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The paper by Lorente et al (Gut 2000; 50: 13-18) demonstrates that H.
pylori stimulates pepsinogen release from human chief cells in vitro. The
precision of the results obtained from cells from 70 different subjects is
to be complimented but several aspects of presentation and interpretation
require further discussion.
The authors report no differences in basal or H. pylori-stimulated
pepsinogen...
The paper by Lorente et al (Gut 2000; 50: 13-18) demonstrates that H.
pylori stimulates pepsinogen release from human chief cells in vitro. The
precision of the results obtained from cells from 70 different subjects is
to be complimented but several aspects of presentation and interpretation
require further discussion.
The authors report no differences in basal or H. pylori-stimulated
pepsinogen release between chief cells from H. pylori infected and
uninfected patients. It would have been particularly interesting if the
authors had reported the effects of H. pylori infection on the responses
to other physiological agonists such as CCK or db-cAMP. The increased
pepsinogen levels in vivo represents the integrated stimulated response of
chief cells, particularly under the influence of the hypergastrinaemia
typical of H. pylori. As such it would have been more relevant to
determine if H. pylori infection altered stimulated rather than basal
pepsinogen, especially as the authors subsequently demonstrated that H.
pylori enhanced db-cAMP in vitro.
Despite the overall pattern of the results, there is striking variability
in the stimulatory effects of H. pylori in the paper. There is a >160%
difference in the stimulatory effects of H. pylori between the experiments
reported in figures 1 and 3 on one hand and figures 2, 5 and 6 on the
other. This absolute difference is greater than the stimulatory effects of
the other physiological agonists. The authors do not account for this
difference; it does not appear to be due differences in recognised H.
pylori virulence factors. If is due to differences in bacterial strains,
it would have been most appropriate to use a consistent strain throughout.
If genuine biological variability explains the difference, it is striking
that it is not manifest in the other stimulated results.
The results are generally consistent with the authors’ assumptions that H.
pylori acts via a Ca++/NO/cGMP-dependent pathway, but in view of the lack
specific controls, the data are not as convincing as the authors contend.
Whilst the inhibition of pepsinogen release by removal of extracelllular
calcium and the additive effect to histamine but not carbachol-stimulated
pepsinogen secretion are supportive of a calcium-dependent pathway, the
lack of control data on the effect of calcium removal on histamine or db-
cAMP-stimulated release does not exclude this being a non-specific effect.
Beil et al showed that either a calmodulin antagonist or inhibition of
Ca++ flux across membranes with lanthanum significantly inhibited
pepsinogen secretion, whether primarily stimulated by H. pylori, a calcium
ionopohore, db-cAMP or direct activation of protein kinase C.[1] This
suggests that calcium flux and calmodulin activation may be an important
final common pathway in pepsinogen secretion and not specific for H.
pylori as suggested by Lorente et al. Similarly although the data do
suggest that nitric oxide and cGMP generation are involved in mediating
the effects of H. pylori, the data in figure 7 and table 2 do not show a
dose response between [cGMP] and pepsinogen release as would be expected
if the two were directly related. An alternative explanation would be that
L-NMMA has wider inhibitory actions that could have been explored by
testing the effects against histamine-stimulated secretion. It is
interesting that Lorente et al failed to find any enhancement of CCK or
carbachol-stimulated release even at submaximal H. pylori concentrations,
they interpret this as implying that H. pylori activates identical
intracellular pathways as these two agonists. This is inconsistent with
the authors' previous work showing that EGF, which is also believed to
activate Ca++/NO/guanylate cyclase pathways,[2] as presently suggested for
H. pylori, had an additive effect with CCK-mediated stimulation.[3]
The authors’ explanation for the different pattern of effects between
histamine and db-cAMP is counterintuitive and inconsistent with available
data. They suggest that the failure of db-cAMP to augment H. pylori-
stimulated pepsinogen release is due to a dependence on Ca++ signalling
for db-cAMP but not histamine. Histamine-2 receptors, the subtype
apparently expressed on human chief cells,[4] are usually coupled to
activation of adenylate cyclase and generation of cAMP as a second
messenger,[5] thus it is difficult to postulate a signalling pathway
activated by db-cAMP acting as a cAMP analogue, which is not also
activated by histamine acting upstream. Conversely it has been shown
(although not yet definitively in chief cells) that the H2 receptor can
couple directly to inositol phosphate turnover and elevations in
[Ca2+]i[6] thus it is more likely that divergent pathways will be
activated by histamine than db-cAMP.
The study of the pathophysiological regulation of chief cell secretion has
been relatively neglected compared to acid or hormone secretion and I look
forward to further studies exploring the mechanisms responsible. It is
essential that such studies are designed to answer pertinent questions.
References (1) Beil W, Wagner S, Piller M, Heim HK, Sewing KF. Stimulation of
pepsinogen release from chief cells by Helicobacter pylori: evidence for a
role of calcium and calmodulin. Microb Pathog 1998;25:181-7.
(2) Fiorucci S, Lanfrancone L, Santucci L, Calabro A, Orsini B,
Frederici B, Morelli A. Epidermal growth factor modulates pepsinogen
secretion in guinea pig gastric chief cells. Gastroenterology 1996;111:945
-58.
(3) Serrano MT, Lanas A, Lorente S, Sainz R. Cytokine effects on
pepsinogen secretion from human peptic cells. Gut 1997;40:42-8.
(4) Lanas A, Anderson JW, Uemura N, Hirschowitz BI. Effects of
cholinergic, histaminergic, and peptidergic stimulation by isolated human
peptic cells. Scand J Gastroenterol 1994;29:678-83.
(5) Del Valle J, Gantz I. Novel insights into histamine H2 receptor
biology. Am J Physiol 1997;273:G987-96.
(6) DelValle J, Wang L, Gantz I, Yamada T. Characterization of H2
histamine receptor: linkage to both adenylate cyclase and [Ca2+]i
signaling systems. Am J Physiol 1992;263:G967-72.
In their letter de Jong et al (Gut 2001;49:874-875) state
that in IBD the efficacy and myelotoxicity of 6-mercaptopurine (6-MP)
and azathioprine (AZA) are related to the 6-thioguanine (6-TG) levels
achieved. It is thought that the 6-thioguanine nucleotides (6-TGN) are the
predominantly active metabolite of AZA/6-MP and that efficacy and
myelotoxicity seem to be related to 6-thioguanine metabolite level...
In their letter de Jong et al (Gut 2001;49:874-875) state
that in IBD the efficacy and myelotoxicity of 6-mercaptopurine (6-MP)
and azathioprine (AZA) are related to the 6-thioguanine (6-TG) levels
achieved. It is thought that the 6-thioguanine nucleotides (6-TGN) are the
predominantly active metabolite of AZA/6-MP and that efficacy and
myelotoxicity seem to be related to 6-thioguanine metabolite levels
(including 6-TGNs)[1]. It is important to note that in the literature the
abbreviation 6-TG can represent both 6-thioguanine and 6-thioguanine
metabolites. 6-Thioguanine is converted to the 6-TGNs by the enzyme
hypoxanthine phosphoribosyltransferase (HPRT). The subtle difference
between 6-thioguanine and 6-TGNs/metabolites is important as the study
quoted by de Jong et al[2] which has now been published in full[3] used 6-
thioguanine as an alternative to Crohn’s disease in patients resistant to
6-MP. 6-thioguanine is partly metabolised by the catabolic enzyme
thiopurine methyltransferase (TPMT)[3](in competition with HPRT) and in
this study Dubinski et al only included patients who had normal TPMT
activity. De Jong et al imply both in the title ("Why measure thiopurine
methyltransferase activity? Direct administration of 6-thioguanine might
be the alternative for 6-mercaptopurine or azathioprine”) and in the text
("6-TG dosing is feasible without measuring TPMT activity”) of their
letter that the use of 6-TG may obviate the need for pre-thiopurine TPMT
evaluation in patients with IBD. It is true to say that the case for
routine pre-thiopurine administration TPMT activity/genotyping remains
unproven but if one believes that TPMT status should be assessed for AZA
or 6-MP then the same must be true when using 6-TG as 6-TG is also partly
metabolized by TPMT. Further work is needed on the role of the 6-TGNs and
TPMT in optimising AZA/6-MP therapy and also on their role in 6-TG
administration.
References
(1) Cuffari C, Hunt S, Bayless TM. Enhanced bioavailability of
azathioprine compared to 6-mercaptopurine therapy in inflammatory bowel
disease: correlation with treatment efficacy. Aliment Pharmacol Ther
2000;14:1009-14
(2) Dubinsky MC, Hassard PV, Abreu MT, et al. Thioguanine (6-TG): a
therapeutic alternative in a subgroup of IBD patients failing 6-
mercaptopurine (6-MP). Gastroenterology 2000;118:A891
(3) Dubinsky MC, Hassard PV, Seidman EG, et al. An open-label pilot study
using thioguanine as a therapeutic alternative in Crohn’s disease patients
resistant to 6-mercaptopurine therapy. Inflamm Bowel Dis 2001;7(3):181-189
Dr. Ely seems to have confounded the definition of "high grade
component" with that of "high grade MALT lymphoma" in our paper. Based on
the previous study by de Jong and colleagues,[1] we used 1% cut off value
for the presence or absence of high grade component. When the high grade
component cells were less than 10% among the neoplastic lymphoid
population, such cases were categorized as low grad...
Dr. Ely seems to have confounded the definition of "high grade
component" with that of "high grade MALT lymphoma" in our paper. Based on
the previous study by de Jong and colleagues,[1] we used 1% cut off value
for the presence or absence of high grade component. When the high grade
component cells were less than 10% among the neoplastic lymphoid
population, such cases were categorized as low grade MALT lymphoma with a
focal high grade component. A diagnosis of high grade MALT lymphoma was
made when the high grade component cells exceeded 10% of the neoplastic
population.[1] A component of low grade MALT lymphoma was also observed
in all of our cases with high grade MALT lymphoma, as described in Results
in our paper. Therefore, according to the recently proposed WHO
classification of lymphoid neoplasms,[2][3] our cases with high grade MALT
lymphoma were categorized into diffuse large B cell lymphoma plus areas of
marginal zone/MALT-type lymphoma.
In our paper, we demonstrated 5 cases with high grade lesions to have
achieved complete regression after eradication of H. pylori (2 with high
grade MALT lymphoma and 3 with low grade MALT lymphoma with a focal high
grade component). Recent publications have also reported such cases in
which high grade B cell gastric lymphoma regressed after eradication
therapy.[4][5][6][7] These observations suggest that high grade MALT
lymphoma (diffuse large B cell lymphoma with areas of marginal zone
lymphoma) in early stage possibly responds to H. pylori eradication.
Further clinicopathologic studies, including molecular genetic analyses,
in a large number of patients are necessary.
(1) de Jong D, Boot H, van Heerde P, et al. Histological grading in gastric
lymphoma: pretreatment criteria and clinical relevance. Gastroenterology
1997;112:1466-74.
(2) Harris NL, Jaffe ES, Diebold J, et al. The World Health Organization
classification of neoplastic diseases of the hematopoietic and lymphoid
tissues: report of the Clinical Advisory Committee Meeting, Airlie House,
Virginia, November, 1997. Ann Oncol 1999;10:1419-32.
(3) Harris NL, Jaffe ES, Diebold J, et al. The World Health Organization
classification of hematologic malignancies report of the Clinical Advisory
Committee Meeting, Airlie House, Virginia, November 1997. Mod Pathol
2000;13:193-207.
(4) Rudolph B, Bayerdšrffer E, Ritter M, et al. Is the polymerase chain
reaction or cure of Helicobacter pylori infection of help in the
differential diagnosis of early gastric mucosa-associated lymphatic tissue
lymphoma? J Clin Oncol 1997;15:1104-9.
(5) Seymour JF, Anderson RP, Bhathal PS. Regression of gastric lymphoma with
therapy for Helicobacter pylori infection. Ann Intern Med 1997;127:247.
(6) Ng W-W, Lam C-P, Chau W-K, et al. Regression of high-grade gastric
mucosa-associated lymphoid tissue lymphoma with Helicobacter pylori after
triple antibiotic therapy. Gastrointest Endosc 2000;51:93-6.
(7) Morgner A, Miehlke S, Fischbach W, et al. Complete remission of primary
high-grade B-cell gastric lymphoma after cure of Helicobacter pylori
infection. J Clin Oncol 2001;19:2041-8.
Although it is valuable in some respects, the study from Nakamura et al (Gut 2001;48:454-460) highlights and potentially exacerbates a critical stumbling block in the diagnosis and treatment of gastric lymphomas.
The authors divide gastric "MALT" lymphomas into low grade and high grade, based on the absence or presence of, "... clusters or sheets of large cells [comprising] at least 1% of the neopla...
Although it is valuable in some respects, the study from Nakamura et al (Gut 2001;48:454-460) highlights and potentially exacerbates a critical stumbling block in the diagnosis and treatment of gastric lymphomas.
The authors divide gastric "MALT" lymphomas into low grade and high grade, based on the absence or presence of, "... clusters or sheets of large cells [comprising] at least 1% of the neoplastic lymphoid population." Although the 1% cut off was used in a previous study, one would be hard pressed to find a hematopathologist who would call such a
lesion "high grade" in clinical practice. Because marginal zone lymphomas tend to remain localized and often respond to antibiotic therapy, while diffuse large B cell lymphomas have aggressive behavior and do not respond
to antibiotics, muddying the waters by the promulgation of the ambiguous term "high grade MALT lymphoma" is a practice that should be discouraged.
Indeed, in order to avoid confusion between marginal zone lymphoma and diffuse large B cell lymphoma, the authors of the upcoming WHO lymphoma classification have urged that marginal zone lymphomas be simply designated as such, and that they not be graded (Harris, et al, Mod Pathol
13;193-207:2000). Part of the reason for this is to underscore the very important distinction of marginal zone lymphoma ("MALT"), an indolent entity that may respond to antibiotics, from diffuse large B cell lymphoma, an aggressive entity that requires surgery and/or multi-agent
chemotherapy.
Lastly, I would like to add that I was prompted to write this letter by a real life manifestation of the type of confusion I attempt to point out. On the day that the Nakamura article was published, I diagnosed a gastric diffuse large B cell lymphoma via an endoscopic biopsy. When I explained to the submitting gastroenterologist that this lymphoma would not respond to antibiotic therapy, he countered with, "There's a paper in today's Gut that says it will. It says that MALT lymphomas will respond,
as long as they're superficial, regardless of grade."
Sadly, a week later I received the patient's bone marrow biopsy, which was completely overtaken by an aggressive diffuse large B cell lymphoma.
The Therapy Update in the May issue highlighted the potential role for
antibiotic therapy in Crohn's disease [1]. Dr Colombel
indicated the need for appropriate antibiotics that are based on current
theories of pathogenesis, namely that they be effective against both
extracellular and intracellular bacteria. The possible role of
Mycobacterium paratuberculosis, although controversial, also should not be
overl...
The Therapy Update in the May issue highlighted the potential role for
antibiotic therapy in Crohn's disease [1]. Dr Colombel
indicated the need for appropriate antibiotics that are based on current
theories of pathogenesis, namely that they be effective against both
extracellular and intracellular bacteria. The possible role of
Mycobacterium paratuberculosis, although controversial, also should not be
overlooked. The review also emphasised that trials of antibiotics should
be of sufficiently long duration to demonstrate any possible benefit.
Based on the observational study of Gui et al,[2] in August 1999 we
commenced a suitably powered Australian multicentre, placebo-controlled,
double-blind trial of clarithromycin, rifabutin and clofazimine in active
Crohn's disease. All subjects receive a tapering regimen of prednisolone
on entry in addition to either antibiotics or matching placebos. If
remission is achieved at 16 weeks, and prednisolone withdrawn, subjects
continue their trial medications for 2 years. There is then a further one
year of clinical and colonoscopic follow-up. The aim of the study is to
determine whether this antibiotic therapy has a long-term benefit for
patients with Crohn's disease. The primary endpoints are relapse rates at
one, two and three years. The latter is particularly important to see if
there is an effect on the natural history of the disorder. Secondary
endpoints include remission at 4 months, safety and quality of life.
As of May 2001, 171 of the 212 subjects required have been enrolled.
Recruitment will continue until the end of July. To date, the likelihood
of being in remission at 16 weeks and continuing in the study is 60%. Once
past this point, 92% are ongoing. Only five patients have been withdrawn
for probable reactions to the trial medication, four with elevated liver
enzymes and one who developed a rash. An Independent Data Monitoring
Committee, which recently conducted the first interim analysis,
unanimously recommended that the trial continue.
Because of the necessary length of therapy the results will not be known
until 2004. The IDMC will continue to assess the progress. We believe this
study will answer the important questions in the treatment of Crohn's
disease raised by Dr Colombel.
W Selby
B Crotty
T Florin
P Pavli
Steering Committee for the Australian IBD Interest Group
References
(1) Colombel J-F, Cortot A, Van Kruiningen HJ. Antibiotics in
Crohn's disease.
(2) Gui GPH, Thomas PRS, Tizard MLV, Lake J, Sanderson JD,
Hermon-Taylor J. Two-year-outcomes analysis of Crohn's disease treated
with rifabutin and macrolide antibiotics. J Antimicrobial chemotherapy
1997;39:393-400.
As therapy of HIV patients with HAART has resulted in long-term
survival, the major burden of "disease" is becoming end-stage liver disease
secondary to HCV infection with rapidly progressive fibrosis and
cirrhosis. We are increasingly being asked to advise on this group of
patients, however, the literature is cautious about treatment and response
rates. Who do we treat? What is the response rate to ac...
As therapy of HIV patients with HAART has resulted in long-term
survival, the major burden of "disease" is becoming end-stage liver disease
secondary to HCV infection with rapidly progressive fibrosis and
cirrhosis. We are increasingly being asked to advise on this group of
patients, however, the literature is cautious about treatment and response
rates. Who do we treat? What is the response rate to achieve HCV
clearance? What are the risks of potential HIV decompensation? Interferon
monotherapy (incl PEG-Inf) or combination therapy?
Should the guidelines include special interest groups such as HCV/HIV
and HCV/HBV co-infections?
Dr Frank Weilert
Gastroenterolist
Waikato Hospital
Hamilton
New Zealand
Editor,
Thoracic outlet syndrome is frequently undiagnosed in patients with
non-cardiac ,non-coronary chest pains.
See www.tos-syndrome.com. Patients with depression or panic attacks can
have associated Thoracic Outlet Syndrome. The diagnosis will remain ignored
unless the symptoms and physical findings are elicited in these patients.
We read with great interest the article of Rasquin-Weber et al (1),
by the title “childhood functional gastrointestinal disorders” in which
the authors try to define criteria for functional gastrointestinal
disorders in infancy, childhood and adolescence. In this paper the authors
consider abdominal migraine as a distinct subgroup of recurrent abdominal
pain. Even though it is known for a l...
We read with great interest the article of Rasquin-Weber et al (1),
by the title “childhood functional gastrointestinal disorders” in which
the authors try to define criteria for functional gastrointestinal
disorders in infancy, childhood and adolescence. In this paper the authors
consider abdominal migraine as a distinct subgroup of recurrent abdominal
pain. Even though it is known for a long time that headache is often
associated with abdominal pain, the existence of abdominal migraine as an
entity is not universally accepted yet (2,3). A present, abdominal
migraine is considered as an episodic disorder with a particular
predilection for time of onset (early in the morning) and is associated
with autonomic features that are clearly lacking in the most children with
recurrent abdominal pain (4).
In a recent study of 475 children, 4 – 14 years of age, with recurrent
abdominal pain (unpublished data) we found only three children, 5, 6 and 8
years old respectively with migraine (two of them with a positive family
history of migraine) and 21 with sporadic episodes of headache, in
correlation with other gastrointestinal symptoms, such as nausea,
vomiting, early satiety etc.
We consider that abdominal migraine is not a distinct entity but a well-
known disorder, which is associated with gastrointestinal manifestations
as happens in asthma and eczema (5,6).
The authors also consider aerophagia as another subgroup of abdominal
pain. Aerophagia is characterized by progressive abdominal distension
during the day, non-distended abdomen in the morning and visible air
swallowing. It is a vary rare condition and only a few cases of known or
unknown origin have been published in the international literature (7,8).
We agree with Ruppin (9) that aerophagia is not a separate entity but only
a complaint met in different disorders such as ingestion of gas-producing
foods, gastric hypersecretion or bacterial overgrowth in the small
intestine.
Based on our experience and previous articles of Boyle (10) and Hyams and
Hyman (11) and until more data are available we suggest that we should
divide recurrent abdominal pain as in the table followed. It must be
stressed that Pediatricians should be familiarized with complaints such as
migraine and aerophagia and ask for these in any child with chronic
abdominal pain.
Chronic abdominal pain
1. Disordesrs with known pattern of symptoms
a. dyspepsia
b. irritable bowel syndrome
2. Disorders with non recognizable pattern of symptoms
a. paroxysmal or isolated
b. somatization of symptoms
c. psychologic or psychogenic disorders
d. Unspecified bowel disorder or idiopathic ?
Spiroglou K, Paroutoglou G#, Nikolaides N,#, Chatziparasidis G,
Demertzidou V, Giuleme O, Eugenides N#
Department of Pediatrics and Department of Gastroenterology#, Aristotelle
University of Thessaloniki, Hippocration Hospital, Thessaloniki, Greece
References
1. Rasquin-Weber A, Hyman PE, Cucchiara S, Fleisher DR, Hyams JS,
Milla PJ, Staiano A. Childhood functional gastrointestinal disorders. Gut
1999;45(suppl 2) : 1160-8
2. Symon DNK. Is there a place for “abdominal migraine” as a separate
entity in the HIS classification? Yes! Cephalalgia 1992;12:345-6
3. Hockaday JM. Is there a place for “abdominal migraine” as a separate
entity in the HIS classification? No! Cephalalgia 1992;12:346-8
4. Hyams JS, Hyman PE. Letter to the editor.Reply. J Pediatr 1999;135:401-
2
5. Caffarelli C, Deriu FM, Terzi V, Perrone F, de Angelis G, Atherton DJ.
Gastrointestinal symptoms in patients with asthma. Arch Dis Child
2000;82:131-5
6. Caffarelli C, Cavagni G, Deriu FM, Zamotti P, Atherton DJ.
Gastrointestinal symptoms in atopic eczema. Arch Dis Child 1998;78:230-4
7. Gauderer MW, Halpin TC Jr, Izant RJ Jr. Pathologic childhood
aerophagia: a recognizeble clinical entity. J Pediatr Surg 1981;16:301-5
8. Lecine T, Michaud L, Gottrand F, Faure C, Bonnevalle M, Vaudour G, Turk
D. Children who swallow air. Arch Pediatr 1998;5:1224-8
9. Ruppin H. Meteorism. Fortsschr Med 1991;109:421-3
10. Boyle JT. Recurrent abdominal pain: an update. Pediatr Rev 1997;18:310-21
11. Hyams JS, Hyman E. Recurrent abdominal pain and the biopsychosocial
model of medical practice. J Pediatr 1998;133:473-8
Dear Editor
The paper by Lorente et al (Gut 2000; 50: 13-18) demonstrates that H. pylori stimulates pepsinogen release from human chief cells in vitro. The precision of the results obtained from cells from 70 different subjects is to be complimented but several aspects of presentation and interpretation require further discussion.
The authors report no differences in basal or H. pylori-stimulated pepsinogen...
Dear Editor
In their letter de Jong et al (Gut 2001;49:874-875) state that in IBD the efficacy and myelotoxicity of 6-mercaptopurine (6-MP) and azathioprine (AZA) are related to the 6-thioguanine (6-TG) levels achieved. It is thought that the 6-thioguanine nucleotides (6-TGN) are the predominantly active metabolite of AZA/6-MP and that efficacy and myelotoxicity seem to be related to 6-thioguanine metabolite level...
1) In the authors' studies, or replications by others, were anti-oxidants other than DA-9601 used (e.g. ascorbic acid)?
2) Have the authors a financial interest in DA-9601?
Dear Editor,
Dr. Ely seems to have confounded the definition of "high grade component" with that of "high grade MALT lymphoma" in our paper. Based on the previous study by de Jong and colleagues,[1] we used 1% cut off value for the presence or absence of high grade component. When the high grade component cells were less than 10% among the neoplastic lymphoid population, such cases were categorized as low grad...
Editor,
Although it is valuable in some respects, the study from Nakamura et al (Gut 2001;48:454-460) highlights and potentially exacerbates a critical stumbling block in the diagnosis and treatment of gastric lymphomas.
The authors divide gastric "MALT" lymphomas into low grade and high grade, based on the absence or presence of, "... clusters or sheets of large cells [comprising] at least 1% of the neopla...
The Therapy Update in the May issue highlighted the potential role for antibiotic therapy in Crohn's disease [1]. Dr Colombel indicated the need for appropriate antibiotics that are based on current theories of pathogenesis, namely that they be effective against both extracellular and intracellular bacteria. The possible role of Mycobacterium paratuberculosis, although controversial, also should not be overl...
Dear Editor,
As therapy of HIV patients with HAART has resulted in long-term survival, the major burden of "disease" is becoming end-stage liver disease secondary to HCV infection with rapidly progressive fibrosis and cirrhosis. We are increasingly being asked to advise on this group of patients, however, the literature is cautious about treatment and response rates. Who do we treat? What is the response rate to ac...
Editor,
Thoracic outlet syndrome is frequently undiagnosed in patients with non-cardiac ,non-coronary chest pains. See www.tos-syndrome.com. Patients with depression or panic attacks can have associated Thoracic Outlet Syndrome. The diagnosis will remain ignored unless the symptoms and physical findings are elicited in these patients.
Editor,
We read with great interest the article of Rasquin-Weber et al (1), by the title “childhood functional gastrointestinal disorders” in which the authors try to define criteria for functional gastrointestinal disorders in infancy, childhood and adolescence. In this paper the authors consider abdominal migraine as a distinct subgroup of recurrent abdominal pain. Even though it is known for a l...
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