma dropped
to
anism. The hypercalcitoninsmia might be explained by ectopic secretion of c.T. (or a peptide sharing common antigenic determinants with c.T.) by the vipoma. This hypothesis is consistent with the finding that most non-thyroid tumours-including
1. Milhaud,
G., Tubiana, M., Parmentier, C., Coutris, G. C.
r.
Acad. Sci.
Paris, 1968, 266, 608. 2. Milhaud, G., Calmette, C., Taboulet, J., Julienne, A., Moukhtar, M. S. Lancet,
1974, i, 462. C., Greenberg, P. B., Hillyard, C., MacIntyre, I. ibid. 1974, i,
3. Coombes, R. 1080. 4. Rambaud, J.
C., Modigliani, R., Matuchansky, C., Bloom, S., Said, S., PesD., Bernier, J. J. Gastroenterology, 1975, 69, 110. 5. Pessayre, D. M.D. thesis, University of Paris VII, 1973. 6. Silva, O. L., Becker, K. L., Primack, A., Doppman, J. L., Snider, R. H. J. Am. med. Ass. 1975, 234, 183. 7. Care, A. D., Bates, R. F. L., Philippo, M., Lequin, R. M., Hackeng, W. H. L., Barlet, J. P., Larvor, P. J. Endocr. 1970, 48, 667. 8. Swaminathan, R., Bates, R. F. L., Bloom, S. R., Ganculi, P. C., Care, A. D. ibid. 1973, 59, 217. 9. Deftos, L. J., Bury, A. E., Habener, J. F., Singer, F. R., Potts, J. T. Jr, Metabolism, 1971, 20, 1129. sayre,
*Resection of pancreatic tumour, hepatic metastasis left.
tNormal value 100 pg/ml. formal value 500 pg/ml.
vipomas-in which circulating ic.T. is raised2 are thought to derive from cells of common embryological origin (i.e., the neural crest).10 In these non-thyroid tumours, the increase of ic.T. is small, whereas our values are within the range of those found in medullary carcinoma of the thyroid. A high concentration of ic.T. has been found in a pancreatic cholera tumour producing multiple hormones including v.I.p.u Moreover, in patient 2, a large concentration gradient of plasma-ic.T. was found between a peripheral vein (4-43 pg/ml, normal 008 pg/ml) and the splenic vein (20.27 pg/ml) simultaneously sampled during laparotomy. The non-parallel changes in circulating v.i.p. and ic.T. after resection of the pancreatic tumour cf patients 1 and 2 could result from differences between the original tumour and the residual metastases in the ratio of the synthesis rates of the two peptides. Extraction of c.T. from the tumours of patients 2 and 3 together with comparative structural studies of vipoma-associated plasma-c.T., normal thyroid c.T., and c.T. produced in medullary carcinoma of the thyroid are in progress. Clinique de Gastroentérologie, Hôpital Saint-Lazare, 75475 Paris, France U.113 Laboratoire de Biophysique, Faculté de Médecine Saint-Antoine, 75012 Paris
Royal Postgraduate Medical School, Hammersmith Hospital, London W12 0HS
J. C. RAMBAUD A. NISARD R. MODIGLIANI C. CALMETTE M. S. MOUKHTAR P. A. HILL H. BESTERMAN
PURPLE URINE BAGS
SiR,-Sometimes the plastic disposable urine bags used with collecting appliances by patients with urinary diversions turn purple. This is usually thought to be associated with infection but the discoloration has not been explained and the manufacturers have been unable to help. We have found that the pigment is readily extracted from the bag with benzene but is almost insoluble in alcohol or isopropanol. The resulting solution in benzene was the same purple colour as the bag. On spectroscopic analysis the visible region spectrum had a broad peak with aX maximum at 555 nm and a shoulder at 600 nm. The spectrum was identical with that of indigo dissolved in benzene. 10. Pearse, A. G. E., Polak, J. M. Med. Biol. 1974, 52, 3. 11. Schmitt, M. G. Jr, Soergel, K. H., Hensley, G. T., Chey, M. Y. Gastroenter-
ology, 1975, 69, 206.
Physical examination was unremarkable except for signs of respiratory distress. The postnatal course was complicated by mild R.D.S. that resolved within 24 h, a sepsis work-up for possible amnionitis, and frequent apnoeic spells treated with theophylline. Laboratory data included negative blood, C.S.F., and urine cultures, haemoglobin 12.4 g/dl, haematocrit 37.4%, reticulocyte-count 10.3%, and 340 000 platelets/pd. Cord-blood IgM was 15 mg/dl. A Venereal Disease Research Laboratory test was non-reactive. Blood type was 0+ and direct Coombs was negative. The absolute w.B.c. count in the first two weeks is shown in the figure. The differential count revealed a predominance of neutrophils and neutrophil precursors, including myelocytes, metamyelocytes, and blast forms. This left shift persisted until the 1 lth day of life. mild
The normal W.B.C. count for a neonate ranges from 9000 to 000/pl with a predominance of neutrophils. The number of neutrophils and neutrophil precursors decreases from 12 to 72 h of age and then remains relatively constant through the first month of life.’ By one week of age the W.B.C. count normally ranges from 5000 to 20 000/1. Between one and four weeks of age the lymphocyte becomes the predominant leucocyte. This patient had a marked deviation from the normal W.B.C. count pattern suggestive of a leukxmoid reaction. Several causes of leukaemoid reaction were investigated in this infant. Infectious processes were ruled out; there was mild anaemia at birth but no evidence of acute blood-loss or haemolysis ; congenital leukaemia was considered but normal platelet and raised reticulocyte counts make this unlikely; V.D.R.L. was negative in both maternal and cord blood. Although unlikely, one possible aetiology for this leukaemoid reaction may have been a hypoxic insult due to perinatal asphyxia, R.D.S., or apnaeic episodes; however, prolonged periods of subnormal oxygen status were not recorded. With other causes of leukaemoid reaction discarded, the prenatal administration of betamethasone has to be considered. Activity of betamethasone has been detected in cord blood as early as one hour after maternal therapy.2 Corticosteroid administration may increase the W.B.C. count by decreasing leucocyte outflow from vessels and by increasing bone-marrow release of neutrophils. The result is not only an increase in 1 w.B.c. but also a shift to the left.’ We are not sure why this leuksemoid reaction occurred but we think that it was related to the prenatal use of betamethasone. Our experience with this drug reflects that of other investigators: unless more serious side-effects are recorded betamethasone remains the treatment of choice for prevention OfR.D.S. 30
Division of Perinatal
Medicine, Department of Pediatrics, Monmouth Medical Center, Long Branch, New Jersey 07740, U.S.A.
DONALD BIELAWSKI I. MARK HIATT THOMAS HEGYI
HYDROGEN-SULPHIDE POISONING
SIR,-I found your warning (Jan. 7, p. 28) on the dangers of hydrogen sulphide excellent, but you state that there is no specific antidote. The toxicity of hydrogen sulphide seems to be due to inhibition of cytochrome oxidase, and in this it resembles cyanide. Smith et al.,3 in experiments on mice, found that the efficacy of nitrite in acute sulphide poisoning was superior to that of oxygen. Nitrite converts some of the haemoglobin to methxmoglobin, and presumably this traps sulphide as sulph-
methsmoglobin. The regimen which we have introduced for the treatment of hydrogen-sulphide poisoning is as follows. The rescuer puts on breathing apparatus and then removes the casualty to the fresh air. The airway is maintained, and, if the casualty is 1. Wetzman, M. Am. J. Dis. Child. 1975, 129, 1183. 2. Anderson, A., and others, Obstet Gynec. 1977, 49, 471. 3. Smith, R. P., Kruszyna, R., Kruszyna, H. Archs envir. Hlth,
1976, 31, 116.
breathing, a capsule of amyl nitrite (which is kept at specific plants) is broken into a cloth and the casualty breathes the vapour. When medical aid is available 10 ml of 3% sodium nitrite is injected intravenously over 2-3 min. If symptoms recur a further 5 ml may be given. We feel it justified, in areas where there is a potential for hydrogen-sulphide poisoning, to keep available capsules of amyl nitrite for use by first-aiders trained in basic life support. Esso Medical Centre, Fawley, Southampton
A. DOWNIE
SO4 1TX
FALSE-POSITIVE IgM ANTI-TOXOPLASMA FLUORESCENT TEST DUE TO RHEUMATOID FACTOR
SIR,-Camargo et al.l detected IgM anti-toxoplasma antiby immunofluorescence (I.F.) in a high percentage of sera containing rheumatoid factor (R.F.). These results, however, were not entirely convincing because treatment of sera with heat-aggregated human gammaglobulin-which was not screened for IgM anti-toxoplasma antibodies2-removed IgM anti-toxoplasma antibodies without modifying the R.F. titres. We have seen an 18-year-old patient with systemic lupus erythematosus who had an anti-toxoplasma IgM titre of 1/800 and a rheumatoid factor titre of 1/320. We found that the IgM bodies
GEL-FILTRATION OF SERUM CONTAINING RHEUMATOID FACTOR AND ANTI-TOXOPLASMA ANTIBODIES
antibodies detectable by LF. were due to R.F. Gel filtration of from this patient on ’Sephadex G200’ under dissociatconditions (pH 4.0) gave three peaks, peakcontaining ing R.F. and IgM without anti-toxoplasma antibodies and peak II containing neither IgM nor R.F. but having anti-toxoplasma activity (see table). Radial immunodiffusion showed that the decrease in protein content during fractionation was negligible. When a fixed concentration of peak i protein was mixed with increasing concentrations of peak II protein IgM anti-toxoplasma I.F. was restored and the titre of IgM LF. increased in parallel with IgG concentration, returning to the activity of whole serum. To confirm the role played by R.F. in this false IgM Of. anti-toxoplasma reaction, we removed R.F. from serum by absorption, either with latex particles coated with IgG or with glutaraldehyde-polymerised IgG. In both cases, despite an insignificant loss of protein, IgM I.F. was abolished by R.F. absorption. R.F. is thus capable of reacting with IgG antibodies bound to the antigen during in-vitro reaction and can subsequently be revealed by the anti-jjt fluorescent antibodies, giving a false-positive reaction in tests for IgM. In further investigations, false reactions were detected in 80% of sera which showed positive latex tests. False-positive IgM antibodies to toxoplasma previously described in patients with juvenile rheumatoid arthritis3 or systemic lupus erythematosus4 may well be due to R.F. R.F. also causes false-positive IgM Of. in some viral and bacterial diseases.s,6 Avoidance of serum
1. Camargo, M.
E., Leser, P. G., Rocca, A.
Rev. Inst. Med. trop. São
Paulo,
1972, 14, 310. 2. Cohen, I. R., Norins, L. C., Julian, A. J. J. Immun. 1967, 98, 143. 3. Cat, I., Marinoni, L. P., Giraldi, D. J., Costa, O. Lancet, 1971, ii, 1156. 4. Araujo, F. G., Barnett, E. V., Gentry, L. O., Remington, J. S. Appl. Microbiol. 1971, 22, 270. 5. Reimer, C. B., Black, C. M., Phillips, D. J., Logan, L. C., Hunter, E. F., Pender, B. J., McGrew, B. E. Ann. N.Y. Acad. Sci. 1975, 254, 77. 6. Robertson, P. W., Kertesz, V., Cloonan, M. J. J. clin. Microbiol. 1977, 6, 174.
220
IgM anti-toxoplasma false reactions is particularly important in pregnancy-in which a diagnosis of evolutive toxoplasmosis may indicate a therapeutic abortion-and in patients with connective tissue diseases in whom toxoplasmosis is particularly severe because they are immunosuppressed and who very frequently have R.F. In these circumstances, sephadex G200 gel filtration under dissociating conditions or R.F. absorption may avoid a falsepositive IgM I.F. anti-toxoplasma reaction. Inserm U 131, Service de Rhumatologie, Hôpital Antoine Béclère, 92141 Clamart, France
IMMUNOREACTIVE CALCITONIN, PROSTAGLANDINS, AND VASOACTIVE INTESTINAL PEPTIDE IN PLASMA OF VIPOMA
PATIENTS
P. YENI P. SEGOND P. MASSIAS
J. PILLOT
HYPERCALCITONINÆMIA IN VIPOMAS
SIR,-Increased circulating immunoreactive calcitonin (ic.T.) which was initially reported in medullary carcinoma of the thyroid,’ has been observed in patients with non-thyroid tumours.2,3 We have found high levels of plasma-ic.T. in three consecutive cases of vipoma (see table), the first of which has been described elsewhere.4 The three patients presented with the usual watery diarrhoea of pancreatic cholera and on laparotomy had an islet-cell carcinoma with hepatic metastases. Immunoreactive prostaglandins E and Fa were raised in the plasma of two cases (see table). Several mechanisms could account for hypercalcitoninaemia in vipoma. It can arise from bone metastases.3 None of our patients had clinical or biological evidence of secondary bonedeposits. These cannot be yet completely ruled out since no skeletal scanning was done and bones were not tested at necropsy in case 2. However, the increase in circulating c.T. in patients with bone metastasis is usually small.3 None of the three patients had clinical or scintiscan evidence of a thyroid tumour and the gland was normal at necropsy in cases 2 and 3. Moreover, medullary thyroid carcinoma has not yet been associated with pancreatic cholera. Stimulation of thyroid c.T. synthesis and release might also produce hypercalcitoninoemia. Hypercalcaemia is observed in nearly half of the patients with pancreatic choleras and could induce a moderate increase in thyroid c.T. production. Our three patients had a normal plasma-calcium. Mild stimulation of thyroid C.T. has been reported in a malignant tumour not associated with hypercalcxmia.6 Glucagon, a peptide structurally and pharmacologically related to the vasoactive intestinal peptide (v.I.P.), releases thyroid C.T. in several animal species7,8 and in some patients with medullary carcinoma of the thyroid.9 However, the persistence of an increased plasma ic.T. level after pancreatic
tumour
patient 2 while the level of v.l.p. in nearly normal, argues against such a mech-
resection in
plasma dropped
to
anism. The hypercalcitoninsmia might be explained by ectopic secretion of c.T. (or a peptide sharing common antigenic determinants with c.T.) by the vipoma. This hypothesis is consistent with the finding that most non-thyroid tumours-including
1. Milhaud,
G., Tubiana, M., Parmentier, C., Coutris, G. C.
r.
Acad. Sci.
Paris, 1968, 266, 608. 2. Milhaud, G., Calmette, C., Taboulet, J., Julienne, A., Moukhtar, M. S. Lancet,
1974, i, 462. C., Greenberg, P. B., Hillyard, C., MacIntyre, I. ibid. 1974, i,
3. Coombes, R. 1080. 4. Rambaud, J.
C., Modigliani, R., Matuchansky, C., Bloom, S., Said, S., PesD., Bernier, J. J. Gastroenterology, 1975, 69, 110. 5. Pessayre, D. M.D. thesis, University of Paris VII, 1973. 6. Silva, O. L., Becker, K. L., Primack, A., Doppman, J. L., Snider, R. H. J. Am. med. Ass. 1975, 234, 183. 7. Care, A. D., Bates, R. F. L., Philippo, M., Lequin, R. M., Hackeng, W. H. L., Barlet, J. P., Larvor, P. J. Endocr. 1970, 48, 667. 8. Swaminathan, R., Bates, R. F. L., Bloom, S. R., Ganculi, P. C., Care, A. D. ibid. 1973, 59, 217. 9. Deftos, L. J., Bury, A. E., Habener, J. F., Singer, F. R., Potts, J. T. Jr, Metabolism, 1971, 20, 1129. sayre,
*Resection of pancreatic tumour, hepatic metastasis left.
tNormal value 100 pg/ml. formal value 500 pg/ml.
vipomas-in which circulating ic.T. is raised2 are thought to derive from cells of common embryological origin (i.e., the neural crest).10 In these non-thyroid tumours, the increase of ic.T. is small, whereas our values are within the range of those found in medullary carcinoma of the thyroid. A high concentration of ic.T. has been found in a pancreatic cholera tumour producing multiple hormones including v.I.p.u Moreover, in patient 2, a large concentration gradient of plasma-ic.T. was found between a peripheral vein (4-43 pg/ml, normal 008 pg/ml) and the splenic vein (20.27 pg/ml) simultaneously sampled during laparotomy. The non-parallel changes in circulating v.i.p. and ic.T. after resection of the pancreatic tumour cf patients 1 and 2 could result from differences between the original tumour and the residual metastases in the ratio of the synthesis rates of the two peptides. Extraction of c.T. from the tumours of patients 2 and 3 together with comparative structural studies of vipoma-associated plasma-c.T., normal thyroid c.T., and c.T. produced in medullary carcinoma of the thyroid are in progress. Clinique de Gastroentérologie, Hôpital Saint-Lazare, 75475 Paris, France U.113 Laboratoire de Biophysique, Faculté de Médecine Saint-Antoine, 75012 Paris
Royal Postgraduate Medical School, Hammersmith Hospital, London W12 0HS
J. C. RAMBAUD A. NISARD R. MODIGLIANI C. CALMETTE M. S. MOUKHTAR P. A. HILL H. BESTERMAN
PURPLE URINE BAGS
SiR,-Sometimes the plastic disposable urine bags used with collecting appliances by patients with urinary diversions turn purple. This is usually thought to be associated with infection but the discoloration has not been explained and the manufacturers have been unable to help. We have found that the pigment is readily extracted from the bag with benzene but is almost insoluble in alcohol or isopropanol. The resulting solution in benzene was the same purple colour as the bag. On spectroscopic analysis the visible region spectrum had a broad peak with aX maximum at 555 nm and a shoulder at 600 nm. The spectrum was identical with that of indigo dissolved in benzene. 10. Pearse, A. G. E., Polak, J. M. Med. Biol. 1974, 52, 3. 11. Schmitt, M. G. Jr, Soergel, K. H., Hensley, G. T., Chey, M. Y. Gastroenter-
ology, 1975, 69, 206.
