In this BMJ case report the authors make conclusions which would
shame a medical or dental undergraduate student.
They dismiss the long term epidemiological data which demonstrates no
increase in incidence of or mortality from infective endocarditis since
the introduction of the NICE guidelinesseveral years ago, using a highly
spurious explanation suggesting that dentists are somehow identifying the
most at risk patients...
In this BMJ case report the authors make conclusions which would
shame a medical or dental undergraduate student.
They dismiss the long term epidemiological data which demonstrates no
increase in incidence of or mortality from infective endocarditis since
the introduction of the NICE guidelinesseveral years ago, using a highly
spurious explanation suggesting that dentists are somehow identifying the
most at risk patients and prescribing against the guidelines regardless.
At the same time they use one anecdotal case where a SBE was diagnosed ten
days after a dental intervention, and presented this as evidence against
the guidelines.
Tragic and all as this case was, there is absolutely no evidence presented
that the relationship to the dental intervention was anything more than a
coincidence.
As dentists we realise that oral commensal bacteraemias are a daily
occurrence in anybody with a natural dentition, as they occur when a
patient eats, brushes their teeth or even clenches and grinds their teeth.
The need for antibiotic prophylaxis prior to the NICE guidelines for
practically every dental intervention probably put such patients at
greater risk of death from SBE rather than the opposite, since they both
acted as a barrier to regular preventative dental care and helped ensure
that their oral commensals were multi antibiotic resistant in the event of
an actual SBE infection.
We, as healthcare professionals, want to do everything we reasonably can
to ensure our patients continued health and welfare.
If the epidemiological data ever suggests that a revision of these
guidelines is desirable, we will be the first to say so.
However we should not be swayed by others making unfounded assumptions
about a single tragic case which don't even satisfy the minimum standards
of scientific rigour.
Yours sincerely
Audoen Healy B Dent Sc, MGDS, FDS, FFGDP, DipImpDent RCS Eng.
Kushwaha et al (1) make the rather positive assertion, regarding the
cause of their patient's symptoms and a possible role of L-DOPA in their
genesis, that it is 'fact that levodopa can contribute to [ST]
occurrence.' Their writing seems to convey an unwarranted confidence in
the strength of this possible, but only remotely possible, association.
I remind readers that the definition of serotonin syndrome (a.k.a....
Kushwaha et al (1) make the rather positive assertion, regarding the
cause of their patient's symptoms and a possible role of L-DOPA in their
genesis, that it is 'fact that levodopa can contribute to [ST]
occurrence.' Their writing seems to convey an unwarranted confidence in
the strength of this possible, but only remotely possible, association.
I remind readers that the definition of serotonin syndrome (a.k.a.
serotonin toxicity) has always been that it is a prerequisite (included in
the benchmark 'Hunter" criteria (2)) that a known (potent) serotonergic
drug must have been administered shortly before symptoms emerge. This
definition became universally accepted ab initio because the
characteristic picture of ST has only ever been reliably described (in
'normal' subjects) following the ingestion of potently serotonergic drugs.
L-dopa is not a 'known serotonergic' drug and there is no evidence that it
produces significant release of serotonin in the human brain. Thus, their
case fails to qualify as ST by the very first criterion of the Hunter
system (Fig 1, (2)).
The authors have failed to adduce any evidence to support the
mechanism they speculate about because the 'supporting' reference they
quote (3) is a letter to a journal which reports no original scientific
data to support their contention: it is an evidence-poor speculation. It
is merely a hypothetical notion that might just possibly warrant
investigation. However it is noteworthy that in the ensuing four decades
no researchers appear to have found it worthy of pursuit and no other
evidence has emerged to support it. Furthermore, of the huge number of
patients (probably many millions) similarly treated over many decades
there are only a couple of rather doubtful case reports. That alone
strongly suggests that the picture reported owes more to the state of
those patients than to L-DOPA.
As a writer involved with many publications on this subject (as both
an author, advisor and referee) it is my common experience that authors
who do not have extensive familiarity with this subject frequently quote
sources which do not contain original data and are frequently speculations
and opinions propounded by people with modest experience or knowledge of
the topic. Such opinions are then reproduced by subsequent writers who
elevate the perception of their status by citing them without critical
comment and without noting that they constitute speculations that have a
scientific foundation that is non-existent or weak. Thus the literature
becomes populated by contributions that are most appropriately described
as rumours: they do not constitute science and have no place in a
'scientific' journal. In my experience there is a widespread failure by
referees to prevent authors from mis-representing references which do not
support the statements concerning which they are cited (or, worse still,
are completely irrelevant). Indeed, Kushwaha et al. mis-cite their two key
ST references, my own review paper (4) and the seminal paper of Dunkerley
et al. There is a widespread failure to recognise that these practices are
a serious academic failing, confuse and impoverish the literature and on
occasions can segue into academic fraud.
A comparable, relevant and topical example of this same type of
careless mis-citation error is the advice/warning about ondansetron (and
related drugs) issued by various regulatory agencies/authorities
(including the WHO, FDA, Health Canada and the Australian TGA). These
warnings are based on similar misconceptions and poor quality mis-quoted
and mis-understood second-hand evidence, as enumerated by Rojas-Fernandes
(5).
I suspect many experienced practitioners who treat organic brain
disease and dementia would agree that atypical side-effects are much more
frequent in this group compared to normal subjects (i.e. those without
organic brain disease). However, it is exceedingly doubtful that
extrapolating to the general population, from rare and unusual reactions
occurring in such cases, is a either a valid or a useful activity. I
suggest it is unlikely to inform us about patho-physiology or treatment:
but it is likely to cause confusion, especially among non-experts and less
critical readers.
References
1. Kushwaha, S, Panda, AK, Malhotra, HS, and Kaur, M, Serotonin
syndrome following levodopa treatment in diffuse Lewy body disease. BMJ
Case Rep, 2014. 2014.
2. Dunkley, EJC, Isbister, GK, Sibbritt, D, Dawson, AH, et al., Hunter
Serotonin Toxicity Criteria: a simple and accurate diagnostic decision
rule for serotonin toxicity. Q. J. Med., 2003. 96: p. 635-642.
3. Sandyk, R, L-Dopa induced "serotonin syndrome" in a parkinsonian
patient on bromocriptine. J Clin Psychopharmacol, 1986. 6([letter]): p.
194-195.
4. Gillman, PK, A review of serotonin toxicity data: implications for the
mechanisms of antidepressant drug action. Biol Psychiatry, 2006. 59(11):
p. 1046-51.
5. Rojas-Fernandes, C, Can 5-HT3 antagonists really contribute to
serotonin toxicity? A call for clarity and pharmacological law and order.
Drugs - Real World Outcomes, 2014: p. [in press].
Thank you for your very clear and concise case report of this elderly
patient who suffered a perforation of a previously undetected gastric
ulcer.
The Xrays and case are good from a basic teaching perspective, but
I'm a bit confused as to what the "learning point" is supposed to be.
What other clinical features would you have expected in the "non-elderly"
to indicate a perforated viscu...
Thank you for your very clear and concise case report of this elderly
patient who suffered a perforation of a previously undetected gastric
ulcer.
The Xrays and case are good from a basic teaching perspective, but
I'm a bit confused as to what the "learning point" is supposed to be.
What other clinical features would you have expected in the "non-elderly"
to indicate a perforated viscus other than worsening abdominal pain,
peritonism and shock? It is certainly good to be vigilant in the elderly
but I'm a bit concerned that this article is teaching us that "vigilance"
is akin to detecting a blow from a sledge-hammer!
I do agree that non-steroidals should be used with care in elderly
patients and in our practice in the UK we might give up to a week or two
(maximum), but always with Ranitidine or PPI cover. I would say this is
more of a learning point that is specific to Elderly Care. Please feel
free to respond to my query.
Yours Sincerely
An air crescent sign describes the crescent of air that can be seen in invasive aspergillosis, or other processes that cause pulmonary necrosis.It should not to be confused with the Monad sign which describes the air that surrounds an aspergilloma. Unfortunately, the air around the fungal ball is also crescent shaped and the term air crescent sign is often used interchangeably as in this case report
An air crescent sign describes the crescent of air that can be seen in invasive aspergillosis, or other processes that cause pulmonary necrosis.It should not to be confused with the Monad sign which describes the air that surrounds an aspergilloma. Unfortunately, the air around the fungal ball is also crescent shaped and the term air crescent sign is often used interchangeably as in this case report
sir,
I disagree with the author in calling them nodules.In fact they are
masses.
The x-ray findings are quite characteristics to be called as a spotter.
In a known case of malignancy elsewhere this is metastasis,unless proved
otherwise
If history is not known,which is the case most often,then it becomes
difficult to make a convincing diagnosis.Therefore a differential
diagnosis is a must.How to differentiate lung masses...
sir,
I disagree with the author in calling them nodules.In fact they are
masses.
The x-ray findings are quite characteristics to be called as a spotter.
In a known case of malignancy elsewhere this is metastasis,unless proved
otherwise
If history is not known,which is the case most often,then it becomes
difficult to make a convincing diagnosis.Therefore a differential
diagnosis is a must.How to differentiate lung masses from different
etiologies ? for eg.hydatid cyst.
Adding most common DD would make this case report complete.
dr.balachandran
The case report by Parthasarathy et al. illustrates that breast
implant-associated anaplastic large cell lymphoma (ALCL) can present as a
locally aggressive tumor mass, and that this tumor can be refractory to
chemotherapy and radiotherapy. In effect, the authors describe that the
tumor was finally felt to be controlled after radical mastectomy including
resection of the implant and its surrounding capsule.
The case report by Parthasarathy et al. illustrates that breast
implant-associated anaplastic large cell lymphoma (ALCL) can present as a
locally aggressive tumor mass, and that this tumor can be refractory to
chemotherapy and radiotherapy. In effect, the authors describe that the
tumor was finally felt to be controlled after radical mastectomy including
resection of the implant and its surrounding capsule.
The authors discuss that this tumor usually presents with an
effusion, and less frequently presents with a tumor mass like the case
that is reported. However, we believe the authors make one contradictory
and one inaccurate statement in the discussion.
First, the authors point on one hand that "The United States Food and
Drug Administration (FDA) noted a possible association between breast
implants and ALCL, and believed that women with breast implants had a
small but increased risk of developing ALCL adjacent to the implant." On
the other hand, later on the discussion, the authors appear to endorse the
opinion that "large clinical studies do not show an increased risk of
lymphoma in women with breast implant. Patients with breast implants
should not be unduly concerned about the risk of developing lymphoma, but
doctors should be wary of patients with breast implants presenting with
vague symptomatology, especially a persisting seroma or a mass lesion."
We believe these statements need to be reconciled.
Second, the authors state that "Cases associated with an effusion
within the implant capsule are typical ALK positive, while those
presenting with a solid mass, like our patient, are typically ALK
negative." The authors don't provide a reference for their statement,
that is also emphasized in the subheading of "Learning Points". In our
experience and in our review of the literature, breast implant-associated
ALCL presenting as an effusion or presenting as a mass appear to represent
different stages of the same disease, and are almost always ALK negative.
Thanks to Dr Kai Ivar M?ller and Dr Svein Ivar Bekkelund for their
very interesting case presented regarding Visual impairment and
posterior cortical atrophy preceding rapid progressive dementia. Posterior
cortical atrophy (PCA) is a neurodegenerative condition regarded as a
progressive loss of visual processing skills and other posterior
functions. Patients have difficulty integrating visual scenes, locating
objects...
Thanks to Dr Kai Ivar M?ller and Dr Svein Ivar Bekkelund for their
very interesting case presented regarding Visual impairment and
posterior cortical atrophy preceding rapid progressive dementia. Posterior
cortical atrophy (PCA) is a neurodegenerative condition regarded as a
progressive loss of visual processing skills and other posterior
functions. Patients have difficulty integrating visual scenes, locating
objects or identify them, and steer their environment.
Some of the symptoms quite often associated with parietal function
deficits symptoms such as calculating numbers, praxis and reading.
Diagnosis is often delayed in as symptoms can be difficult for the patient
to express and for the clinician to spot. Although the diagnosis is
particularly challenging in the earliest stages of the disease but in
general it depend on the clinical, features.
On direct comparison between Alzheimer's disease and PCA, there was no
difference in the distribution of amyloid, as measured by Pittsburgh
Compound B (PIB) PET (Dr. Rabinovici and his colleagues study). In
contrast, PCA patients showed more severe hypometabolism in occipital
cortex, concordant with their more severe visual dysfunction. Functional
imaging and fMRI, as well as structural imaging may help to better
understand network degeneration in AD variants.
REFERENCE:
Rosenbloom MH, Alkalay A, Rabinovici GD, et al. Distinct clinical and
metabolic deficits in PCA and AD are not related to amyloid distribution.
Neurology 2011; E-pub 2011 April 27.
Dr Os hammer MBBch.,MSC.,MRCPsych .,IAPA
I read with great interest the article concerning amplification of
ALK gene detected in a IMT of breast, largely because ALK gene
amplification was recently described in inflammatory breast cancer.
However, judging from the figure 3B illustrated, I suspect that a
rearrangement rather than amplification occur as most nuclei demonstrate
one yellow fused signal, one red signal and one green signal. ALK g...
I read with great interest the article concerning amplification of
ALK gene detected in a IMT of breast, largely because ALK gene
amplification was recently described in inflammatory breast cancer.
However, judging from the figure 3B illustrated, I suspect that a
rearrangement rather than amplification occur as most nuclei demonstrate
one yellow fused signal, one red signal and one green signal. ALK gene
translocation should be more commonly encountered in IMT in general.
I did like this case report- honestly. However, I required more
information to satisfy my curiosity of the case and had reluctance in
accepting the conclusion regarding how this case validates the possibility
that quetiapine is soley responsible for the apparent positive outcome. I
would prefer to know why in 2009 he decided he wanted to curtail his
drinking? Given that his recovery co-incided with a diagnosis of bi-polar...
I did like this case report- honestly. However, I required more
information to satisfy my curiosity of the case and had reluctance in
accepting the conclusion regarding how this case validates the possibility
that quetiapine is soley responsible for the apparent positive outcome. I
would prefer to know why in 2009 he decided he wanted to curtail his
drinking? Given that his recovery co-incided with a diagnosis of bi-polar
disorder and quetiapine whether any other interventions( counselling,
psychotherapy etc) occurred?
His persistently elevated GTT with normal Trans. No FBCor CDT, and no
mentioned liver disease diagnosis?
I put it forward that treatment of his bipolar disorder successfully-
regardless of the the 'drug-specific'is as likely , and has far more
evidence-base than the drug Que
In this BMJ case report the authors make conclusions which would shame a medical or dental undergraduate student. They dismiss the long term epidemiological data which demonstrates no increase in incidence of or mortality from infective endocarditis since the introduction of the NICE guidelinesseveral years ago, using a highly spurious explanation suggesting that dentists are somehow identifying the most at risk patients...
Kushwaha et al (1) make the rather positive assertion, regarding the cause of their patient's symptoms and a possible role of L-DOPA in their genesis, that it is 'fact that levodopa can contribute to [ST] occurrence.' Their writing seems to convey an unwarranted confidence in the strength of this possible, but only remotely possible, association.
I remind readers that the definition of serotonin syndrome (a.k.a....
Dear Dr Lobao
Thank you for your very clear and concise case report of this elderly patient who suffered a perforation of a previously undetected gastric ulcer.
The Xrays and case are good from a basic teaching perspective, but I'm a bit confused as to what the "learning point" is supposed to be. What other clinical features would you have expected in the "non-elderly" to indicate a perforated viscu...
Conflict of Interest:
...sir, I disagree with the author in calling them nodules.In fact they are masses. The x-ray findings are quite characteristics to be called as a spotter. In a known case of malignancy elsewhere this is metastasis,unless proved otherwise If history is not known,which is the case most often,then it becomes difficult to make a convincing diagnosis.Therefore a differential diagnosis is a must.How to differentiate lung masses...
The case report by Parthasarathy et al. illustrates that breast implant-associated anaplastic large cell lymphoma (ALCL) can present as a locally aggressive tumor mass, and that this tumor can be refractory to chemotherapy and radiotherapy. In effect, the authors describe that the tumor was finally felt to be controlled after radical mastectomy including resection of the implant and its surrounding capsule.
The...
Thanks to Dr Kai Ivar M?ller and Dr Svein Ivar Bekkelund for their very interesting case presented regarding Visual impairment and posterior cortical atrophy preceding rapid progressive dementia. Posterior cortical atrophy (PCA) is a neurodegenerative condition regarded as a progressive loss of visual processing skills and other posterior functions. Patients have difficulty integrating visual scenes, locating objects...
Dear Editor,
The photomicrograph in this case report is not that of a Brunner gland adenoma. It is of an adenomatous polyp of the surface epithelium.
Yours sincerely, Andrew Mitchell MD
Conflict of Interest:
None declared
Dear Sir,
I read with great interest the article concerning amplification of ALK gene detected in a IMT of breast, largely because ALK gene amplification was recently described in inflammatory breast cancer. However, judging from the figure 3B illustrated, I suspect that a rearrangement rather than amplification occur as most nuclei demonstrate one yellow fused signal, one red signal and one green signal. ALK g...
I did like this case report- honestly. However, I required more information to satisfy my curiosity of the case and had reluctance in accepting the conclusion regarding how this case validates the possibility that quetiapine is soley responsible for the apparent positive outcome. I would prefer to know why in 2009 he decided he wanted to curtail his drinking? Given that his recovery co-incided with a diagnosis of bi-polar...
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