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Recent eLetters

Displaying 11-20 letters out of 200 published

  1. Trismus, the first symptom in a challanging diagnosis of Tetanus

    Although Tetanus has become a rare disease in most of the developed countries it had been quite common disease with high mortality in the developing countries like India. We have seen a variety of presenting symptoms in patients who ultimately were diagnosed as Tetanus. Now of course it is rare to find a patient developing Tetanus because of the universal immunization against the same. The authors are right in expressing the concern in suspecting the diagnosis of Tetanus in this patient. A high index of suspession is needed to think of the possibility and start the management early to have the best prognosis

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  2. Ramaria rufescens photo

    The photo above the caption "Ramaria rufescens" is clearly not in the genus Ramaria, the "coral fungi". A quick Google search of the name would have revealed this. As an amateur mycologist, I find it hard to believe that this article received peer review by anyone with professional training in mycology.

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  3. mistake

    In trans sccaphoid perilunate dislocation as shown on the radiographs the lunate is not dorsaly dislocated.the lunate stays in its place the peri lunate carpal bones are dorsaly displaced.

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  4. Once again, the "the MRI sequence dilemma!"

    Many thanks go the authors for reporting this very interesting finding.

    A minor comment, please:

    Figure 1, although it is somewhat blurred and dark, the MRI sequence it contains seems be to the "T2 FLAIR" one, not the T1 with Gadolinium, as the manuscript reads. Therefore, the lesions it demonstrates are the non- suppressed hyper-intensities from the T2-weighted film (which is not shown).

    Thanks!

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  5. Associated hypoparathyroidism?

    Sir,

    Wilson's disease is known to directly affect parathyroid function resulting in hypoparathyroidism. In a patient with rickets, one would expect secondary hypoparathyroidism. Moreover, this patient likely suffered from vitamin D resistant rickets due to renal calcium and phosphate wasting. Were PTH and serum vitamin D levels assayed in this instance?

    Yours sincerely,

    Kushal Naha, MD

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  6. Details and Interpretation

    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

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  7. In response to Brunneroma with duodenojejunal intussusception: a rare cause of gastric outlet obstruction

    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

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  8. Breast implant-associated ALCL is ALK negative

    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.

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  9. Monad sign and air crescent sign are not synonyms

    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

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  10. Comment on 'Serotonin syndrome following levodopa treatment in diffuse Lewy body disease'

    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].

    Conflict of Interest:

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