The recent guidelines for the management of inflammatory bowel disease in
adults[1] have not covered a common clinical scenario where Crohn’s
disease presents as a pure terminal ileal lesion and biopsies are either
unobtainable or inconclusive and decision of treatment rests on
interpretation of radiological findings only. Under such conditions one
will have to depend on the balance of probabilities...
The recent guidelines for the management of inflammatory bowel disease in
adults[1] have not covered a common clinical scenario where Crohn’s
disease presents as a pure terminal ileal lesion and biopsies are either
unobtainable or inconclusive and decision of treatment rests on
interpretation of radiological findings only. Under such conditions one
will have to depend on the balance of probabilities and effects of trial
of empirical treatment. Terminal ileum is less accessible to endoscopic
procedures than the rest of the colon even in expert hands. It is doubtful
if capsule endoscopy will overcome this problem, as the procedure should
not be carried out on these very patients who may have narrowing of the
ileum from inflammation. A fortuitous positive histological diagnosis from
blind biopsies taken from elsewhere in the alimentary canal or from the
peri-anal tags cannot be relied upon as in 20% of cases of Crohn’s disease
the disease activity may be restricted to the terminal ileum only.
Moreover, the histological diagnosis of Crohn’s disease from blind mucosal
biopsies from areas, which are not affected visibly, is difficult to
interpret and can even be misleading.
In terms of frequency of occurrence of clinical conditions affecting
terminal ileum, Crohn’s disease far outweigh other conditions. Although
primary non-Hodgkin’s lymphoma and stromal tumors are known to involve
terminal ileum in an isolated way, the frequency of such occurrence is so
rare (1% of GI tumors) that according to one study in more than 75% cases
the diagnoses of these tumors were made either accidentally or at post-
mortem. It is therefore not at all surprising that survival from primary
malignancies have not improved during the last four decades.[2]
There is also little information in the literature on the biological
behaviour of these tumors. Whilst intestinal obstruction and bleeding
brings such diagnoses to light early, some tumors can lie indolent for
long periods of time only to present later as subacute obstruction or
perforation. Early diagnosis of these tumors is essential as not only some
of these can be removed by resection in its entirety but specific
chemotherapy is also available for certain tumors eg, gastrointestinal
stromal tumor (GIST).
It is therefore imperative that those cases of Crohn’s disease where
biopsy confirmation has not been achieved for one reason or another are
periodically reviewed at multidisciplinary meeting with surgeons. A
laparoscopic examination should be carried out where there is the
slightest suspicion of a non-Crohn's illness like secondary metastasis or
TB that may cause peritoneal involvement. However, if the lesion is
endoluminal like Crohn’s or tumor a full laparotomy becomes the only
alternative. A drastic measure though it may seem for those few who
respond to steroids and hence may be reluctant to undergo surgery, it
would, however, form a safeguard against misdiagnosis of an early
resectable ileal tumor as Crohn’s disease.
References
1. Guidelines for the management of inflammatory bowel disease in
adults. Carter MJ, Lobo AJ, Travis SPL. Gut;53:v1-16v
2. The role of the physician in the late diagnosis of primary malignant
tumors of the small intestine. Am J Gastroenterology 1991 Mar;86(3):304-8
I congratulate the authors of the recently revised BSG 'Guidelines for the
investigation of diarrhoea' for their excellent overview of this important
clinical problem.[1] I would however take issue with guideline’s
suggestion that measurement of stool volumes in outpatients is
impractical. In my experience such measurement is readily achievable and
cheap, merely requiring a suitable container and some we...
I congratulate the authors of the recently revised BSG 'Guidelines for the
investigation of diarrhoea' for their excellent overview of this important
clinical problem.[1] I would however take issue with guideline’s
suggestion that measurement of stool volumes in outpatients is
impractical. In my experience such measurement is readily achievable and
cheap, merely requiring a suitable container and some weighing scales. A 3-day stool collection should be considered early in the investigation of
chronic diarrhoea particularly if a factitious aetiology is suspected
which is unfortunately often under-diagnosed and over investigated.[2]
References
(1) Thomas PD, Forbes A, Green J et al. Guidelines for the investigation of chronic diarrhoea (2nd edition)
Gut 2003;52(suppl V): v1-v15.
Jowett and colleagues have recently reported in their elegant study,
the role of diet to maintain remission in patients with ulcerative
colitis.[1] Surely, the effect of diet has an
essential, but often forgotten, role in altering the course of the disease
in all types of inflammatory bowel diseases. This role does not
necessarily act by maintaining patients in remission clinically, but
perhaps mo...
Jowett and colleagues have recently reported in their elegant study,
the role of diet to maintain remission in patients with ulcerative
colitis.[1] Surely, the effect of diet has an
essential, but often forgotten, role in altering the course of the disease
in all types of inflammatory bowel diseases. This role does not
necessarily act by maintaining patients in remission clinically, but
perhaps more importantly by minimising the activities of the disease and
rendering it quiescent.
We have recently reported a case of active
stricturing Crohn’s disease in an adult female patient with high stoma
output.[2]
She was treated solely with casein-base formula (Modulen IBD-Nestle,
Vevey, Switzerland) for 3 weeks. Her stoma output was reduced from 2,800
ml to 400 ml per day by day 10. The serum albumin and serum protein has
significantly risen as well. She subjectively felt better and pain free
and she stopped her opiate and non opiate formula. The casein-based
formula is a nutritionally complete formulation containing a natural anti-
inflammatory growth factor TGF-â2. The mechanism for inducing
remission in our patient is possibly by inhibiting the expression of MHC
class II protein to down-regulate the inflammatory response.[3]
Previous
studies have shown that there is a decrease in the plasma anti-oxidant
defences in all types of inflammatory bowel disease.[4] This is mirrored
by increase in the free radical peripheral leukocyte DNA damage. It is
therefore possible that casein-based formula acts as an anti-oxidant to
minimise the oxidative stress that occurs in patients with active Crohn’s
disease. The other possible mechanism is that this formula might have a
role of a prebiotic by stimulating the activity of bacteria which is
already present in the gut.
The remission induced in our case study
highlights the part played by a casein-based formula in the management of
adult Crohn’s disease. The encouraging result demonstrates the need to
treat similar cases with dietary measures first. This opportunity should
not be missed as it may well obviate the need for surgical intervention or
administration of potent pharmacotherapy, which has the risk of several
comorbidities.
References
(1) Jowett SL, Seal CJ, Pearce MS, Phillips E, Gregory W, Barton JR, Welfare MR. Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study. Gut 2004;53:1479-1484.
(2) S. Jones, H. Shannon, E. Srivastava, N Haboubi. A novel approach
to a patient with Crohn’s disease and a high stoma output: a missed
opportunity? Scand J Gastroenterol 2004, 4, 398 - 400
(3) Donnet-Hughes A, Duc N, Serrant P, Vidal K, Schiffrin EJ. Bioactive
molecules in milk and their role in health and disease: the role of
transforming growth factor-â. Immunol Cell Biol 2000;34:49-53
(4) D’Odorico A, BortolanS, Gaardin R, et al. Reduced plasma antioxidant
concentrations and increased oxidative DNA damage in inflammatory bowel
disease.
Scand J Gastroenteral 2001;36:1289-94
Early diagnosis to distinguish between malignant pancreatic tumor and chronic pancreatitis is still difficult despite significant progress in imaging techniques. Moreover the patients with chronic pancreatitis are in a higher risk of pancreatic cancer development.
The recently published study performed by Malka et al.[1] clearly
confirms these difficulties independently of rigorous selection...
Early diagnosis to distinguish between malignant pancreatic tumor and chronic pancreatitis is still difficult despite significant progress in imaging techniques. Moreover the patients with chronic pancreatitis are in a higher risk of pancreatic cancer development.
The recently published study performed by Malka et al.[1] clearly
confirms these difficulties independently of rigorous selection criteria
of patients with chronic pancreatitis. To exclude the possibility that
chronic pancreatitis may be caused by early potentially premalignant
lesions, the authors eliminated from their investigations even the
patients with chronic pancreatitis in whom pancreatic cancer was
recognized during the first 2 years of follow-up.
Several studies indicate the value of circulating
tumor markers evaluation as a simple, sensitive and reliable tests
facilitating the differential diagnosis between chronic pancreatitis and
cancer.[2-8] To improve the effectiveness of serological diagnosis of patients
with pancreatic carcinoma different tumor markers have been assessed
including CEA, CA 242, CA 50, CA 72-4.[2-5,8] However, the
sensitivity and specificity of these markers appeared to be insufficient
for the differentiation of pancreatic carcinoma and chronic pancreatitis.
In 1996 CAM 17-1 [6] was described as a new useful diagnostic marker in
pancreatic carcinoma. It showed a sensitivity similar to that of CA 19-9
but higher specificity, giving only 10% false positive results in patients
with chronic pancreatitis.
Tissue polypeptide specific antigen (TPS) is a different type of
antigen that does not correlate with tumor mass but reflects the tumor
proliferative activity.[9] Our study [7] revealed that the elevated
levels of TPS detected preoperatively 100% of patients with pancreatic
carcinoma. The introduction of 200 U/L as a decision criterion for TPS
level allowed to increase the specificity of this marker to 98% and
eliminated all but 2% of the false positive results in patients with
chronic pancreatitis. Moreover, the TPS is useful for detection of early
stages of clinical advancement of pancreatic carcinoma.
It seems to be that measurement of TPS, using 200 U/L as its cut off
value should facilitate the more precise discrimination between early
stages of pancreatic carcinoma and chronic pancreatitis.
References
(1) Malka D, Hammel P, Maire F, et al. Risk of pancreatic adenocarcinoma in
chronic pancreatitis. Gut 2002;51:849-52.
(2) Banfi G, Zerbi A, Pastori S, et al. Behavior of tumor markers CA 19-9,
CA 195, CAM 43, CA 242 and TPS in diagnosis and follow-up of pancreatic
cancer. Clin Chem 1993;39:420-3.
(3) Ventrucci M, Ubalducci GM, Cipolla A, et al. Serum CA 242: the search
for a valid marker of pancreatic cancer. Clin Chem Lab Med 1998;36:179-84.
(4) Kawa S, Tokoo M, Hasebe O, et al. Comparative study of CA 242 and CA 19
-9 for the diagnosis of pancreatic cancer. Br J Cancer 1994;70:481-6.
(5) Sperti C, Pasquali C, Guolo P, et al. Serum tumor markers and cyst
fluid analysis are useful for the diagnosis of pancreatic cystic tumors. Cancer 1996;78:237-43.
(6) Gansauge F, Gansauge S, Parker N, et al. CAM 17-1 – A new diagnostic
marker in pancreatic cancer. Br J Cancer 1996;74:1997-2002.
(7) Slesak B, Harlozinska-Szmyrka A, Knast W, et al. Tissue polypeptide
specific antigen (TPS), a marker for differentiation between pancreatic
carcinoma and chronic pancreatitis. Cancer 2000;89:83-8.
(8) Pasanen PA, Eskelinen M, Partanen K, et al. Diagnostic value of tissue
polypeptide specific antigen in patients with pancreatic carcinoma. Tumor Biol 1994;15:52-60.
(9) Rydlander L, Ziegler E, Bergman T, et al. Molecular characterization of
tissue-polypeptide-specific-antigen epitope and its relationship to human
cytokeratin 18. Eur J Biochem 1996;241:309-14.
Penagini and Cantù should be congratulated for the remarkable results they
were able to obtain in 11 patients with achalasia treated by pneumatic
dilation.[1] To my knowledge, not a single study has so far produced similar
results. A review of prospective studies in patients undergoing pneumatic
dilation with the Rigiflex dilator[2] indicated that approximately 80%
will have a good or excellent short term response. Howev...
Penagini and Cantù should be congratulated for the remarkable results they
were able to obtain in 11 patients with achalasia treated by pneumatic
dilation.[1] To my knowledge, not a single study has so far produced similar
results. A review of prospective studies in patients undergoing pneumatic
dilation with the Rigiflex dilator[2] indicated that approximately 80%
will have a good or excellent short term response. However, if such
patients are observed for prolonged periods, the results obtained do not
differ significantly from those observed following treatment with the
older balloons. In a recent study, in which 56 patients were treated with
the Rigiflex dilator and observed for more than 10 years, the long-term
success rate was 55%.[3] Thus, it is my impression that differences in
treatment results are not so much related to differences in technique and
operator experience, but rather to the number of patients investigated,
the length of follow-up and finally the quality of the study design. It is
hoped that carefully designed randomized studies, which are now in
progress, will more definitely tell us whether we still should continue to
offer pneumatic dilation to the great majority of patients with achalasia
or whether we should advise them to undergo surgery instead.
References
1. Penagini R, Cantù. Efficacy and strategy of pneumatic dilatation in achalasia [electronic response to Eckardt V F, Gockel I, Bernhard G. Pneumatic dilation for achalasia: late results of a prospective follow up investigation] gutjnl.com 2004URL direct link to eLetter.
2. Kadakia SC, Wong RKH. Pneumatic balloon dilation for esophageal
achalasia. Gastrointest Endosc Clin N Am 2001;11:325-345.
3. West RL, Hirsch DP, Bartelsman JFWM, de Borst J, Ferwerda G, Tytgat
GNJ, Boeckxstaens GE. Long term results of pneumatic dilation in achalasia
followed for more than 5 years. Am J Gastroenterol 2002;97:1346-51.
We were interested to read the case report by Rampertab et al. about
small bowel neoplasia in coeliac disease.[1] The
findings are very much in accord with ours from the BSG National UK Survey
published earlier this year.[2]
Over a two-year period (1998-2000) we collected details of 175 cases
of primary small intestinal adenocarcinoma, of which 13% were associated
with coeliac disease,...
We were interested to read the case report by Rampertab et al. about
small bowel neoplasia in coeliac disease.[1] The
findings are very much in accord with ours from the BSG National UK Survey
published earlier this year.[2]
Over a two-year period (1998-2000) we collected details of 175 cases
of primary small intestinal adenocarcinoma, of which 13% were associated
with coeliac disease, and another 7% with Crohn's disease. As regards the
coeliac-associated adenocarcinomas, similar to Rampertab et al,[1] we found
a predominance of males (2:1) and an equal distribution between duodenum
and jejunum. The age range was 47-80 years. Fifty five per cent
presented acutely, predominantly with obstruction, and 45% chronically
with anaemia, weight loss or abdominal pain. The mean time of symptoms
prior to diagnosis was 14 months, which was reflected in a relatively poor
30-month overall survival of 58%. In 63% coeliac disease had been
diagnosed a mean of 8.2 years prior to the diagnosis of adenocarcinoma; in
almost all these patients there had been a good clinical and mucosal
response to a gluten-free diet. In 37% coeliac disease was diagnosed at
the same time as the adenocarcinoma.
Although 13% of small bowel adenocarcinomas being associated with
coeliac disease implied that the risk of these cancers in coeliac disease
is very high, such an increase translates into a very small absolute life-
time risk of less than 1%, since these tumours are rare and coeliac
disease is very common. Nevertheless, we agree that coeliac patients
require long-term follow-up for this, and other, complications. However,
the best means of surveillance needs to be determined.
Of most concern is the long delay in the diagnosis of small bowel
adenocarcinoma, irrespective of whether or not coeliac disease is present.
This leads to a poor survival, since 40% have metastasised by the time the
diagnosis is made. A high index of suspicion is required by all
gastroenterologists for this rare, but eminently treatable, type of
adenocarcinoma.
References
(1) Rampertab SD, Forde KA, Green PHR. Small bowel neoplasia in coeliac disease. Gut 2003;52:1211-1214.
(2) Howdle PD, Jalal PK, Holmes GKT et al. Primary small bowel
malignancy in the UK and its association with coeliac disease. Quarterly Journal of Medicine 2003;96:345-353.
We read with interest the article by Atkinson et al[1]. The authors describe an important
advance in our understanding of the putative role of inflammation in
irritable bowel syndrome (IBS). However we wonder whether their conclusion
that assay of IgG antibodies may have a role in identifying candidate
foods for elimination to treat patients with IBS may be a step too far.
The four foods to...
We read with interest the article by Atkinson et al[1]. The authors describe an important
advance in our understanding of the putative role of inflammation in
irritable bowel syndrome (IBS). However we wonder whether their conclusion
that assay of IgG antibodies may have a role in identifying candidate
foods for elimination to treat patients with IBS may be a step too far.
The four foods to which the patients most commonly formed antibodies and
hence the four foods most commonly eliminated from the "true diet", were
yeast (86.7%), milk (84.3%), whole egg (58.3%) and wheat (49.3%). The
"sham diet" involved eliminating foods to which the patients had not
formed antibodies and, therefore, in the sham group the exclusion rates
for yeast, milk, whole egg and wheat were very low (0%, 1.3%, 26.7%, and
8% respectively). It is therefore difficult to assess whether a diet
excluding these foods would have lead to symptomatic improvement in all
patients, regardless of their antibody status.
Furthermore, the foods to which the study group commonly formed
antibodies are similar to those already identified as leading to
symptomatic benefit in patients with IBS when excluded from their diet.
In a review cited by Atkinson et al,[2] it was noted that in eight trials
of exlusion diets in IBS, seven identified dairy products, and five wheat
as worsening symptoms. It is not clear whether the difference in
improvement in symptoms seen in the current study between true and sham
groups can be explained simply by the omission of these foods. This
could, in practice eliminate the need for antibody testing.
References
1. Atkinson W, Sheldon TA, Shaath N et al. Food elimination based on
IgG antibodies in irritable bowel syndrome: a randomised controlled trial.
Gut 2004; 53: 1459-1464
2. Burden S. Dietary treatment of irritable bowel syndrome: current
evidence and guidelines for future practice. J Hum Nutr Dietet
2001;14:231-41
We welcome Dr Pollock's comments on the use of a three day stool
collection
in the investigation
of chronic diarrhoea.[1] Our concern about its use in the out-patient
setting, and
particularly when factitious
diarrhoea is suspected, is that the collection is unsupervised and
potentially susceptible to
interference. It was for this reason that in-patient collection was
suggested. Furthermore, we think
t...
We welcome Dr Pollock's comments on the use of a three day stool
collection
in the investigation
of chronic diarrhoea.[1] Our concern about its use in the out-patient
setting, and
particularly when factitious
diarrhoea is suspected, is that the collection is unsupervised and
potentially susceptible to
interference. It was for this reason that in-patient collection was
suggested. Furthermore, we think
there will be widespread doubt by clinicians about the acceptability of
this approach. Excepting these
caveats, we agree that it is a relatively simple and effective way to
assess stool volume which may limit
the need for other investigations in these patients.
Reference
(1) Pollock RCG. Investigation of chronic diarrhoea [electronic response to Thomas PD et al.
Guidelines for the investigation of chronic diarrhoea, 2nd edition] gutjnl.com 2003 http://gut.bmjjournals.com/cgi/eletters/52/suppl_5/v1#107
The recent paper by Atkinson et al[1] regarding IgG food antibodies
and irritable bowel syndrome (IBS) fails to compare like with like.
Regardless of the IgG results, the treatment group excluded significantly
different food to the control group, particularly those foods which appear
to exacerbate symptoms of IBS. Of particular concern is the 'yeast
exclusion' diet. A low yeast diet is not a r...
The recent paper by Atkinson et al[1] regarding IgG food antibodies
and irritable bowel syndrome (IBS) fails to compare like with like.
Regardless of the IgG results, the treatment group excluded significantly
different food to the control group, particularly those foods which appear
to exacerbate symptoms of IBS. Of particular concern is the 'yeast
exclusion' diet. A low yeast diet is not a recognised diet in standard
textbooks of dietetics and nutrition. However, alternative practitioners
offering such a 'yeast exclusion diet' sometimes recommend exclusion of a
wide range of foods such as: bakery products, alcoholic beverages, many
other beverages including commercial fruit juices, cereals, condiments,
dairy produce, fungi, meat products (hamburgers, sausages and cooked meats
made with bread or breadcrumbs), yeast extracts (Bisto, Marmite, Oxo,
Bovril, Vegemite, gravy browning and all similar extracts), all B-vitamin
preparations, and sometimes most worryingly, 'sugar foods' (sugar,
sucrose, fructose, maltose, lactose, glycogen, glucose milk, sweets,
chocolate, sweet biscuits, cakes, candies, cookies, puddings, desserts,
canned food, packaged food, hamburgers, honey, mannitol, sorbitol,
galactose, monosaccharides, polysaccharides, date sugar, turbinado sugar,
molasses, maple syrup, most bottled juices, all soft drinks, tonic water,
milkshakes, raisins, dried apricots, dates, prunes, dried figs, other
dried fruit).
So regardless of IgG antibody status, the dietary restrictions in one
group are not controlled for by the other group, and hence the conclusion
may not be valid.
It would also be helpful to know if any of the patients with IgG
antibodies to a particular antigen also had IgE antibodies to the same
antigen.
References
1. Atkinson W, Sheldon TA, Shaath N et al. Food elimination based on IgG
antibodies in irritable bowel syndrome: a randomised controlled trial. Gut
2004; 53: 1459-1464
I read with interest the article of Vaughan RB et al,[1] and was
pleased to see my novel studies,[2,3] partially reproduced in patients with
decompensated cirrhosis. I disagree with some of its results as it involves
substancial design, methodology, and analysis problems.
The authors said that advanced cirrhotic patients have “generalised
vasodilatation”. Vasodilatation does occur in...
I read with interest the article of Vaughan RB et al,[1] and was
pleased to see my novel studies,[2,3] partially reproduced in patients with
decompensated cirrhosis. I disagree with some of its results as it involves
substancial design, methodology, and analysis problems.
The authors said that advanced cirrhotic patients have “generalised
vasodilatation”. Vasodilatation does occur in these patients, but only in
the splanchnic and pulmonary beds.[4] Indeed, I and others have shown
vasoconstriction in the bracheal, femoral, cerebral and renal territories
especially in advanced cirrhosis.[5-7] Therefore, I stress that with
advancing cirrhosis, further activation of the neurohumoral systems
occurs, with consequent peripheral vasoconstriction. However, blood
pooling, particularly in the splanchnic bed, lowers the systemic vascualr
resistance.
Measuring forearm blood flow (FBF) in one arm is a major critics to
this study.[1] Changing levels of alertness and external stimuli produce
similar fluctuations in blood flow of both arms, and lead to significant
misleading alterations in the measured responses if unilateral
measurements are used. Thus, responses to intra-arterial infusions should
have been measured in both arms with the results expressed as ratios of
concurrent FBFs in the infused and non-infused arms, where the latter
serves as a contemporaneous control for the drug effects in the former.[8-10] Furthermore, FBF ratios are significantely more reproducible than
unilateral FBF measurements both at rest and following the infusions of
vasoconstrictors.[10]
The authors, surprisingly, demonstrated an increase in FBF (~35-40%)
in response to the infusion of a locally-active dose of the potent
vasoconstrictor endothelin-1 (ET-1), which reached its maximum within 5
minutes from the start. They attributed their finding to an enhanced ETB
receptor-mediated vasodilatation. This needs to be tested by selectively
blocking ETB receptors, using BQ-788. So far, ETB receptors upregulation has
been reported in the splanchnic and pulmonary vasculature, but not in the
forearm.[11,12] How can the maximum response to the slowly-acting ET-1 be
reached within 5 minutes? Also, dose-response curves of the effects of ET-1 and BQ-123 should have beed done.
According to the authors, ETA receptor-mediated responses are
unaltered, while those mediated by the ETB receptor are enhanced in
pateints with decompensated cirrhosis. Thus, one would expect that
blocking the ETA receptors, with BQ-123, allows ET-1 to act unopposed on
the ETB receptors, and produces enhanced vaodilatation. However, this was
not the case (Figure 2). What adds to my surprise here is that BQ-123
infusion also increased FBF by ~35-40%. How can the infusion ET-1 produce
the same percentage change in FBF as the infusion of its selective ETA receptor
antagonists?!
Many of the included patients were on
diuretics, beta-blockers, and immuno-suppressive medications, which were withheld only on the day of testing.
These medications affects the circulating volume, vascular tone and the
activity of the neurohumoral systems. To eliminate these effects, drugs
need to be stopped for at least 5 times their half-lives. Alternatively,
control subjects on the same medications should be used (e.g. renal
transplant recepients with nomal liver).
Vaughans et al, reported normal plasma ET-1 concentrations in
decompensated cirrhosis, without measuring preproendothelin-1 mRNA or big
ET-1, the biological precursor of ET-1. Due to its autocrine, paracrine
and endocrine nature, plasma concentrations of ET-1 alone do not reflect
the activity of the endothelin system or the status of ET-1 production.[13]
This should have been stated by the authors. We also recommend collecting
samples in tubes containing 1000 KIU aprotinin and EDTA.
In conclusion, the scientific contents of this article would have
been greater if the authors had: 1. Measured FBF in both arms; 2. Presented their data as % change in the ratio of flows in both arms at
every time point; 3. Assessed plasma big ET-1 or preproendothelin mRNA
concentrations; 4. Examined the reponses to ETB receptor antagonist; 5. Performed a dose response curve; 6. Selected a comparable control group on
similar medications as the patients.
References
(1) Vaughan RB, Angus PW, Chin- Dusting JPF. Evidence for altered vascular
responses to exogenous endothelin-1 in patients with advanced cirrhosis
with restoration of the normal vasoconstrictor response following
successful liver transplantation. Gut 2003;52:1505-10.
(2) Helmy A, Newby DE, Jalan R, et al. Enhanced vasodilatation to
endothelin antagonism in patients with compensated cirrhosis and the role
of nitric oxide. Gut 2003;52:410-15.
(3) Helmy A, Jalan R, Newby DE, et al. Altered peripheral vascular
responses to exogenous and endogenous endothelin-1 in patients with well-
compensated cirrhosis. Hepatology 2001;33:826–31.
(4) Newby DE, Hayes PC. Hyperdynamic circulation in liver cirrhosis: not
peripheral vasodilatation but 'splanchnic steal'. QJM 2002;95:827-30.
(5) Helmy A, Jalan R, Newby DE, et al. Role of angiotensin II in regulation
of basal and sympathetically stimulated vascular tone in early and
advanced cirrhosis. Gastroenterology 2000;118:565–72.
(6) Fernandez-Seara J, Prieto J, Quiroga J, et al. Systemic and regional
hemodynamics in patients with liver cirrhosis and ascites with and without
renal failure. Gastroenterology 1989;97:1304-12.
(7) Maroto A, Gines P, Arroyo V, et al. Brachial and femoral artery blood
flow in cirrhosis: relationship to kidney dysfunction. Hepatology
1993;17:788-93.
(8) Benjamin N, Calver A, Collier J, et al. Measuring forearm blood flow
and interpreting the responses to drugs and mediators. Hypertension
1995;25:918-923.
(9) Webb DJ. The pharmacology of human blood vessels in vivo. J Vasc Res
1995;32:2-15.
(10) Petrie JR, Ueda S, Morris AD, et al. How reproducible is bilateral
forearm plethysmography? Br J pharmacol 1998;45:131-9.
(11) Cahill PA, Hou MC, Hendrickson R, et al. Increased expression of
endothelin receptors in the vasculature of portal hypertensive rats: role
in splanchnic hemodynamics. Hepatology 1998;28:396-403.
Dear Editor
The recent guidelines for the management of inflammatory bowel disease in adults[1] have not covered a common clinical scenario where Crohn’s disease presents as a pure terminal ileal lesion and biopsies are either unobtainable or inconclusive and decision of treatment rests on interpretation of radiological findings only. Under such conditions one will have to depend on the balance of probabilities...
Dear Editor
I congratulate the authors of the recently revised BSG 'Guidelines for the investigation of diarrhoea' for their excellent overview of this important clinical problem.[1] I would however take issue with guideline’s suggestion that measurement of stool volumes in outpatients is impractical. In my experience such measurement is readily achievable and cheap, merely requiring a suitable container and some we...
Dear Editor
Jowett and colleagues have recently reported in their elegant study, the role of diet to maintain remission in patients with ulcerative colitis.[1] Surely, the effect of diet has an essential, but often forgotten, role in altering the course of the disease in all types of inflammatory bowel diseases. This role does not necessarily act by maintaining patients in remission clinically, but perhaps mo...
Dear Editor
Early diagnosis to distinguish between malignant pancreatic tumor and chronic pancreatitis is still difficult despite significant progress in imaging techniques. Moreover the patients with chronic pancreatitis are in a higher risk of pancreatic cancer development.
The recently published study performed by Malka et al.[1] clearly confirms these difficulties independently of rigorous selection...
Penagini and Cantù should be congratulated for the remarkable results they were able to obtain in 11 patients with achalasia treated by pneumatic dilation.[1] To my knowledge, not a single study has so far produced similar results. A review of prospective studies in patients undergoing pneumatic dilation with the Rigiflex dilator[2] indicated that approximately 80% will have a good or excellent short term response. Howev...
Dear Editor
We were interested to read the case report by Rampertab et al. about small bowel neoplasia in coeliac disease.[1] The findings are very much in accord with ours from the BSG National UK Survey published earlier this year.[2]
Over a two-year period (1998-2000) we collected details of 175 cases of primary small intestinal adenocarcinoma, of which 13% were associated with coeliac disease,...
Dear Editor
We read with interest the article by Atkinson et al[1]. The authors describe an important advance in our understanding of the putative role of inflammation in irritable bowel syndrome (IBS). However we wonder whether their conclusion that assay of IgG antibodies may have a role in identifying candidate foods for elimination to treat patients with IBS may be a step too far. The four foods to...
Dear Editor
We welcome Dr Pollock's comments on the use of a three day stool collection in the investigation of chronic diarrhoea.[1] Our concern about its use in the out-patient setting, and particularly when factitious diarrhoea is suspected, is that the collection is unsupervised and potentially susceptible to interference. It was for this reason that in-patient collection was suggested. Furthermore, we think t...
Dear Editor
The recent paper by Atkinson et al[1] regarding IgG food antibodies and irritable bowel syndrome (IBS) fails to compare like with like. Regardless of the IgG results, the treatment group excluded significantly different food to the control group, particularly those foods which appear to exacerbate symptoms of IBS. Of particular concern is the 'yeast exclusion' diet. A low yeast diet is not a r...
Dear Editor
I read with interest the article of Vaughan RB et al,[1] and was pleased to see my novel studies,[2,3] partially reproduced in patients with decompensated cirrhosis. I disagree with some of its results as it involves substancial design, methodology, and analysis problems.
The authors said that advanced cirrhotic patients have “generalised vasodilatation”. Vasodilatation does occur in...
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