Firstly, Dr Canavese and colleagues' interest in the guideline
document is much appreciated.
Before responding specifically, it is worth noting that there are two main
diagnostic decisions to make when a patient presents with suspected
chronic idiopathic inflammatory bowel disease (IBD): distinguishing IBD
from other causes of inflammation; and classifying IBD as ulcerative
colitis (UC) or Crohn's disease (CD). Even wit...
Firstly, Dr Canavese and colleagues' interest in the guideline
document is much appreciated.
Before responding specifically, it is worth noting that there are two main
diagnostic decisions to make when a patient presents with suspected
chronic idiopathic inflammatory bowel disease (IBD): distinguishing IBD
from other causes of inflammation; and classifying IBD as ulcerative
colitis (UC) or Crohn's disease (CD). Even with full clinical details,
comprehensive sampling, and assessment by a well-informed pathologist
there will be a significant minority of IBD biopsies that cannot be
classified confidently as UC or CD.[1, 2] There will also be a number
that cannot even be categorised as IBD or non-IBD. However, I agree
entirely that several other factors beyond the pathologist's control may
also contribute to diagnostic uncertainty. Indeed, the proven importance
of adequate clinical details and of thorough sampling are often noted in
clinical guidelines.[1, 3-8] For example, limited sampling within and
between sites may be one of the reasons why histopathologists are
apparently less successful at diagnosing CD than diagnosing UC.[7-9]
I also agree that pathologists have a responsibility to convey the level
of diagnostic certainty as clearly as possible to the clinical teams.
Proposed categories for the conclusion of an IBD biopsy report have been
included in the BSG guideline ("PAID" scheme, Table 14).[10] The
suggested terminology represents a consensus view on the best way to
express probability. Accordingly, its adoption is recommended.
Similarly, vague terms such as "in keeping with" are best avoided or used
sparingly (Table 13).[10]
Dr Canavese and colleagues' suggested solutions are helpful. I agree that
the pathologist should insist on a minimum standard of clinical input.
Indeed, provision of the endoscopy report to the pathologist will be
recommended strongly in a forthcoming guideline for clinicians.[11]
Similarly, identifiable deficiencies in the process should be noted by the
pathologist interpreting the biopsies, especially if they interfere with
assessment. Also, a statement in a histology report that repeat endoscopy
and sampling might be informative would oblige the clinician to consider
this option. However, enforcement of minimum clinical standards can be
difficult. Overall, better communication between pathologists and
clinicians, ideally in the setting of a regular clinicopathological
meeting, is an excellent way to enhance diagnostic accuracy.[4, 10, 12]
On a more general note, the scope and quality of IBD services and the
reasons for suboptimal management may vary within and between countries.
Attempts are being made to remedy the inconsistencies. Reassuringly, a UK
services standards document for IBD includes guidance on the use of
histopathology services and is cognisant both of the value of biopsy
assessment and of the importance of interaction between pathologists and
clinicians.[13]
Having read Kennedy et al's short report on finding increased neutrophil apoptosis in patients with chronic fatigue syndrome, I am
unable to agree with their conclusion that "these findings provide new
evidence that patients with CFS have an underlying abnormality in their
immune cells" [1]. They provide no evidence that the immune defect is
causative, and, on the contrary, there is a wealth of...
Having read Kennedy et al's short report on finding increased neutrophil apoptosis in patients with chronic fatigue syndrome, I am
unable to agree with their conclusion that "these findings provide new
evidence that patients with CFS have an underlying abnormality in their
immune cells" [1]. They provide no evidence that the immune defect is
causative, and, on the contrary, there is a wealth of data suggesting that
primary depressive illnesses are associated with immune function defects.
Research papers in neuropsychology journals over the last year have
described abnormalities of natural killer cell function, T cell function,
and neutrophil function in psychological stress, depression, and
associated loneliness [2-5]. As somebody who has spent an albeit
relatively short time working as an SHO in a CFS specialist ward, I would
suggest that a more likely explanation for the group's findings are that
CFS patients have a primary psychological disorder with the secondary
expected immune dysfunction predicted by the referenced papers above.
References
(1) Kennedy G, Spence V, Underwood C. Increased neutrophil apoptosis
in chronic fatigue syndrome. J Clin Pathol 2004;57:891-3.
(2) Frank MG, Hendricks SE, Burke WJ et al. Clinical response
augments NK cell activity independent of treatment modality. Psychol Med
2004 Apr; 34(3)491-8.
(3) Steptoe S, Owen N, Kunz-Ebrecht SR et al. Loneliness and
neuroendocrine, cardiovascular and inflammatory stress response in middle-
aged men and women. Psychoneuroendocrinology 2004 Jun 29(5)593-611.
(4) Silberman DM, Ayelli-Edgar V, Zorilla-Zubilete M et al. Impaired
T cell dependent humoral response and its relationship with T lymphocyte
sensitivity to stress hormones in a chronic mild stress model of
depression. Brain Behav Immuno 2004 Jan 18(1)81-90.
(5) Irie M, Asami S, Ikeda M et al. Depressive state relates to
female oxidative DNA damage via neutrophil activation. Biochem Biophys Res
Commun 2003 Nov 28;311(4)1014-18.
In their review article "Challenges and controversies in the
diagnosis of mesothelioma: Part 1. Cytology-only diagnosis, biopsies,
immunohistochemistry, discrimination between mesothelioma and reactive
mesothelial hyperplasia, and biomarkers", Henderson et al.1 describe and
illustrate "rod-like or cylindrical crystalloids as seen in numerous
mesothelial cells in the pleural effusion of a malignan...
In their review article "Challenges and controversies in the
diagnosis of mesothelioma: Part 1. Cytology-only diagnosis, biopsies,
immunohistochemistry, discrimination between mesothelioma and reactive
mesothelial hyperplasia, and biomarkers", Henderson et al.1 describe and
illustrate "rod-like or cylindrical crystalloids as seen in numerous
mesothelial cells in the pleural effusion of a malignant mesothelioma".
The authors state "so far as we are aware they have been reported only in
epithelioid malignant mesothelioma (MM)".
In an effort to clarify/correct the impression that these inclusions are
specifically associated with epithelioid MM, I report a series of 16
benign pleural fluids and 1 benign pericardial fluid each containing
mesothelial cells with these rod-like or crystalloid inclusions (Figure
1,2). None of the 17 patients had a diagnosis of MM and none developed MM
during follow-up (range from 1 to 7 yrs). The patients (13 males, 4
females) ranged from 13 to 91 years in age (median 78.5 yrs.) at
thoracentesis/ pericardiocentesis. Clinical diagnoses included congestive
heart failure, chronic renal disease, end stage liver disease, pneumonia,
and CLL. Three of the 17 patients had a diagnosis of carcinoma
(endometrioid endometrial, renal clear cell, and cutaneous squamous cell);
none of these tumors involved the effusion. Others have also reported
similar appearing crystalloids within mesothelial cells in effusions in a
variety of benign conditions. 2, 3
References:
1. Henderson DW, Reid G, Kao SC, et al. Challenges and controversies in
the diagnosis of mesothelioma: Part 1. Cytology-only diagnosis, biopsies,
immunohistochemistry, discrimination between mesothelioma and reactive
mesothelial hyperplasia, and biomarkers. J Clin Pathol 2013;66:847-853.
2. Zaharopoulos P, Wen JW, Wong J. Membranous lamellar cytoplasmic
inclusions in histiocytes and mesothelial cells of serous fluids. Acta
Cytol 1998;42:607-613.
3. Lang E, Uthman M. Pseudo-Gaucher cells in peritoneal fluid: An uncommon
manifestation of extramedullary hematopoiesis. Diagn Cytopathol
1999;20:379-381.
Please note Figs 1,2 (jpgs) have been emailed to Mr. Rinon along with
a copy of this letter.
Ian Chandler's response to this study, insisting that any immune
abnormality is secondary to depression is without scientific merit.
Several studies comparing ME/CFIDS patients with patients suffering
from clinical depression have found important physical differences. SPECT
brain imaging studies sh...
Ian Chandler's response to this study, insisting that any immune
abnormality is secondary to depression is without scientific merit.
Several studies comparing ME/CFIDS patients with patients suffering
from clinical depression have found important physical differences. SPECT
brain imaging studies show ME/CFIDS patients suffer from hypoperfusion
that gets worse, rather than better, after exercise, a pattern not found
in depressed patients.
Studies have also show a reduced pain threshold in ME/CFIDS patients,
which again responds to exercise in a manner opposite to that found in
healthy and depressed control groups - pain thresholds get lower, instead
of higher.
These studies amount to clinical confirmation of a simple but often-
ignored distinction. When people suffering from depression exercise they
feel better, when people suffering from ME/CFIDS exercise they feel much
worse, often for days afterwards.
As an adult male diagnosed with ME/CFIDS, I can tell you that few
things are more 'depressing' than encountering medical professionals like
Mr. Chandler, who discount all evidence of organic illness in ME/CFIDS
patients because of a willful, even perverse attachment to the belief that
our symptoms are 'all in our heads'.
To hold to that position despite all evidence to the contrary
demonstrates a mindset in which empathy and scientific curiosity are
markedly absent - in other words, a mindset uniquely unsuited for
responsible diagnosis and treatment of complex illnesses like this one.
Mr. Chandler's position is one which cannot be altered by encounters
with contrary facts. If presented with undisputable evidence of, say,
chronic bacterial infection in a patient with ME/CFIDS, Mr. Chandler will
acknowledge the infection but deny that it has anything at all to do with
ME/CFIDS itself.
Do depressed people experience symptom remission when treated with
Ampligen, an immune-modulating drug? Do depressed people regain their
health and vitality after long-courses of antibiotics? The answer, of
course, is no. Patients with ME/CFIDS, however, do.
Mr. Chandler would no doubt object that the studies demonstrating
this improvement are not large enough to be considered definitive. The
point, of course, is that views such as his are the primary reason that
adequate research budgets for these illnesses are not forthcoming.
Answers to the letter
Dear Dr. Sir.
1. We confirmed that the patient was 79 years-old man on case 2. As the
mitosis index and the Ki-67 labeling index were estimated with newly
prepared sections, the indices were a bit different. We confirmed that
the tumor cells were focally positive for chromogranin-A, but negative for
synaptophysin on case 2.
2. Certainly, at the writing step of the review article (ref.3), the
progno...
Answers to the letter
Dear Dr. Sir.
1. We confirmed that the patient was 79 years-old man on case 2. As the
mitosis index and the Ki-67 labeling index were estimated with newly
prepared sections, the indices were a bit different. We confirmed that
the tumor cells were focally positive for chromogranin-A, but negative for
synaptophysin on case 2.
2. Certainly, at the writing step of the review article (ref.3), the
prognosis of our series of M-LCNEC was relatively good, but the prognosis
became worse one year after that time. We concluded that the prognosis of
M-LCNEC was relatively worse, like the LCNEC of other organs, in this
recent paper (ref. 1). Moreover, we confirmed that three cases of M-LCNEC
were positive for thyroid transcription factor(TTF)-1.
3. We confirmed that the age ranged from 52 to 74 years old in our M-LCNEC
series and that four patients were alive without disease (31 months, 18
months, 24 months and 90 months).
Dr. Kimihide Kusafuka, D.D.S., Ph.D.
Pathology Division, Shizuoka Cancer Center Hospital and Research Institute
It is disappointing to read Ian Chandler's comments on this work. Dr
Chandler's rather simplified logic seems to work like this:
- Depression is a psychiatric illness.
- Immunological abnormalities can be found in depression.
- CFS is also a psychiatric disorder and so there is no point in
measuring immunological parameters because any findings will be redundant.
CFS remains a debilitating condition for which more pathological data
is desperately needed. Psychiatric studies, whilst having been of value in
the past, are failing to provide new insight into disease aetiology, nor
are they providing effective treatments, particularly for those patients
who are most seriously affected by the condition.
Immunological profiling will undoubtedly lead to immunomodulatory
interventions for a number of medical conditions. Perhaps one of these
will be CFS, perhaps not. It may even be the case for certain subgroups
with clinical depression. The point is, we'll never know unless we
encourage this type of research.
I hope that medical professionals like Dr Chandler are prepared to
adjust their views on CFS if and when further findings are published.
I entirely agree with the authors of 'A Survey of reporting of
colorectal cancer in Scotland: compliance with guidelines and effect of
proforma reporting'1 that proforma reporting should be standard across
Scotland for reporting colorectal caner excision specimens. Although
obvious, I feel it should be stated the 2007 RCPath dataset standards 2
were issued for a symptomatic population and, as stat...
I entirely agree with the authors of 'A Survey of reporting of
colorectal cancer in Scotland: compliance with guidelines and effect of
proforma reporting'1 that proforma reporting should be standard across
Scotland for reporting colorectal caner excision specimens. Although
obvious, I feel it should be stated the 2007 RCPath dataset standards 2
were issued for a symptomatic population and, as stated in the study,
these audited cases were both screening and symptomatic. Also, in their
conclusions they allude to the potential impact that neo-adjuvant therapy
could play in Serosal Involvement (SI), Lymph node retrieval and
extramural venous invasion (EMVI) but state that this aspect could not be
accurately assessed in this study. All reported cases in our Health Board
are staged using TNM5 and, as such, will be prefixed with 'y' to identify
them as having had neo-adjuvant therapy. If this was not known prior to
reporting, a supplementary report will be issued after the case has
undergone MDT discussion when the patient history is reviewed. This may
be unique to our health board but, as it is part of the RCPath dataset, it
should also be recorded.
I do find the wording used in 'What this paper adds', where it states
that "....this is likely to have serious adverse consequences for patient
care." hard to extract from the data presented and this claim is not
reported in the article by the authors themselves. The data suggests that
there may be a group of patients that are falsely node 'negative' due to
insufficient nodal sampling and a further group in whom the EMVI or SI is
not identified. However, it does not state the cross over between these
groups or if the ones 'missing' the EMVI/SI are node positive patients.
Taken together this suggests that a small percentage of patients may have
been excluded the option of adjuvant therapy, but without looking at
specific patient outcomes and the case slides is it fair to label this as
'serious adverse consequences for patient care'?
I do look forward to the results of the repeat data collection which
will, hopefully, show proformas being used across all NHS Scotland boards
as well as an uplift in the percentage of boards reaching all the
standards. Further investigation of a national electronic dataset would
also be welcomed especially if the data required for such audits can be
extracted easily and possibly centrally from this. Given the existence of
one in Norway maybe we should be moving to access that and use it
throughout Scotland? I am sure the follow up audit will also take into
account the influences of neo-adjuvant therapies on the audited adverse
factors in the rectum, a treatment which is an established local practice,
but also the emerging use of neo-adjuvant therapy in advanced colonic
cancers. These data could be collated to allow reporting of all cases
together and in different cohorts (Treatment naive V's neo-adjuvant) to
try to identify the changes attributable to therapy.
Conflict of Interest:
I report GI resection specimens in a health board in Scotland that provided raw data for this survey. (Our board median nodal count is above 17 for both colonic and rectal excisions including post treatment cases)
I welcome the latest research on neutrophil
apoptosis from a educated, experienced, and motivated M.E. expert.
I am very concerned, and thoroughly disappointed again, that, despite
the concerns raised, by hundreds of well educated people, involved with
M.E. worldwide, for many years, someone who ha...
I welcome the latest research on neutrophil
apoptosis from a educated, experienced, and motivated M.E. expert.
I am very concerned, and thoroughly disappointed again, that, despite
the concerns raised, by hundreds of well educated people, involved with
M.E. worldwide, for many years, someone who has admitted to being "quite
new" to a SHO post, on a Chronic Fatigue ward, has assumed, that he has
the authority and education, to criticise the outcome of this research, at
this stage, when most people admit they are not 100% sure about the
aetiology M.E.
This seems to be a pre-determined blinkered
attitude, that screams out "l know all there is to know". I will not tolerate,
on behalf of the members of the M.E.Association, the approach
perpetrated by information solely provided by the Psychiatrists, who have
continually reported, that M.E. is an illness belief, that one has a real
illness that must not be encouraged, by validating, or providing medical
testing, for a non-illness.
The Department of Health have on many occasions, declared
that they are duty bound, to take account of all national and international
information and evidence, from all sources so as to provide as broad a spectrum of ideas and treatment plans as
is reasonable. And to provide the least damaging and most helpful, practical
treatment or advice for all. The Canadian Guidelines have the potential to be adapted for world
wide use, but l have been told the government appears to use international advice only, when it suits
them, and ignore it when it suits patients.
Has the DOH considered fully, the possible financial implications,
for us all, if there is no research into the physical, epidemiological and
biological cause of M.E.?
This has resulted in many cases of long term physical damage,<see 25%
Report 2002-2004> which has resulted in the death of hundreds of people
every year.
A high proportion are those have been young adults, who have been
constantly, denied referrals, to the independent, M.E. specialists that we
have in our files.
The correspondent points out that the RCPath standards of 2007 were
written for a symptomatic population. This is not specifically stated in
the standards, which were written just as the UK pilots of FOB screening
were concluding. The current proposed standards (2014) are still in draft
stage. It seems clear however that it will apply equally to all cancers.
The issue of the effect of preoperative therapy on reporting of...
The correspondent points out that the RCPath standards of 2007 were
written for a symptomatic population. This is not specifically stated in
the standards, which were written just as the UK pilots of FOB screening
were concluding. The current proposed standards (2014) are still in draft
stage. It seems clear however that it will apply equally to all cancers.
The issue of the effect of preoperative therapy on reporting of SI, EMVI
and node number is important. Unfortunately in our retrospective audit the
use of the prefix "y" in staging patients who have had preoperative
therapy was not universally applied. It is also true that in many units,
including our own, the pathologist is not always informed that the patient
has been treated by an oncologist. A tighter prospective study is needed.
It should be noted that the revised national standards do not make any
allowance for the effect of chemotherapy and radiotherapy.
The comment that the failure of some units to meet minimum standards
"....is likely to have serious adverse consequences for patient care" is ,
we feel, justified. There is significant crossover in under-reporting as
can be seen by inspection of the tabulated data. Unit 10 on our tables,
for example, did not report serosal invasion in any rectal cancer, reports
only 10% EMVI and has a mean node yield of 5 for rectum and 10 for colon.
It is certain that this will have led to understaging and possibly to
denial of treatment to patients who would have benefitted.
I agree that electronic reporting systems would be a major asset.
We would certainly hope to ask for documentation of preoperative treatment
in our follow-up audit!
In his letter of the letter 18th August 2004, Dr Chandler makes some
interesting comments on our paper “Increased neutrophil apoptosis in
chronic fatigue syndrome” [1]. He states that “a more likely explanation
for the group's findings are that CFS patients have a primary
psychological disorder with the secondary expected immune dysfunction”. We
strongly disagree with this statement.
In his letter of the letter 18th August 2004, Dr Chandler makes some
interesting comments on our paper “Increased neutrophil apoptosis in
chronic fatigue syndrome” [1]. He states that “a more likely explanation
for the group's findings are that CFS patients have a primary
psychological disorder with the secondary expected immune dysfunction”. We
strongly disagree with this statement.
It is noteworthy that many research findings that support a physical
basis to CFS are constantly under attack and are commonly reduced to the
lowest common denominator i.e. that CFS is “psychological in origin”. Dr
Chandler comments that, “there is a wealth of data suggesting that primary
depressive illnesses are associated with immune function defects”. That
may be true, however, we are not aware of a study which shows that
neutrophils are significantly apoptotic in depressed patients and that
this is associated with an increase in the pro-inflammatory cytokine,
transforming growth factor â-1. Furthermore, the CFS patients in our study
were not depressed or excessively anxious and we have already reported on
their psychological status in a separate report [2]. Indeed, three groups
of CFS patients are mentioned in that report [2]: those with self-reported
symptoms which developed sporadically (CFS, n =48); after Gulf War service
(GW, n =24); and following exposure to organophosphate insecticides (OP, n
=25). All of these patients underwent a clinical examination which
included psychiatric status, they all completed the MOS SF-36 quality of
life and Hospital Anxiety and Depression scales, and fulfilled major and
minor criteria for CDC-1994 CFS. The GW and OP cohorts had significant
impairments to both emotional and mental health measures (GW > OP) when
compared to their own controls and to the sporadic CFS patients. We have
not yet reported on the neutrophil apoptosis data on the GW and OP
patients (or in other studies of their lymphocyte function) but neither
cohort had any difference in the percentage of neutrophils undergoing
apoptosis when compared with their respective controls. We additionally
found that the GW and OP cohorts had no difference in the percentages of
tumour necrosis factor receptor-1 death receptor molecules expressed on
their neutrophils or levels of platelet poor plasma activated transforming
growth factor â-1. This data is at variance with Dr Chandlers comment that
“a more likely explanation for the group's findings are that CFS patients
have a primary psychological disorder”.
What is clear is that the term CFS is heterogeneous and lacks
specificity as others have reported [3, 4]. The CFS patients in our study
should more accurately be described as those having myalgic
encephalomyelitis (ME) as defined by Ramsay [5] which has recently been
reported to be operationally distinct from those with chronic fatigue and
chronic fatigue syndrome [6] especially in the neurological and
neuropsychiatric areas reported in our recent study [2]. Fatigue is a
symptom and not a disease and, ultimately, “an operational CFS case
definition will need to be based on empirical studies designed to
delineate the possibly distinct biological pathways that result in
illness” [3]: such a case definition already exists [7]. Our paper on
increased neutrophil apoptosis in a specific subset of patients within the
CFS construct goes some way to assisting in this process of
classification.
References
(1) Kennedy G, Spence V, Underwood C. Increased neutrophil apoptosis
in chronic fatigue syndrome. J Clinical Pathology 2004; 57: 891-3
(2) Kennedy G, Abbot NC, Spence V, Underwood C, Belch JJF. The
specificity of the CDC-1994 criteria for chronic fatigue syndrome: a
comparison of health status in three groups of patients who fulfill the
criteria. Annals of Epidemiology 2004; 14: 95-100
(3) Reeves WC, Lloyd A, Vernon SD et al. Identification of
ambiguities in the 1994 chronic fatigue syndrome research case definition
and recommendations for resolution. BMC Health Services Research 2003,
3:25
(4) Jason LA, King CP, Richman JA, et al. US case definition of
Chronic Fatigue Syndrome: Diagnostic and theoretical issues. J Chronic
Fatigue Syndrome 1999; 5: 3–33.
(5) Ramsay, M. A. (1988). Myalgic encephalomyelitis and post-viral
fatigue states: The saga of Royal Free disease (2nd ed.). Hampshire, UK:
Gower.
(6) Jason LA, Helgerson J, Torres-Harding SR et al. Variability in
diagnostic criteria for chronic fatigue syndrome may result in substantial
differences in patterns of symptoms and disability. Evaluation & the
Health Professions 2003; 26: 3-22
(7) Carruthers BM, Jain AK, De Meirleir KL, Peterson DL, Klimas NG,
Lerner AM, et al. Myalgic encephalomyelitis/chronic fatigue syndrome:
Clinical working case definition, diagnostic and treatment protocols. J
Chronic Fatigue Syndrome 2003; 11: 7–116.
Firstly, Dr Canavese and colleagues' interest in the guideline document is much appreciated. Before responding specifically, it is worth noting that there are two main diagnostic decisions to make when a patient presents with suspected chronic idiopathic inflammatory bowel disease (IBD): distinguishing IBD from other causes of inflammation; and classifying IBD as ulcerative colitis (UC) or Crohn's disease (CD). Even wit...
Dear Editor
Having read Kennedy et al's short report on finding increased neutrophil apoptosis in patients with chronic fatigue syndrome, I am unable to agree with their conclusion that "these findings provide new evidence that patients with CFS have an underlying abnormality in their immune cells" [1]. They provide no evidence that the immune defect is causative, and, on the contrary, there is a wealth of...
To the Editor:
In their review article "Challenges and controversies in the diagnosis of mesothelioma: Part 1. Cytology-only diagnosis, biopsies, immunohistochemistry, discrimination between mesothelioma and reactive mesothelial hyperplasia, and biomarkers", Henderson et al.1 describe and illustrate "rod-like or cylindrical crystalloids as seen in numerous mesothelial cells in the pleural effusion of a malignan...
Dear Editor
Ian Chandler's response to this study, insisting that any immune abnormality is secondary to depression is without scientific merit.
Several studies comparing ME/CFIDS patients with patients suffering from clinical depression have found important physical differences. SPECT brain imaging studies sh...
Answers to the letter Dear Dr. Sir. 1. We confirmed that the patient was 79 years-old man on case 2. As the mitosis index and the Ki-67 labeling index were estimated with newly prepared sections, the indices were a bit different. We confirmed that the tumor cells were focally positive for chromogranin-A, but negative for synaptophysin on case 2. 2. Certainly, at the writing step of the review article (ref.3), the progno...
Dear Editor
It is disappointing to read Ian Chandler's comments on this work. Dr Chandler's rather simplified logic seems to work like this:
- Depression is a psychiatric illness.
- Immunological abnormalities can be found in depression.
- CFS is also a psychiatric disorder and so there is no point in measuring immunological parameters because any findings will be redundant.
...
Dear Editor,
I entirely agree with the authors of 'A Survey of reporting of colorectal cancer in Scotland: compliance with guidelines and effect of proforma reporting'1 that proforma reporting should be standard across Scotland for reporting colorectal caner excision specimens. Although obvious, I feel it should be stated the 2007 RCPath dataset standards 2 were issued for a symptomatic population and, as stat...
Dear Editor
I welcome the latest research on neutrophil apoptosis from a educated, experienced, and motivated M.E. expert.
I am very concerned, and thoroughly disappointed again, that, despite the concerns raised, by hundreds of well educated people, involved with M.E. worldwide, for many years, someone who ha...
The correspondent points out that the RCPath standards of 2007 were written for a symptomatic population. This is not specifically stated in the standards, which were written just as the UK pilots of FOB screening were concluding. The current proposed standards (2014) are still in draft stage. It seems clear however that it will apply equally to all cancers. The issue of the effect of preoperative therapy on reporting of...
Dear Editor
In his letter of the letter 18th August 2004, Dr Chandler makes some interesting comments on our paper “Increased neutrophil apoptosis in chronic fatigue syndrome” [1]. He states that “a more likely explanation for the group's findings are that CFS patients have a primary psychological disorder with the secondary expected immune dysfunction”. We strongly disagree with this statement.
It is n...
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