- Email: [email protected]
Screening relatives of coeliacs with the sugar absorption test
Abstracts
/Netherlands
Journal
only GSTlr (755 + 96) and GST+ (83 + 54) could be detected. As a result of the dietary regimen rectal GST-(Y and -rr levels were slightly increased at the end of the sprouts period by 30 and 15%, respectively. Glutathione content was uninfluenced by the dietary regimen. Conclusions: Consumption of glucosinolate-containing Brussels sprouts for 1 week results in increased rectal GST-(Y and +r isozyme levels. We hypothesize that these enhanced detoxification enzyme levels may partly explain the epidemiological association between a high intake of glucosinolates (cruciferous vegetables) and a decreased risk for colorectal cancer. Effect of intraduodenal gastrin-stimulated gastric
tkt acid
and non-absorbable secretion. T. v.d.
fat
on
Wijk, M.I.M. Maas, W.P.M. Hopman, M.B. Katan, J.B.M.J. Jansen. Department of Gastroenterology tal, Nijmegen, Netherlands.
& Hepatology,
University
Hospi-
Fat in the small intestine stimulates CCK and inhibits gastric acid secretion. It is not known whether intact or hydrolysed triglycerides are responsible for this enterogastrone effect. In the present study we have investigated whether digestible fat (frying oil) or non-digestible fat (sucrose polyester, SPE) containing fatty acids of comparable chain length inhibits gastrin-stimulated gastric acid secretion and stimulates CCK. Eight healthy volunteers (8 M; 23 +2 yrl were studied. Three experiments were performed in each volunteer in random order on different days. In all experiments gastrin-17 was infused for 180 min in a dose of 10 pmol/kg h. This dose results in plasma gastrin concentrations comparable to those after a meal. After 1 h the duodenum was perfused with equimolar amounts of fatty acids (62 mmol/h) of either digestible fat or sucrose polyester (SPE) for 90 min, at a perfusion rate comparable to the gastric emptying rate of fat after a meal. In the third experiment saline instead of fat was perfused. We measured gastric acid secretion by a phenol red recovery technique, and plasma gastrin and CCK concentrations by sensitive and specific radioimmunoassays. Infusion of gastrin resulted in plasma gastrin concentrations ranging from 46f4 to 55 &5 pM. Fat (+ 66.3 f 10.9 pM.60 mitt) but not SPE ( - 24.7 f 14.5 pM. 60 min) stimulated plasma CCK when compared with saline (- 5.4 f 13.9 pM .60 min; p = 0.0092). Gastrin-stimulated gastric acid secretion during saline perfusion was inhibited (p = O.OCkI4)by fat (9.6 + 2.7 mmol H+/h) but not by SPE (17.9 + 2.4 mmol H+/h) when compared with saline (21.Ok1.6 mmol H+/h). Conclu.rionr: Intraduodenal perfusion of fat hut not of SPE inhibits gastrin-stimulated gastric acid secretion. Fat but not SPE stimulates the release of CCK. Our data demonstrate that hydrolysis of fat is important for the enterogastrone effect of fat and for the release of CCK. Is circulating cholecystokinio involved in the inhibition gastrin-stimwlsted gastric acid secretion by intraduodenal long-chain trigiyccrides and medinm-chain triglycerides?
of
M.I.M. Maas, W.P.M. Hopman, M.B. Katan, J.B.M.J. Jansen.
of Medicine
47 (1995)
Al5
Al -A42
Department of Gastroenterology pital, Nijmegen, Netherlands.
& Hepatology,
Unit,ersity
Hos-
Fat in the small intestine stimulates cholecystokinin (CCKI and inhibits gastric acid secretion. It is not known whether the chain length of fatty acids is of importance for this effect of triglycerides. In the present study we have investigated the role of fatty acid chain length and the role of circulating CCK in the inhibition of gastrin-stimulated gastric acid secretion. Eight healthy volunteers (8 M; 23 f21 were studied. Four experiments were performed in random order on different days. In all experiments gastrin-17 was infused for 150 min in a dose of 10 PM/kg. h. This dose results in plasma gastrin concentrations comparable to those after a meal. During the last 90 min the duodenum was perfused with equimolar amounts of fatty acids (124 mmol/h) of either corn oil, mainly containing Cl8 fatty acids (LCI), or Ceres-MCT oil, mainly containing C8 and Cl0 fatty acids (MCT) or with saline at a perfusion rate comparable to the gastric emptying rate of fat (n = 8). In the fourth experiment CCK-33 was infused intravenously for the last 90 min of the experiment in amounts that resulted in plasma concentrations that were somewhat higher than during perfusion of LCT (n = 6). We measured gastric acid secretion by a phenol red recovery technique, and plasma gastrin and CCK concentrations by sensitive and specific radioimmunoassays. Infusion of gastrin resulted in plasma gastrin concentrations ranging from 46 + 4 to 55 rt 5 pM. LCT (+19.0*4.1 pM.30 min) but not MCI (-4.8k4.2 pM.30 min) stimulated plasma CCK when compared with saline (+ 1.3 + 5.3; p = 0.0022). During infusion of CCK, plasma concentrations of CCK increased by 108.8+ 10.5 pM.30 min. Gastrin-stimulated gastric acid output was inhibited by LCT by 74+ 6% (p = 0.0003 vs. control) and by MCT by 43+ 9% (p = 0.0426 versus control). LCT inhibited gastric acid output significantly more than MCI (p = 0.0499). CCK failed to inhibit gastrin-stimulated gastric acid output (18 i 6%) compared to saline (17 f 4%). Conclusions: Intraduodenal perfusion of both LCT and MCI inhibits gastrin-stimulated gastric acid secretion. LCT was significantly more effective than MCT. LCT but not MCT stimulated the release of CCK. However, infusion of CCK to plasma concentrations somewhat higher than during perfusion of LCT did not inhibit gastrin-stimulated gastric acid secretion. Screening
relatives
of coeliacs
with
tbe sugar
absorption
test.
F.M. van Gverbeek ‘, R.M. van Elburg ‘, J.J. Uil ,, C.J.J. Mulder *, H.S.A. Heymans ‘. ’ Beatrix Children i Hospital, University Hospital, Groningen; ogy, R&state Hospital, Arnhem,
’ Department Netherlands.
of Gastroenterol-
Subclinical and thus untreated coeliacs have an increased risk of developing serious, but avoidable, complications during life. Therefore, it seems reasonable to screen relatives of coeliacs, whose risk of developing coeliac disease (CD) is increased. Former research has shown that the sugar absorption test (SAT) is a sensitive marker for CD-related enteropathy. The aim of this prospective study was to evaluate the SAT as a screening parameter for CD. Serological IgA-anti-
Al6
Abstracts/Netherlands
Journal
gliadin antibodies (IgA-AGA) levels were also measured. An annual follow-up will take place to evaluate the SAT as a predictive tool for developing CD in the future. We would like to present the first-year screening results. In the SAT a solution of lactulose (L), mannitol (M) and sucrose was ingested and the L/M ratio was measured in 5-h urine. A ratio > 0.089 was considered aberrant. 126 first-degree relatives of biopsy-proven coeliacs and 84 controls were investigated. The SAT was performed and in 80 relatives IgA-AGA levels were also measured. Relatives with an aberrant L/M ratio or IgA-AGA level were biopsied. For statistical analysis the Mann-Whitney U-test was used. A p-value < 0.05 was considered significant. L/M ratios were significantly higher in the relatives group (mean 3t SEM: 0.092+0.006) than in the controls (0.039+ 0.003) (p < 0.001). In the relatives group 45/126 (36%) had an aberrant L/M ratio, in the controls 3/84 (4%). So far, 34 relatives with an aberrant L/M ratio have been biopsied: 5 had (subkotal villous atrophy and 8 infiltrative lesions (Marsh classification: l-2/4). In 2/80 relatives an elevated level of IgA-AGA was found: one had an aberrant L/M ratio and total villous atrophy in biopsy, the other had a normal L/M ratio and infiltrative lesions in biopsy. Three relatives with (subhotal villous atrophy were IgA-AGA-negative. Conclusions: Relatives of coeliacs have higher L/M ratios than controls as measured with the SAT. An aberrant L/M ratio may be related to constitutional factors, a low-grade immunological reaction to gluten or latent CD. IgA-AGA analyses were not useful in screening for CD. A follow-up study will be performed to investigate whether an aberrant SAT, without histological changes at first biopsy, is a predictive tool for the development of clinical CD in the future. Influence of medium-chain mononuclear phagocyte
and structured triglycerides on the system in postoperative patients. J.W.
Kruimel ‘, A.H.J. Naber i, J.W.M. Vehof ‘, E. Koenders ‘, J.A. van der Vliet 3, F.G.M. Buskens 3, F.H.M. Corstens 2, J.B.M.J. Jansen I. Departments of I Gastroenterology, 2 Nuclear Medicine imegen, Netherlands.
and
3 Surgery,
lJniversi@
Hospital,
Ni-
We studied the effects of parenteral infusion of structured triglycerides (STG) and an emulsion containing 50% rnediumchain and 50% long-chain triglycerides (MCT/LCT) on the mononuclear phagocyte system (MPS) in postoperative patients, measuring 99m-technetium-sulfur colloid (TSCJ clearance. TSC clearance is known to be reduced after administration of long-chain triglyceride emulsions. Thirteen wellnourished patients underwent elective implantation of an aortic prosthesis and were treated with total parenteral nutrition (TPN) for the first 5 days postoperatively. Amino acids were supplied in a dose of 0.2 g N/kg/day; $ of the non-protein energy was given as a lipid emulsion (STG or MCT/LCTI and 3 as carbohydrates. The lipid emulsion was infused in 6 h, daily; one group received the STG emulsion (n = 6) and the other group received the MCT/LCT emulsion (n = 7). TSC clearance was measured before the start of TPN and after 5 days of TPN. A bolus of 12-20 MBq TSC was injected
of Medicine
47 (1995)
Al -A42
intravenously. At 1.5, 3, 4.5, 6, 9, 12, 15, 30 and 60 min after injection, venous blood samples were drawn and radioactivity was measured. The two-tail probation test was used. Before the start of TPN, TSC clearance in the STG group was 192 f 66 ml/min (n = 6) and in the MCT/LCT group 202 + 34 ml/min (n = 7) (n.s.). Two patients did not complete the study. After 5 days of TPN, TSC clearance was 206+ 62 ml/min (n = 6) in the STG group and 183 + 94 ml/min (n = 5) (n.s.1 in the MCT/LCT group. The change in TSC clearance, during 5 days of TPN, was + 14 f 74 ml/min (n.s.) in the STG group and -20+57 ml/min (n.s.) in the MCT/LCT group. There was no significant difference between the change in TSC clearance in the STG group and the MCT/LCT group. Conclusions: In contrast to long-chain triglyceride emulsions, lipid emulsions containing medium-chain triglycerides do not suppress the functioning of the mononuclear phagocyte system. In this respect, there is no difference between the effects of a physical mixture of medium-chain and long-chain triglycerides and a structured triglyceride emulsion. Dietary man.
sulfate
might
inhibit
colonic
methane
production
in
A. Tangerman i, W. Wesseling *, M.B. Katan 2, F.M. Nagengast ‘. t Department of Gastroenterology, University Hospital, Nijmegen; lands.
2 Agricultural
University,
Wageningen,
Nether-
Hydrogen produced during colonic fermentation is consumed by methanogens to form methane or by sulphate-reducing bacteria (SRB) to form toxic hydrogen sulphide (H,S). Impairment of colonocyte nutrition by H,S and involvement of H,S in the pathogenesis of ulcerative colitis have been postulated. It is controversial whether methanogens outcompete SRB for H, consumption. Problems in quantitating sulphide in faeces have hampered research in this field. The aim of the present study was to establish the role of SRB in the human colon in relation to that of methanogens. In a cross-over study, 12 normal subjects with methanogenie activity (CH,-producers) and 8 subjects without (CH,non-producers) received a l-week diet rich (S-rich period) or poor (S-poor period) in dietary sulphate. Both periods were separated by a wash-out of 1 week. At the end of each period, faeces was sampled and faecal sulphide concentrations (free, bound and total) were measured by means of gas chromatography. No differences in total faecal sulphide levels were found between the S-rich (1.79+1.15 mmol/kg dry weight, meanf SD) and the S-poor period (1.96+ 1.61 mmol/kgI. The CH,-producers and non-producers had also similar sulphide levels. Nearly all sulphide was bound to the insoluble particulate faeces fraction. During the S-rich period a significant reduction in breath methane was observed in the CH,group. Of the 12 CH,-producers, 4 became non-producers, 3 showed a strong reduction and 5 remained unchanged. This reduction was accompanied by a reduced CH, production in the corresponding faecal samples during in vitro faecal incubation experiments. In vitro faecal incubation with 20 mM NasSO, showed a huge increase in free sulphide concentrations, reaching levels of 30 mmol/kg dry weight, in both the S-rich and S-poor samples. This increase was even more
/Netherlands
Journal
only GSTlr (755 + 96) and GST+ (83 + 54) could be detected. As a result of the dietary regimen rectal GST-(Y and -rr levels were slightly increased at the end of the sprouts period by 30 and 15%, respectively. Glutathione content was uninfluenced by the dietary regimen. Conclusions: Consumption of glucosinolate-containing Brussels sprouts for 1 week results in increased rectal GST-(Y and +r isozyme levels. We hypothesize that these enhanced detoxification enzyme levels may partly explain the epidemiological association between a high intake of glucosinolates (cruciferous vegetables) and a decreased risk for colorectal cancer. Effect of intraduodenal gastrin-stimulated gastric
tkt acid
and non-absorbable secretion. T. v.d.
fat
on
Wijk, M.I.M. Maas, W.P.M. Hopman, M.B. Katan, J.B.M.J. Jansen. Department of Gastroenterology tal, Nijmegen, Netherlands.
& Hepatology,
University
Hospi-
Fat in the small intestine stimulates CCK and inhibits gastric acid secretion. It is not known whether intact or hydrolysed triglycerides are responsible for this enterogastrone effect. In the present study we have investigated whether digestible fat (frying oil) or non-digestible fat (sucrose polyester, SPE) containing fatty acids of comparable chain length inhibits gastrin-stimulated gastric acid secretion and stimulates CCK. Eight healthy volunteers (8 M; 23 +2 yrl were studied. Three experiments were performed in each volunteer in random order on different days. In all experiments gastrin-17 was infused for 180 min in a dose of 10 pmol/kg h. This dose results in plasma gastrin concentrations comparable to those after a meal. After 1 h the duodenum was perfused with equimolar amounts of fatty acids (62 mmol/h) of either digestible fat or sucrose polyester (SPE) for 90 min, at a perfusion rate comparable to the gastric emptying rate of fat after a meal. In the third experiment saline instead of fat was perfused. We measured gastric acid secretion by a phenol red recovery technique, and plasma gastrin and CCK concentrations by sensitive and specific radioimmunoassays. Infusion of gastrin resulted in plasma gastrin concentrations ranging from 46f4 to 55 &5 pM. Fat (+ 66.3 f 10.9 pM.60 mitt) but not SPE ( - 24.7 f 14.5 pM. 60 min) stimulated plasma CCK when compared with saline (- 5.4 f 13.9 pM .60 min; p = 0.0092). Gastrin-stimulated gastric acid secretion during saline perfusion was inhibited (p = O.OCkI4)by fat (9.6 + 2.7 mmol H+/h) but not by SPE (17.9 + 2.4 mmol H+/h) when compared with saline (21.Ok1.6 mmol H+/h). Conclu.rionr: Intraduodenal perfusion of fat hut not of SPE inhibits gastrin-stimulated gastric acid secretion. Fat but not SPE stimulates the release of CCK. Our data demonstrate that hydrolysis of fat is important for the enterogastrone effect of fat and for the release of CCK. Is circulating cholecystokinio involved in the inhibition gastrin-stimwlsted gastric acid secretion by intraduodenal long-chain trigiyccrides and medinm-chain triglycerides?
of
M.I.M. Maas, W.P.M. Hopman, M.B. Katan, J.B.M.J. Jansen.
of Medicine
47 (1995)
Al5
Al -A42
Department of Gastroenterology pital, Nijmegen, Netherlands.
& Hepatology,
Unit,ersity
Hos-
Fat in the small intestine stimulates cholecystokinin (CCKI and inhibits gastric acid secretion. It is not known whether the chain length of fatty acids is of importance for this effect of triglycerides. In the present study we have investigated the role of fatty acid chain length and the role of circulating CCK in the inhibition of gastrin-stimulated gastric acid secretion. Eight healthy volunteers (8 M; 23 f21 were studied. Four experiments were performed in random order on different days. In all experiments gastrin-17 was infused for 150 min in a dose of 10 PM/kg. h. This dose results in plasma gastrin concentrations comparable to those after a meal. During the last 90 min the duodenum was perfused with equimolar amounts of fatty acids (124 mmol/h) of either corn oil, mainly containing Cl8 fatty acids (LCI), or Ceres-MCT oil, mainly containing C8 and Cl0 fatty acids (MCT) or with saline at a perfusion rate comparable to the gastric emptying rate of fat (n = 8). In the fourth experiment CCK-33 was infused intravenously for the last 90 min of the experiment in amounts that resulted in plasma concentrations that were somewhat higher than during perfusion of LCT (n = 6). We measured gastric acid secretion by a phenol red recovery technique, and plasma gastrin and CCK concentrations by sensitive and specific radioimmunoassays. Infusion of gastrin resulted in plasma gastrin concentrations ranging from 46 + 4 to 55 rt 5 pM. LCT (+19.0*4.1 pM.30 min) but not MCI (-4.8k4.2 pM.30 min) stimulated plasma CCK when compared with saline (+ 1.3 + 5.3; p = 0.0022). During infusion of CCK, plasma concentrations of CCK increased by 108.8+ 10.5 pM.30 min. Gastrin-stimulated gastric acid output was inhibited by LCT by 74+ 6% (p = 0.0003 vs. control) and by MCT by 43+ 9% (p = 0.0426 versus control). LCT inhibited gastric acid output significantly more than MCI (p = 0.0499). CCK failed to inhibit gastrin-stimulated gastric acid output (18 i 6%) compared to saline (17 f 4%). Conclusions: Intraduodenal perfusion of both LCT and MCI inhibits gastrin-stimulated gastric acid secretion. LCT was significantly more effective than MCT. LCT but not MCT stimulated the release of CCK. However, infusion of CCK to plasma concentrations somewhat higher than during perfusion of LCT did not inhibit gastrin-stimulated gastric acid secretion. Screening
relatives
of coeliacs
with
tbe sugar
absorption
test.
F.M. van Gverbeek ‘, R.M. van Elburg ‘, J.J. Uil ,, C.J.J. Mulder *, H.S.A. Heymans ‘. ’ Beatrix Children i Hospital, University Hospital, Groningen; ogy, R&state Hospital, Arnhem,
’ Department Netherlands.
of Gastroenterol-
Subclinical and thus untreated coeliacs have an increased risk of developing serious, but avoidable, complications during life. Therefore, it seems reasonable to screen relatives of coeliacs, whose risk of developing coeliac disease (CD) is increased. Former research has shown that the sugar absorption test (SAT) is a sensitive marker for CD-related enteropathy. The aim of this prospective study was to evaluate the SAT as a screening parameter for CD. Serological IgA-anti-
Al6
Abstracts/Netherlands
Journal
gliadin antibodies (IgA-AGA) levels were also measured. An annual follow-up will take place to evaluate the SAT as a predictive tool for developing CD in the future. We would like to present the first-year screening results. In the SAT a solution of lactulose (L), mannitol (M) and sucrose was ingested and the L/M ratio was measured in 5-h urine. A ratio > 0.089 was considered aberrant. 126 first-degree relatives of biopsy-proven coeliacs and 84 controls were investigated. The SAT was performed and in 80 relatives IgA-AGA levels were also measured. Relatives with an aberrant L/M ratio or IgA-AGA level were biopsied. For statistical analysis the Mann-Whitney U-test was used. A p-value < 0.05 was considered significant. L/M ratios were significantly higher in the relatives group (mean 3t SEM: 0.092+0.006) than in the controls (0.039+ 0.003) (p < 0.001). In the relatives group 45/126 (36%) had an aberrant L/M ratio, in the controls 3/84 (4%). So far, 34 relatives with an aberrant L/M ratio have been biopsied: 5 had (subkotal villous atrophy and 8 infiltrative lesions (Marsh classification: l-2/4). In 2/80 relatives an elevated level of IgA-AGA was found: one had an aberrant L/M ratio and total villous atrophy in biopsy, the other had a normal L/M ratio and infiltrative lesions in biopsy. Three relatives with (subhotal villous atrophy were IgA-AGA-negative. Conclusions: Relatives of coeliacs have higher L/M ratios than controls as measured with the SAT. An aberrant L/M ratio may be related to constitutional factors, a low-grade immunological reaction to gluten or latent CD. IgA-AGA analyses were not useful in screening for CD. A follow-up study will be performed to investigate whether an aberrant SAT, without histological changes at first biopsy, is a predictive tool for the development of clinical CD in the future. Influence of medium-chain mononuclear phagocyte
and structured triglycerides on the system in postoperative patients. J.W.
Kruimel ‘, A.H.J. Naber i, J.W.M. Vehof ‘, E. Koenders ‘, J.A. van der Vliet 3, F.G.M. Buskens 3, F.H.M. Corstens 2, J.B.M.J. Jansen I. Departments of I Gastroenterology, 2 Nuclear Medicine imegen, Netherlands.
and
3 Surgery,
lJniversi@
Hospital,
Ni-
We studied the effects of parenteral infusion of structured triglycerides (STG) and an emulsion containing 50% rnediumchain and 50% long-chain triglycerides (MCT/LCT) on the mononuclear phagocyte system (MPS) in postoperative patients, measuring 99m-technetium-sulfur colloid (TSCJ clearance. TSC clearance is known to be reduced after administration of long-chain triglyceride emulsions. Thirteen wellnourished patients underwent elective implantation of an aortic prosthesis and were treated with total parenteral nutrition (TPN) for the first 5 days postoperatively. Amino acids were supplied in a dose of 0.2 g N/kg/day; $ of the non-protein energy was given as a lipid emulsion (STG or MCT/LCTI and 3 as carbohydrates. The lipid emulsion was infused in 6 h, daily; one group received the STG emulsion (n = 6) and the other group received the MCT/LCT emulsion (n = 7). TSC clearance was measured before the start of TPN and after 5 days of TPN. A bolus of 12-20 MBq TSC was injected
of Medicine
47 (1995)
Al -A42
intravenously. At 1.5, 3, 4.5, 6, 9, 12, 15, 30 and 60 min after injection, venous blood samples were drawn and radioactivity was measured. The two-tail probation test was used. Before the start of TPN, TSC clearance in the STG group was 192 f 66 ml/min (n = 6) and in the MCT/LCT group 202 + 34 ml/min (n = 7) (n.s.). Two patients did not complete the study. After 5 days of TPN, TSC clearance was 206+ 62 ml/min (n = 6) in the STG group and 183 + 94 ml/min (n = 5) (n.s.1 in the MCT/LCT group. The change in TSC clearance, during 5 days of TPN, was + 14 f 74 ml/min (n.s.) in the STG group and -20+57 ml/min (n.s.) in the MCT/LCT group. There was no significant difference between the change in TSC clearance in the STG group and the MCT/LCT group. Conclusions: In contrast to long-chain triglyceride emulsions, lipid emulsions containing medium-chain triglycerides do not suppress the functioning of the mononuclear phagocyte system. In this respect, there is no difference between the effects of a physical mixture of medium-chain and long-chain triglycerides and a structured triglyceride emulsion. Dietary man.
sulfate
might
inhibit
colonic
methane
production
in
A. Tangerman i, W. Wesseling *, M.B. Katan 2, F.M. Nagengast ‘. t Department of Gastroenterology, University Hospital, Nijmegen; lands.
2 Agricultural
University,
Wageningen,
Nether-
Hydrogen produced during colonic fermentation is consumed by methanogens to form methane or by sulphate-reducing bacteria (SRB) to form toxic hydrogen sulphide (H,S). Impairment of colonocyte nutrition by H,S and involvement of H,S in the pathogenesis of ulcerative colitis have been postulated. It is controversial whether methanogens outcompete SRB for H, consumption. Problems in quantitating sulphide in faeces have hampered research in this field. The aim of the present study was to establish the role of SRB in the human colon in relation to that of methanogens. In a cross-over study, 12 normal subjects with methanogenie activity (CH,-producers) and 8 subjects without (CH,non-producers) received a l-week diet rich (S-rich period) or poor (S-poor period) in dietary sulphate. Both periods were separated by a wash-out of 1 week. At the end of each period, faeces was sampled and faecal sulphide concentrations (free, bound and total) were measured by means of gas chromatography. No differences in total faecal sulphide levels were found between the S-rich (1.79+1.15 mmol/kg dry weight, meanf SD) and the S-poor period (1.96+ 1.61 mmol/kgI. The CH,-producers and non-producers had also similar sulphide levels. Nearly all sulphide was bound to the insoluble particulate faeces fraction. During the S-rich period a significant reduction in breath methane was observed in the CH,group. Of the 12 CH,-producers, 4 became non-producers, 3 showed a strong reduction and 5 remained unchanged. This reduction was accompanied by a reduced CH, production in the corresponding faecal samples during in vitro faecal incubation experiments. In vitro faecal incubation with 20 mM NasSO, showed a huge increase in free sulphide concentrations, reaching levels of 30 mmol/kg dry weight, in both the S-rich and S-poor samples. This increase was even more