- Email: [email protected]
Fecal fat concentration: Determinants and diagnostic value
CORRESPONDENCE
July 1985
Fecal Fat Concentration: Diagnostic Value
Determinants
and
Dear Sir: Recently, Bo-Linn and Fordtran presented data indicating that fecal fat concentration (fecal fat weight/total fecal weight x 100) was higher in patients with pancreatic insufficiency than in patients with other causes of steatorrhea. They suggested that the measurement of fecal fat concentration (FFC] might provide information of diagnostic value (11. This report caused us to exhume some data on fecal composition collected and collated some 15 years ago at the Mayo Clinic. The stimulus to these studies was the recognition of the syndrome of bile acid diarrhea (z), which had led us to consider whether colonic bile acids were the major determinant of fecal weight even in healthy individuals. If this hypothesis is true, fecal weight should be lower in patients with decreased bile acid excretion, such as should occur in cholestatic conditions. To test this hypothesis, we collated data on fecal composition from patients with hepatobiliary disease using analyses performed by the Mayo Clinic Laboratories during the preceding 3 years. We found that our hypothesis was not correct, as patients with hepatobiliary disease and presumed decreased bile acid secretion into the intestine had increased fecal weight. (Data from some individual patients are given in Table 1.) The majority of these patients had steatorrhea; and thus, to our astonishment, it seemed that increased fecal fat per se caused increased fecal water. An explanation was obtained a few years later when it was found in clinical studies that dietary fat contributes to fecal weight in patients with steatorrhea caused by severe bile acid malabsorption (3). Later, Ammon and Phillips (4) demonstrated directly the secretory action of long-chain fatty acids in the human colon using a perfusion technique. In the course of this work, we decided it might be of interest to take a look at fecal composition in all patients with digestive disease. Accordingly, we collated data on fecal composition for all fecal analyses (about 1600 samples!). At the Mayo Clinic, fecal fat measurements are made on 3- to 6-day collections during which the patient ingests a 100-g fat/day diet (5). The fecal collection is weighed; one aliquot is combusted, the weight of the residue representing total solids. Fecal fat is determined by saponification, acidification, extraction into petroleum hydrocarbon, and weighing of the residue after evaporation of the solvent. Thus, the percentages of water and of fat can be obtained; one can then
Table
1. Fecal
Weight,
Fecal
Hepatobiliary
Fat,
and Fecal
Composition
231
calculate the percentage of nonfat solids (NFS). As there are three values that add up to lOO%, the results are easily plotted on triangular coordinates. One can also show the weight of the stool by plotting data in the form of a prism, with the altitude representing fecal weight. Selected results are shown in Table 2. (Unfortunately, data for daily fecal fat output were not collated, as this was not the purpose of the study. The original data sheets were discarded some years ago.) In their article, Bo-Linn and Fordtran suggest that patients with steatorrhea due to nonpancreatic causes should have increased fecal water because of poor absorption of fluid as well as the osmotic and secretory effects of unabsorbed food, especially fatty acids; in contrast, in patients with pancreatic insufficiency in whom fat malabsorption is the major pathophysiologic defect, the secretory stimulus caused by fat passing into the colon should be less, because presumably it would be in the form of insoluble higher glycerides. The equation describing FFC may be written as follows: FFC (%) Fecal
= Fecal
water
weight
+ fecal
fat weight fat weight
+ fecal NFS weight x 100,
where FFC is the fecal fat concentration and NFS is nonfat solids. The first question is whether fat malabsorption in patients with pancreatic insufficiency should influence fecal weight in any way other than by the increased quantity of fat. Some years ago, in an important abstract, Bliss and Small (6) showed that in some patients with pancreatic insufficiency, there is hydrolysis of malabsorbed fat in the colon, presumably by bacterial lipases, although possibly continuing lipolysis by lingual and gastric lipases might also contribute. Thus, FFC might not be increased in those patients with pancreatic insufficiency if the malabsorbed glycerides were hydrolyzed to fatty acids which induced colonic secretion of water. Another component of feces is the NFS portion, which is in the denominator of the FFC equation. Patients with pancreatic insufficiency may also have protein and carbohydrate malabsorption, and if the mass of the malabsorbed nutrients was appreciable, FFC would decrease. (Note values below 10% in patients with total pancreatectomy.) It seems likely, however, that these malabsorbed
in Individual
Patients
With Hepatitis
or Obstructive
Obstruction’ Fecal
Name
Diagnosis
Weight
Fat
(g/day)
(g/day1
% Fat
composition
% Nonfat solids
% Water
Hepatitis Sm Me Au Fo co Hepatobiliary Bo MO De Ka " Data based
Acute Acute Acute Acute Chronic
hepatitis hepatitis hepatitis hepatitis hepatitis
90 124 194 167 230
7 12
8
20 21 13
9 10 13 6
22 13 11 10 11
70 78 79 78 83
400 203 204
56 36 28
14 18 14
4 9 11
82 73 75
294
38
13
9
78
obstruction Carcinoma of common duct Carcinoma of common duct Common duct stone with biliary obstruction Biliary cirrhosis on 3- to 6-day
fecal collections
for all patients.
232
Table
CORRESPONDENCE
2.
GASTROENTEROLOGY
Fecal Weight and Fecal Composition
in Patients
n Pancreatic disease Chronic pancreatitis Cystic fibrosis Status postpancreatomy (Whipple procedure) Hepatobiliary disease Biliary cirrhosis Postnecrotic cirrhosis Gastric surgery Vagotomy and gastroenterostomy Vagotomy and pyloroplasty Billroth I Billroth II Ileal dysfunction (presumed bile acid malabsorption) Ileal resection Regional enteritis Regional enteritis with resection Short bowel syndrome Mucosal disease causing fat malabsorption Sprue Diabetic enteropathy Diabetic retinopathy Diabetes without retinopathy Colonic disease Ulcerative colitis Miscellaneous conditions Acute gastroenteritis No gastrointestinal disease (but includes constipation] Normal a Data based
Mean
2 SD
(g/day] Range
89, No. 1
With and Without Digestive Diseasea Fecal
Weight
Vol.
% Fat Mean
2 SD
composition
% Nonfat Range
Mean
2 SD
solids Range
% Water Mean
2 SD
Range
276 2 277 252 -c 262 182 C 113
16-1429 lo-724 31-435
8 * 6.1 13 * 7.2 13 k 6.1
l-24 7-26 4-31
15 iz 7.1 17 2 3.1 14 _f 4.1
14-22 8-21
77 '- 9.1 70 _t 7.2 73 2 6.1
56-77 59-83
(71
197 4 133 147 t 86
60-434 56-320
10 2 7.2 13 * 9.3
1-21 l-27
12 2 4.1 13 rt 5.2
6-18 7-21
78 2 9.3 74 2 10.4
62-91 64-92
(221
286 + 266
55-1162
B&l
3-19
12 2 1
b
80 2 1
b
(11)
266 * 361
39-1223
4+1
2-8
12 +- 2
b
83 k 3
b
(9) (72)
105 t 68 218 2 216
23-186 21-1260
622 821
3-16 1-18
16 2 1 15 2 1
b b
77 t 2 78 ? 1
77-86 b
(15) (521 (40)
400 k 226 397 t 247 331 2 268
154-981 34-1094 21-1169
4 -r-3.1 3 t 3.0 4 2 3.0
o-11 1-18 1-12
10 t 6.2 9 2 4.1 12 k 7.1
O-27 3-25 5-41
86 ? 7.2 88 2 6.1 84 + 9.1
71-100 68-95 52-94
132-4621
5 ? 3.1
1-9
8 + 3.1
5-12
87 ? 5.2
82-94
(611
(8) (20)
(11)
(71 1019 2 1608
4-39
55-95
(631
255 + 296
26-1988
7 + 4.1
1-16
13 2 6.1
3-27
80 2 8.1
64-95
(181 (22)
219 A 174 174 2 97
16-623 8-384
4 + 4.1 4 2 5.1
o-15 O-20
14 + 11.2 15 k 8.2
5-39 l-33
82 + 13.3 82 2 11.2
60-95 36-99
(25)
347 + 383
14-1516
2 2 2.0
O-8
10 2 5.1
3-27
88 k 6.1
72-96
(42)
202 k 217
36-610
421
80 +- 3
72-95
79 -e 9.1
46-94
(108)
on 3- to B-day stool
120 t 92 collection.
9-488
4 + 3.0
b
O-17
16 k 3
17 2 7.1
b
6-53
b Data not available.
nutrients undergo a complex fate in the colon. They may be digested by bacterial enzymes and the products absorbed; this would increase FFC. Alternatively, either the malabsorbed nutrients or their digestion products by their osmotic activity might diminish colonic water absorption. Accordingly, the denominator of the equation would not change and FFC would remain low. Thus, increased FFC should reflect fat malabsorption in the absence of a marked increase in fecal water or NFS. If the malabsorbed fat was hydrolyzed to fatty acids during colonic transit and these induced water secretion, or if malabsorbed protein or carbohydrate induced water secretion, FFC would decrease. Accordingly, in patients with pancreatic insufficiency, increased FFC should be specific, but not sensitive. The data in Table 2 confirm this, but note that FFC values exceeding 10% were also observed in patients with gastric surgery, bile acid malabsorption, diabetic enteropathy, and sprue. Bo-Linn and Fordtran also suggest that FFC should be increased in patients with cholestasis and bacterial overgrowth syndromes.
Our data indicate that their surmise is correct. Fecal fat concentration is markedly increased in cholestatic conditions. Finally, FFC may also be increased in healthy subjects with severe constipation. In most individuals, feces are about 80% water. In individuals with constipation, fecal water may fall to as low as 46%, and FFC will show the expected reciprocal increase. Other types of malabsorption should manifest increases in both the numerator and denominator [if steatorrhea is present), or in the denominator only (if steatorrhea is not present). For example, in patients with bacterial overgrowth or with greatly increased inflammatory exudates, the NFS may be increased. In patients with simple diarrhea of colonic origin, fecal water alone will be increased. To summarize, our data of some years ago confirm, extend, and may help to clarify the observations of Bo-Linn and Fordtran. Our data indicate that increased FFC is neither very specific nor sensitive (as values
July
CORRESPONDENCE
1985
is easily detectable
by histochemical staining of stool (7,8). To establish the diagnosis of mild pancreatic insufficiency, we SUSpect that it is going to be better to carry out a Lundh test meal and measure enzyme concentrations in the jejunal aspirates (91, or to perform the usual cholecystokinin-stimulation test (10). Several new noninvasive tests for assessment of pancreatic exocrine function have recently been reported (ll-131, and it will be of interest to compare these tests with not only results from invasive procedures, but also with FFC measurement in patients with varying degrees of pancreatic exocrine hypofunction. In the meantime, if fecal fat measurements are made to quantitate the degree of steatorrhea in a patient with malabsorption (who does not have hepatobiliary disease or previous gastrointestinal surgery), the astute clinician who observes an elevated FFC (>lO%) in the lab report may immediately make a presumptive diagnosis of pancreatic insufficiency with some confidence.
ALAN F. HOFMANN,
M.D. Division of Gastroenterology Department of Medicine University of California, San 225 Dickinson Street San Diego, California 92103
2.
3.
4.
5.
6. 7. 8.
Dear Sir: It does not surprise us that operations and medication designed to reduce gastric activity and thus hormonal stimulation of the pancreas are not very successful in relieving the pain of chronic pancreatitis. It is evident now that even during prolonged fasting the gland is spontaneously active at 100-min intervals. In dogs we obtain half-maximal protein secretion and about one-eighth maximal juice volume at spontaneous peak activity. Spontaneous peaking is completely abolished by ganglion blocking agents (1,2) and our evidence is that cholecystokinin and secretin release are abolished also (3,4). Might not a long-acting blocker, like pentolinium tartrate, be worth a trial in the disease? The argument that these agents cause hypotension is not really relevant as the orthostatic hypotension that can result is of little consequence to patients in bed. Creighton
Diego
Bo-Linn GW, Fordtran JS. Fecal fat concentration in patients with steatorrhea. Gastroenterology 1984;87:319-22. Hofmann AF. The syndrome of ileal disease and the broken enterohepatic circulation: cholerheic enteropathy. Gastroenterology 1967:52:752-7. Hofmann AF, Poley JR. Role of bile acid malabsorption in pathogenesis of diarrhea and steatorrhea in patients with ileal resection. I. Response to cholestyramine or replacement of dietary long chain triglyceride by medium chain triglyceride. Gastroenterology 1972;62:1191-9. Ammon HV, Phillips SF. Inhibition of colonic water and electrolyte secretion by fatty acids in man. Gastroenterology 1973;65:744-9. Dornberger GR, Comfort MW, Wollaeger EE, Power MH. Total fecal solids, fat and nitrogen: study of patients with chronic relapsing pancreatitis. Gastroenterology 1948;11:691-700. Bliss CM, Small DM. A comparison of ileal and fecal lipid in pancreatic steatorrhea (abstr). Gastroenterology 1970;58:928. Luk CD. Screening for steatorrhea (letter). Gastroenterology 1979;77:205-6. Newcomer AD, Hofmann AF, DiMagno EP, Thomas PJ. Carl-
son CL. Triolein breath test: a sensitive and specific test for fat malabsorption. Gastroenterology 1979;76:6-13. 9. Braganza JM. Herman K, Hine P, Kay G, Sandle GI. Pancreatic enzymes in human duodenal juice-a comparison of responses in secretin pancreocymin and Lundh Borgstrom tests. Gut 1978;19:358-66. 10.
Pain in Chronic Pancreatitis
D. F. MAGEE, M.D., Ph.D
JAMES W. MANIER Lovelace Medical Center Albuquerque, New Mexico 1.
233
DiMagno EP, Go VLW, Summerskill WHJ. Relations between pancreatic enzyme outputs and malabsorption in severe pancreatic insufficiency. N Engl J Med 1973;288:813-5. 11. Braganza JM, Kay GH, Tetlow VA, Herman KJ. Observations on the BT PABAIl%-PABA tubeless test of pancreatic function. Clin Chim Acta 1983:130:339-47. 12. Lankisch PG, Schreiber A, Otto J. Pancreolauryl test. Evaluation of a tubeless pancreatic function test in comparison with other indirect and direct tests for exocrine pancreatic function. Dig Dis Sci 1983;28:490-3. 13. Cole S, Rossi S, Stern A, Hofmann AF, Mundlos S. A cholesterol octanoate breath test for pancreatic exocrine function: feasibility studies (abstr). Am J Gastroenterol (in press).
University
School of Medicine 2500 California Street Omaha, Nebraska 68178 S. NARUSE. M.D. National Institute
for Physiological
Sciences
Department of Molecular Physiology Laboratory of Cellular Metabolism Myodaiji, Okazaki, 444 Japan Magee DF, Naruse S. Neural control of periodic secretion of the pancreas and the stomach in fasting dogs. J Physiol 1983; 344:153-60. Magee DF, Naruse S. Characteristics of secretin stimulated pancreatic secretion in dogs. J Physiol 1983;346:115P. Hong SS, Magee DF, Crewdson F. The physiological regulation of gallbladder evacuation. Gastroenterology 1956;30:625-30. Hong SS, Magee DF. Pharmacological studies on the regulation of pancreatic secretion in pigs. Ann Surg 1970;172:41-8.
Diagnosis of IBS Dear Sir: We enjoyed reading the excellent editorial by Drossman (1) that summarized the difficulties encountered in the diagnostic workup and classification of patients suspected to suffer from irritable bowel syndrome (IBS). It was mentioned that the determination of whether a patient has either IBS or organic disease cannot always be made in clinical practice. We would like to add some further information. The protocol of our study (2) was designed to develop a weighted score for the diagnosis of IBS and to test the diagnostic accuracy of this scoring system in two patient groups to be defined as precisely as possible. Thus, we created the scoring system using the data of patients with symptoms of IBS but without any recognizable organic disease and of other patients also with symptoms compatible with IBS, but with some organic disease diagnosed. Patients with organic disease but with the additional diagnosis of IBS were excluded from all calculations. In this group, IBS was diagnosed because the complaints seemed not to be fully explained by the organic disease and were typical of IBS. This may appear arbitrary because the symptoms complained about by patients classified into the group “organic disease” may also not necessarily be related to the underlying organic disease. However, in the absence of a “gold” standard for the diagnosis of IBS, as discussed in the editorial, arbitrary decisions cannot be eliminated completely.
July 1985
Fecal Fat Concentration: Diagnostic Value
Determinants
and
Dear Sir: Recently, Bo-Linn and Fordtran presented data indicating that fecal fat concentration (fecal fat weight/total fecal weight x 100) was higher in patients with pancreatic insufficiency than in patients with other causes of steatorrhea. They suggested that the measurement of fecal fat concentration (FFC] might provide information of diagnostic value (11. This report caused us to exhume some data on fecal composition collected and collated some 15 years ago at the Mayo Clinic. The stimulus to these studies was the recognition of the syndrome of bile acid diarrhea (z), which had led us to consider whether colonic bile acids were the major determinant of fecal weight even in healthy individuals. If this hypothesis is true, fecal weight should be lower in patients with decreased bile acid excretion, such as should occur in cholestatic conditions. To test this hypothesis, we collated data on fecal composition from patients with hepatobiliary disease using analyses performed by the Mayo Clinic Laboratories during the preceding 3 years. We found that our hypothesis was not correct, as patients with hepatobiliary disease and presumed decreased bile acid secretion into the intestine had increased fecal weight. (Data from some individual patients are given in Table 1.) The majority of these patients had steatorrhea; and thus, to our astonishment, it seemed that increased fecal fat per se caused increased fecal water. An explanation was obtained a few years later when it was found in clinical studies that dietary fat contributes to fecal weight in patients with steatorrhea caused by severe bile acid malabsorption (3). Later, Ammon and Phillips (4) demonstrated directly the secretory action of long-chain fatty acids in the human colon using a perfusion technique. In the course of this work, we decided it might be of interest to take a look at fecal composition in all patients with digestive disease. Accordingly, we collated data on fecal composition for all fecal analyses (about 1600 samples!). At the Mayo Clinic, fecal fat measurements are made on 3- to 6-day collections during which the patient ingests a 100-g fat/day diet (5). The fecal collection is weighed; one aliquot is combusted, the weight of the residue representing total solids. Fecal fat is determined by saponification, acidification, extraction into petroleum hydrocarbon, and weighing of the residue after evaporation of the solvent. Thus, the percentages of water and of fat can be obtained; one can then
Table
1. Fecal
Weight,
Fecal
Hepatobiliary
Fat,
and Fecal
Composition
231
calculate the percentage of nonfat solids (NFS). As there are three values that add up to lOO%, the results are easily plotted on triangular coordinates. One can also show the weight of the stool by plotting data in the form of a prism, with the altitude representing fecal weight. Selected results are shown in Table 2. (Unfortunately, data for daily fecal fat output were not collated, as this was not the purpose of the study. The original data sheets were discarded some years ago.) In their article, Bo-Linn and Fordtran suggest that patients with steatorrhea due to nonpancreatic causes should have increased fecal water because of poor absorption of fluid as well as the osmotic and secretory effects of unabsorbed food, especially fatty acids; in contrast, in patients with pancreatic insufficiency in whom fat malabsorption is the major pathophysiologic defect, the secretory stimulus caused by fat passing into the colon should be less, because presumably it would be in the form of insoluble higher glycerides. The equation describing FFC may be written as follows: FFC (%) Fecal
= Fecal
water
weight
+ fecal
fat weight fat weight
+ fecal NFS weight x 100,
where FFC is the fecal fat concentration and NFS is nonfat solids. The first question is whether fat malabsorption in patients with pancreatic insufficiency should influence fecal weight in any way other than by the increased quantity of fat. Some years ago, in an important abstract, Bliss and Small (6) showed that in some patients with pancreatic insufficiency, there is hydrolysis of malabsorbed fat in the colon, presumably by bacterial lipases, although possibly continuing lipolysis by lingual and gastric lipases might also contribute. Thus, FFC might not be increased in those patients with pancreatic insufficiency if the malabsorbed glycerides were hydrolyzed to fatty acids which induced colonic secretion of water. Another component of feces is the NFS portion, which is in the denominator of the FFC equation. Patients with pancreatic insufficiency may also have protein and carbohydrate malabsorption, and if the mass of the malabsorbed nutrients was appreciable, FFC would decrease. (Note values below 10% in patients with total pancreatectomy.) It seems likely, however, that these malabsorbed
in Individual
Patients
With Hepatitis
or Obstructive
Obstruction’ Fecal
Name
Diagnosis
Weight
Fat
(g/day)
(g/day1
% Fat
composition
% Nonfat solids
% Water
Hepatitis Sm Me Au Fo co Hepatobiliary Bo MO De Ka " Data based
Acute Acute Acute Acute Chronic
hepatitis hepatitis hepatitis hepatitis hepatitis
90 124 194 167 230
7 12
8
20 21 13
9 10 13 6
22 13 11 10 11
70 78 79 78 83
400 203 204
56 36 28
14 18 14
4 9 11
82 73 75
294
38
13
9
78
obstruction Carcinoma of common duct Carcinoma of common duct Common duct stone with biliary obstruction Biliary cirrhosis on 3- to 6-day
fecal collections
for all patients.
232
Table
CORRESPONDENCE
2.
GASTROENTEROLOGY
Fecal Weight and Fecal Composition
in Patients
n Pancreatic disease Chronic pancreatitis Cystic fibrosis Status postpancreatomy (Whipple procedure) Hepatobiliary disease Biliary cirrhosis Postnecrotic cirrhosis Gastric surgery Vagotomy and gastroenterostomy Vagotomy and pyloroplasty Billroth I Billroth II Ileal dysfunction (presumed bile acid malabsorption) Ileal resection Regional enteritis Regional enteritis with resection Short bowel syndrome Mucosal disease causing fat malabsorption Sprue Diabetic enteropathy Diabetic retinopathy Diabetes without retinopathy Colonic disease Ulcerative colitis Miscellaneous conditions Acute gastroenteritis No gastrointestinal disease (but includes constipation] Normal a Data based
Mean
2 SD
(g/day] Range
89, No. 1
With and Without Digestive Diseasea Fecal
Weight
Vol.
% Fat Mean
2 SD
composition
% Nonfat Range
Mean
2 SD
solids Range
% Water Mean
2 SD
Range
276 2 277 252 -c 262 182 C 113
16-1429 lo-724 31-435
8 * 6.1 13 * 7.2 13 k 6.1
l-24 7-26 4-31
15 iz 7.1 17 2 3.1 14 _f 4.1
14-22 8-21
77 '- 9.1 70 _t 7.2 73 2 6.1
56-77 59-83
(71
197 4 133 147 t 86
60-434 56-320
10 2 7.2 13 * 9.3
1-21 l-27
12 2 4.1 13 rt 5.2
6-18 7-21
78 2 9.3 74 2 10.4
62-91 64-92
(221
286 + 266
55-1162
B&l
3-19
12 2 1
b
80 2 1
b
(11)
266 * 361
39-1223
4+1
2-8
12 +- 2
b
83 k 3
b
(9) (72)
105 t 68 218 2 216
23-186 21-1260
622 821
3-16 1-18
16 2 1 15 2 1
b b
77 t 2 78 ? 1
77-86 b
(15) (521 (40)
400 k 226 397 t 247 331 2 268
154-981 34-1094 21-1169
4 -r-3.1 3 t 3.0 4 2 3.0
o-11 1-18 1-12
10 t 6.2 9 2 4.1 12 k 7.1
O-27 3-25 5-41
86 ? 7.2 88 2 6.1 84 + 9.1
71-100 68-95 52-94
132-4621
5 ? 3.1
1-9
8 + 3.1
5-12
87 ? 5.2
82-94
(611
(8) (20)
(11)
(71 1019 2 1608
4-39
55-95
(631
255 + 296
26-1988
7 + 4.1
1-16
13 2 6.1
3-27
80 2 8.1
64-95
(181 (22)
219 A 174 174 2 97
16-623 8-384
4 + 4.1 4 2 5.1
o-15 O-20
14 + 11.2 15 k 8.2
5-39 l-33
82 + 13.3 82 2 11.2
60-95 36-99
(25)
347 + 383
14-1516
2 2 2.0
O-8
10 2 5.1
3-27
88 k 6.1
72-96
(42)
202 k 217
36-610
421
80 +- 3
72-95
79 -e 9.1
46-94
(108)
on 3- to B-day stool
120 t 92 collection.
9-488
4 + 3.0
b
O-17
16 k 3
17 2 7.1
b
6-53
b Data not available.
nutrients undergo a complex fate in the colon. They may be digested by bacterial enzymes and the products absorbed; this would increase FFC. Alternatively, either the malabsorbed nutrients or their digestion products by their osmotic activity might diminish colonic water absorption. Accordingly, the denominator of the equation would not change and FFC would remain low. Thus, increased FFC should reflect fat malabsorption in the absence of a marked increase in fecal water or NFS. If the malabsorbed fat was hydrolyzed to fatty acids during colonic transit and these induced water secretion, or if malabsorbed protein or carbohydrate induced water secretion, FFC would decrease. Accordingly, in patients with pancreatic insufficiency, increased FFC should be specific, but not sensitive. The data in Table 2 confirm this, but note that FFC values exceeding 10% were also observed in patients with gastric surgery, bile acid malabsorption, diabetic enteropathy, and sprue. Bo-Linn and Fordtran also suggest that FFC should be increased in patients with cholestasis and bacterial overgrowth syndromes.
Our data indicate that their surmise is correct. Fecal fat concentration is markedly increased in cholestatic conditions. Finally, FFC may also be increased in healthy subjects with severe constipation. In most individuals, feces are about 80% water. In individuals with constipation, fecal water may fall to as low as 46%, and FFC will show the expected reciprocal increase. Other types of malabsorption should manifest increases in both the numerator and denominator [if steatorrhea is present), or in the denominator only (if steatorrhea is not present). For example, in patients with bacterial overgrowth or with greatly increased inflammatory exudates, the NFS may be increased. In patients with simple diarrhea of colonic origin, fecal water alone will be increased. To summarize, our data of some years ago confirm, extend, and may help to clarify the observations of Bo-Linn and Fordtran. Our data indicate that increased FFC is neither very specific nor sensitive (as values
July
CORRESPONDENCE
1985
is easily detectable
by histochemical staining of stool (7,8). To establish the diagnosis of mild pancreatic insufficiency, we SUSpect that it is going to be better to carry out a Lundh test meal and measure enzyme concentrations in the jejunal aspirates (91, or to perform the usual cholecystokinin-stimulation test (10). Several new noninvasive tests for assessment of pancreatic exocrine function have recently been reported (ll-131, and it will be of interest to compare these tests with not only results from invasive procedures, but also with FFC measurement in patients with varying degrees of pancreatic exocrine hypofunction. In the meantime, if fecal fat measurements are made to quantitate the degree of steatorrhea in a patient with malabsorption (who does not have hepatobiliary disease or previous gastrointestinal surgery), the astute clinician who observes an elevated FFC (>lO%) in the lab report may immediately make a presumptive diagnosis of pancreatic insufficiency with some confidence.
ALAN F. HOFMANN,
M.D. Division of Gastroenterology Department of Medicine University of California, San 225 Dickinson Street San Diego, California 92103
2.
3.
4.
5.
6. 7. 8.
Dear Sir: It does not surprise us that operations and medication designed to reduce gastric activity and thus hormonal stimulation of the pancreas are not very successful in relieving the pain of chronic pancreatitis. It is evident now that even during prolonged fasting the gland is spontaneously active at 100-min intervals. In dogs we obtain half-maximal protein secretion and about one-eighth maximal juice volume at spontaneous peak activity. Spontaneous peaking is completely abolished by ganglion blocking agents (1,2) and our evidence is that cholecystokinin and secretin release are abolished also (3,4). Might not a long-acting blocker, like pentolinium tartrate, be worth a trial in the disease? The argument that these agents cause hypotension is not really relevant as the orthostatic hypotension that can result is of little consequence to patients in bed. Creighton
Diego
Bo-Linn GW, Fordtran JS. Fecal fat concentration in patients with steatorrhea. Gastroenterology 1984;87:319-22. Hofmann AF. The syndrome of ileal disease and the broken enterohepatic circulation: cholerheic enteropathy. Gastroenterology 1967:52:752-7. Hofmann AF, Poley JR. Role of bile acid malabsorption in pathogenesis of diarrhea and steatorrhea in patients with ileal resection. I. Response to cholestyramine or replacement of dietary long chain triglyceride by medium chain triglyceride. Gastroenterology 1972;62:1191-9. Ammon HV, Phillips SF. Inhibition of colonic water and electrolyte secretion by fatty acids in man. Gastroenterology 1973;65:744-9. Dornberger GR, Comfort MW, Wollaeger EE, Power MH. Total fecal solids, fat and nitrogen: study of patients with chronic relapsing pancreatitis. Gastroenterology 1948;11:691-700. Bliss CM, Small DM. A comparison of ileal and fecal lipid in pancreatic steatorrhea (abstr). Gastroenterology 1970;58:928. Luk CD. Screening for steatorrhea (letter). Gastroenterology 1979;77:205-6. Newcomer AD, Hofmann AF, DiMagno EP, Thomas PJ. Carl-
son CL. Triolein breath test: a sensitive and specific test for fat malabsorption. Gastroenterology 1979;76:6-13. 9. Braganza JM. Herman K, Hine P, Kay G, Sandle GI. Pancreatic enzymes in human duodenal juice-a comparison of responses in secretin pancreocymin and Lundh Borgstrom tests. Gut 1978;19:358-66. 10.
Pain in Chronic Pancreatitis
D. F. MAGEE, M.D., Ph.D
JAMES W. MANIER Lovelace Medical Center Albuquerque, New Mexico 1.
233
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University
School of Medicine 2500 California Street Omaha, Nebraska 68178 S. NARUSE. M.D. National Institute
for Physiological
Sciences
Department of Molecular Physiology Laboratory of Cellular Metabolism Myodaiji, Okazaki, 444 Japan Magee DF, Naruse S. Neural control of periodic secretion of the pancreas and the stomach in fasting dogs. J Physiol 1983; 344:153-60. Magee DF, Naruse S. Characteristics of secretin stimulated pancreatic secretion in dogs. J Physiol 1983;346:115P. Hong SS, Magee DF, Crewdson F. The physiological regulation of gallbladder evacuation. Gastroenterology 1956;30:625-30. Hong SS, Magee DF. Pharmacological studies on the regulation of pancreatic secretion in pigs. Ann Surg 1970;172:41-8.
Diagnosis of IBS Dear Sir: We enjoyed reading the excellent editorial by Drossman (1) that summarized the difficulties encountered in the diagnostic workup and classification of patients suspected to suffer from irritable bowel syndrome (IBS). It was mentioned that the determination of whether a patient has either IBS or organic disease cannot always be made in clinical practice. We would like to add some further information. The protocol of our study (2) was designed to develop a weighted score for the diagnosis of IBS and to test the diagnostic accuracy of this scoring system in two patient groups to be defined as precisely as possible. Thus, we created the scoring system using the data of patients with symptoms of IBS but without any recognizable organic disease and of other patients also with symptoms compatible with IBS, but with some organic disease diagnosed. Patients with organic disease but with the additional diagnosis of IBS were excluded from all calculations. In this group, IBS was diagnosed because the complaints seemed not to be fully explained by the organic disease and were typical of IBS. This may appear arbitrary because the symptoms complained about by patients classified into the group “organic disease” may also not necessarily be related to the underlying organic disease. However, in the absence of a “gold” standard for the diagnosis of IBS, as discussed in the editorial, arbitrary decisions cannot be eliminated completely.