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Recent eLetters

Displaying 1-10 letters out of 222 published

  1. Diagnosis unconfirmed

    This could possibly be anti-GBM disease, though bloody diarrhoea isn't a feature of that condition. But there wasn't a renal biopsy to confirm, or specificity tests on the antibody (e.g. Western blotting with it) so evidence is only the ELISA result. Most such assays encounter occasional false positives.

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  2. Neurosarcoidosis: Diagnosis towards Clinical Insight

    Dear Sir, We have read your impressive article "Neurosarcoidosis presenting as a large dural mass lesion" published in BMJ Case report on 8 November 2016. I have read about neurosarcoidosis thoroughly because of my previous exposure with few patients who were recovered as per diagnosis and prognosis.

    First, your esteem has mentioned that the biopsy confirmed the diagnosis while the diagnosis of sarcoidosis depends on multiple factors. Infact, histopayhology is only one of the diagnostic steps that we totally agreed to be included in the investigative process but histopathological changes are non-specific because of unidentified molecular and cellular events. Indeed, Sarcoidosis has neither distinctive clinical features [1] exclusive changes in pulmonary function studies, diagnostic labarotary investigations,[2] definite disease activity marker,[3] special imaging findings nor specific histological picture.[4-6]

    Consequently, the diagnosis of sarcoidosis is based on clinico- radiographic ?ndings which are supported by histologic evidence of the presence of noncaseating granulomatous in?ammation with the exclusion of similar presenting diseases such as tuberculosis, brucellosis, lymphoma, and lung cancer,[7] autoimmunity disorders (primary biliary cirrhosis and Wegener's granulomatosis), drug reactions, occupational and environmental exposures (e.g. beryllium, talc), farmer's lung disease (hypersensitivity pneumonitis) and infections.[4-6]

    So, when the diagnosis of sarcoidosis is considered, stains and culture for fungi and mycobacteria should always be obtained.[6] Approching patient with sarcoidosis is based on the following criteria:[8] 1) a compatible clinical and/or radiological picture; 2) histological evidence of non-caseating granulomas; and 3) exclusion of other diseases capable of producing a similar histological or clinical picture.

    Second, your esteem has mentioned that your case has been treated with steroids and as you now there is no global / international consensus about the dose and duration. Most recommend prednisolone 20 - 40 mg for not less than 12 months. [9] While we have treated ourpatient with prednisolone tablet orally started with 40 mg daily in divided doses and tapered for as short as two months. We are egger to know what type of steroids you have prescribed and more importantly what was the dose and for how long was the treatment spectrum of this neurosarcoidosis case?

    References 1. Baughman RP, Drent M, Kavuru M, Judson MA, Costabel U, Du BR, Albera C, Brutsche M, Davis G, Donohue JF, et al. In?iximab therapy in patients with chronic sarcoidosis and pulmonary involvement. Am J Respir Crit Care Med 2006;174:795-802. 2. Keir G, Wells AU. Assessing pulmonary disease and response to therapy: which test? Semin Respir Crit Care Med 2010;31:409-418. 3. Chesnutt AN. Enigmas in sarcoidosis. West j Med 1995; 162:519-526. 4. Nunes H, Bouvry D, Soler P, Valeyre D. Sarcoidosis. Orphanet J Rare Dis 2007; 2: 46. 5. Warshauer DM, Lee JKT. Imaging manifestations of abdominal sarcoidosis. AJR 2004; 182: 15-28. 6. Jundson MA. Sarcoidosis: clinical presentation, diagnosis and approach to treatment. Am J Med Sci 2008; 335: 26-33. 7. Iannuzzi MC, Rybicki BA, Teirstein AS. Sarcoidosis. N Engl J Med. 2007;357(21):2153-2165. 8. U. Costabel. Sarcoidosis: clinical update. Eur Respir J 2001; 18: Suppl. 32, 56s-68s. 9. Eishi Y, Suga M, Ishige I, Kobayashi D, Yamada T, Takemura T, Takizawa T, Koike M, Kudoh S, Costabel U, et al. Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis. J Clin Microbiol 2002;40(1):198-204.

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  3. A daily dose of 3,000 IU vitamin D should be safe in a 4-year-old child

    The case report from Dr. Boyd and Dr. Moodambail highlights the potential for over-zealous administration of vitamin D to result in toxicity (1). However, we contend that it is very unlikely that the reported daily dose of 3,000 IU (75 micrograms) vitamin D would elevate serum 25-hydroxyvitamin D (25[OH]D) concentrations to over 2000 nmol/L in a 4-year-old child. The US Institute of Medicine specifies a safe Upper Level Intake of 3000 IU vitamin D per day for children aged 4-8 years (2), and vitamin D intoxication in children typically arises when very much larger doses of vitamin D (240,000 IU to 4,500,000 IU) are administered (3). Mutations in genes encoding enzymes in the vitamin D metabolic pathway have been associated with hypercalcaemia in individuals with relatively modest vitamin D intakes, but circulating 25(OH)D concentrations in these cases are below the thresholds associated with toxicity (4). It is therefore likely that the dose of vitamin D taken by this child was far in excess of the reported 3,000 IU per day; determination of the vitamin D content of the supplements that he was taking would be instructive.

    1. Boyd C, Moodambail A. Severe hypercalcaemia in a child secondary to use of alternative therapies. BMJ Case Reports. 2016; 2016. 2. Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press; 2011. 3. Vogiatzi MG, Jacobson-Dickman E, DeBoer MD. Vitamin D supplementation and risk of toxicity in pediatrics: a review of current literature. J Clin Endocrinol Metab. 2014; 99(4): 1132-41. 4. Schlingmann KP, Kaufmann M, Weber S, Irwin A, Goos C, John U, et al. Mutations in CYP24A1 and idiopathic infantile hypercalcemia. N Engl J Med. 2011; 365(5): 410-21.

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  4. Optimum management of Femoral Neck Stress Fractures.

    We would like to thank Petrin et al for an informative case report[1] on an important injury sustained in athletes and service personnel. We agree that a high degree of suspicion for stress fractures should be maintained as we have previously reported the problems with a missed femoral neck stress fracture[2], and the more literature that is available highlighting these training injuries is useful for medical staff looking after athletes and servicemen[3].

    We note and thank you, that you reference our paper a couple of times in your article[4]. However, we believe that you have inadvertently slightly miss represented our work and we would like to take this opportunity to correct it.

    We do not state that "surgical fixation with percutaneous nail fixation is the treatment of choice in the management of tension type femoral neck fractures", as whilst we strongly believe that operative management is the most appropriate treatment for these fractures, we also think that the fracture should be treated with the most appropriate device available, as in our case report[2], where the patient was treated with a dynamic hip screw. Whilst in some cases an inter-medullary device would be appropriate, there is a higher cost and periprosthetic fracture risk using these devices. To our knowledge there is no evidence supporting the use of an inter-medullary device over a dynamic hip screw in the treatment of tension-type femoral stress fractures. We would also draw your attention to our paper Femoral Neck Stress Fractures in Sport: A Current Concepts Review[5] which details this type of stress fracture further.

    We thank the authors for an excellent case report and are grateful for the opportunity to clarify our stance on internal fixation of these fractures.

    References:

    1. Petrin Z, Sinha A, Gupta S, Patel MK. Young man with sudden severe hip pain secondary to femoral neck stress fracture. BMJ Case Rep 2016. doi:10.1136/bcr-2016-216820

    2. Thomas R, Wood AM, Watson J, Arthur CHC, Nicol AM. Delay in Diagnosis of Neck of Femur Stress Fracture in a female military recruit. J Royal Naval Medical Service 2012, Vol 98.2 27-29

    3. Wood AM, Keenan ACM, Arthur C, Wood IM. Common Training Injuries Concerning Potential Royal Marine Applicants. J Royal Naval Medical Service 2011, 97.3 106-109

    4. Wood AM, Hales R, Keenan A, et al. Incidence and time to return to training for stress fractures during military basic training. J Sports Med 2014;2014:282980.

    5. Robertson G, Wood AM. Femoral Neck Stress Fractures in Sport: A Current Concepts Review. Under Consideration Sports Medicine International SMIO-10-2016-0014-re

    Conflict of Interest:

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  5. Non-Disclosure of CAM usage: a case of "for every complex problem, there is a solution that is plain, simple and wrong"?

    We thank Dr. Boyd and Dr. Moodambail for their recent article in BMJ Case Reports, which describes the case of a four-year old boy with hypercalcaemia and hypervitaminosis D that was possibly attributed to the inappropriate prescribing of nutrient supplements. The case was complicated by the fact that the parent failed to disclose the use of these supplements until several days into the child's admission.

    Patient underreporting of complementary and alternative medicine (CAM) use during clinical encounters with conventional health care providers is a well-documented concern. It is estimated that 50% to 77% of people consuming CAM do not inform their medical practitioner (1-5), which is alarming. Drs. Boyd and Moodambail suggest that the issue of non- disclosure could be resolved if medical practitioners routinely gathered information about CAM use as part of the history taking process. This proposed solution is underpinned by a rather simplistic view of a complex problem.

    Myriad factors undoubtedly determine whether a patient divulges the use of CAM to a medical practitioner or other health care provider. Drs. Boyd and Moodambail allude to just one of these factors - 'opportunity' - highlighting that the health care provider should at least ask the patient if they are taking any CAM. Evidence suggests that communication is merely one of many factors impacting patient disclosure of CAM use. Yet another reason for non-disclosure are patient concerns regarding a potential negative response (such as being judged) by a medical practitioner (4). What this means is that even if the appropriate questions are posed by the medical practitioner, the patient may not divulge relevant information about CAM use because of fear.

    Given the complexity underpinning this issue, we propose a multifaceted strategy to overcome barriers associated with the disclosure of CAM use. In addition to improving communication, strategies to improve the disclosure of CAM use should draw attention to shared decision making between patient and medical practitioner (6), and to fostering positive relationships between patient and health care provider (5). Medical practitioners would also benefit from seeking relevant and unbiased information about CAM and to have a greater respect for patient decision making (7). This is especially poignant given the emergence of patient- centered and consumer-directed care, where the patient plays the role of an active and informed decision maker. The onus is not just on the medical practitioner and patient, however; CAM practitioners also need to be aware of their limitations and the potential adverse effects of their treatments, and to encourage patients to share relevant details with other health care providers such as medical professionals and pharmacists.

    Ultimately, all health care providers, conventional and complementary, should work towards ensuring that their patients receive timely, quality and safe health care. This can only be achieved if conventional and complementary health care providers: (1) communicate effectively with each other and with the patient, (2) openly and respectfully discuss each other's roles in the patient's care, and (3) acknowledge the patient's right to privacy, respect, access to all forms of health care, and their own personal belief system. By adopting a multi- faceted approach to such a complex issue, it is more likely that patients - the primary stakeholders in health care - would have the opportunity and confidence to disclose CAM usage to their health care providers.

    References

    1. MacLennan A, Myers S, Taylor A. The continuing use of complementary and alternative medicine in South Australia: costs and beliefs in 2004. Medical Journal Australia. 2006;184(1):27-31. 2. World Health Organization. WHO traditional medicine strategy 2002-2005. Geneva World Health Organization; 2002. 3. Crawford NW, Cincotta DR, Lim A, Powell CVE. A cross-sectional survey of complementary and alternative medicine use by children and adolescents attending the University Hospital of Wales. BMC Complementary and Alternative Medicine. 2006;6. 4. Robinson A, McGrail MR. Disclosure of CAM use to medical practitioners: a review of qualitative and quantitative studies. Complementary Therapies in Medicine. 2004;12(2-3):90-8. 5. Faith J, Thorburn S, Tippens KM. Examining CAM use disclosure using the Behavioral Model of Health Services Use. Complementary Therapies in Medicine. 2013;21(5):501-8. 6. Wallen GR, Brooks AT. To Tell or Not to Tell: Shared Decision Making, CAM Use and Disclosure Among Underserved Patients with Rheumatic Diseases. Integrative Medicine Insights. 2012;7:15-22. 7. Saxe GA, Madlensky L, Kealey S, Wu DP, Freeman KL, Pierce JP. Disclosure to physicians of CAM use by Breast cancer patients: Findings from The women's healthy eating and living study. Integrative Cancer Therapies. 2008;7(3):122-9.

    Conflict of Interest:

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  6. Re: Trandermal Hyoscine Induced Unilateral Mydriasis

    A 4 year old patient with a known diagnosis of a brainstem glioma, ventriculo-peritoneal shunt and ventricular access device was referred to our paediatric district general ward for review following a head injury. She had been knocked over at nursery by her brother on a bicycle and sustained an occipital head injury. Following this, the nursery staff noticed that her pupils were asymmetrical. Mum had collected her from nursery and brought her to the ward. There was no history of loss of consciousness or vomiting. On examination she was very well, bright and playful with a heart rate of 104 and blood pressure 99/56. There was a small, non boggy swelling to her occiput. Her right pupil was a size 6, fixed and dilated. Her left pupil was size 2 with an intact direct and consensual response to light. The accommodation reflex was intact and eye movements were also normal. Fundoscopy showed a slightly blurred optic disc on the right and was difficult to visualise on the left. Neurological examination was otherwise normal for this patient and mum described her as 'the best she has been in ages'. On further discussion of current medication it transpired that the hyoscine patch which had been applied that morning was missing from behind her right ear. The clinical impression was that the head injury was coincidental and that given how clinically well she was, the right sided pupillary findings were most in keeping with topical contamination of the eye with hyoscine presumably by fingertip innoculation. In our literature search for the half life of hyoscine we came across the above BMJ case report. In this report, Hannon et al very helpfully summarise an easy clinical test involving the instillation of Pilocarpine eye drops to establish if a pharmacological blockade is the cause for the underlying pupillary dilatation. We therefore administered pilocarpine and reviewed. Our patient continued to have one fixed and dilated pupil at 30 minutes, confirming pharmacological blockade as the cause of her dilated pupil. This avoided an hour long journey to a tertiary centre, possible general anaesthetic for a CT scan and potential aspiration of ventricular access device. This case reinforces the need for a detailed medication history and the management was significantly improved by the BMJ case report. Case reports remain a very helpful resource for patient management and we were exceptionally grateful to these authors for their thorough and helpful discussion.

    Sarah Alexander, Locum Paediatric Consultant Clare Irving, Consultant Paediatrician, Borders General Hospital

    Conflict of Interest:

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  7. Aspirin unmasking acquired haemophilia A in a patient with prostatic cancer

    Malignancy of the prostate is very well known to liberate lots of tissue factors controlling the coagulation process. This patient must have developed some sort of Disseminated intra vascular coagulation which was enhanced by the simultaneous administration of Aspirin. Most of the tests used to diagnose a particular coagulation deficiency have a considerable overlap in clinical setting. To say that this patient has developed haemophilia A at the age of seventy plus years and to call it as acquired haemohilia is not justified. The aspirin of course had contributed to the bleeding problems in this patient. It is fortunate that the patient improved with the appropriate effective management.

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  8. Vitamin D

    I think it is irresponsible of this author not to mention that there has indeed been research linking vitamin D to Autism and it is quite reasonable for parents to consider that supplements might improve their child's symptoms. https://www.vitamindcouncil.org/health-conditions/autism/ I have certainly seen in clinical practice a reduction in autistic symptoms in patients over the summer months.

    There is also evidence that low vitamin D in pregnancy might acutally increase the likelihood of autism. A Swedish study found significantly lower levels of vitamin D in chord blood in siblings who went on to develop autism compared with the siblings who did not. https://www.autismspeaks.org/science/science-news/swedish-study-suggests- low-vitamin-d-birth-may-increase-autism-risk Part of the problem is that the UK guidelines suggest levels of vitamin D supplementation which have been shown by research to be too low, but there is no clear consensus as to what the levels should be, particularly in children and no access to blood tests for families. Given that an adult can produce 10,000 iu a day of vitamin D in full sun, whilst 3000iu sounds a lot, it might be other factors such as the amount of calcium which was at fault in this case. More research is urgently needed. The author should at least advocate adherence to current advice that everyone should take at least a low dose vitamin D supplement in the winter months and vulnerable groups year round. http://www.nhs.uk/news/2016/07July/Pages/The-new- guidelines-on-vitamin-D-what-you-need-to-know.aspx

    Parents can also be blamed when their children develop rickets which is sometimes misdiagnosed as child abuse. This can be due to avoiding the sun as they are told to do and not taking supplements in pregnancy or giving children supplements through ignorance.

    This website gives some useful information for parents https://scotsneedvitamind.com/why-we-need-vitamin-d/pregnancy/

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  9. Anisakidosis as an emerging problem

    A relevant warning, particularly in front of an Anisakis' wide diffusion outside its traditional environment as a consequence of global warming.

    Nowadays, Anisakis is frequently present in anchovies, sardines and mackerels in Northern Mediterranean too, causing infestations after consuming uncooked or half-cooked fish.

    It is very difficult to recognize Anisakidosis if the suspect doesn't arise and this paper is very useful for increasing awareness of the problem.

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  10. Mouthpiece intermittent positive pressure ventilation: An old yet underutilized technique for long-term management of respiratory muscle failure.

    Dear Authors,

    We applaud your recognition that daytime mouthpiece intermittent positive pressure ventilation (IPPV) can serve as a practical alternative in cases of end stage respiratory muscle failure in which tracheostomy is usually the eventual conventional intervention of choice among the majority of today's clinicians. Lack of familiarity indeed seems to be the reason open-circuit mouthpiece ventilation, among other interfaces for IPPV, remains infrequently used among physicians today, despite first being described as an alternative to tracheotomy decades ago. In 1953 Dr. John Affeldt reported his experience working with polio patients with little to no vital capacity--how a simple mouthpiece attached to a positive pressure ventilator was able to provide ventilatory support for patients both during the day and while asleep.1 The application of mouthpiece rather than invasive IPPV for patients with neuromuscular disease (NMD) respiratory failure was greatly facilitated by the advent of portable positive pressure ventilators in 1957, the Puritan Bennett lip seal in 1964, nasal and oral-nasal interfaces after 1985, and mechanical in-exsufflation (MIE) devices in 1993.2, 3 While the on-demand mouthpiece mode (2013) for the Trilogy ventilator may represent the latest technologic development in mouthpiece IPPV, its earliest, far more simplistic predecessors, such as the Zephyr positive pressure blower (early 1950s), Monaghan portable respirator (1953), Thompson Bantam (1956), and Bird Mark 7 (commercially available 1958) have all been used to the same effect, to free polio and other NMD patients from negative pressure ventilators and tracheostomy mechanical ventilation.4,5,6

    Regarding the superiority of volume and pressure targeted modes, we prefer volume cycling since only it permits active lung volume recruitment (air stacking) that serves to maintain or improve lung compliance, permits effective coughing without personal assistance, increasing voice volume, etc., for those with glottis function.7 We only resort to pressure cycling when patients experience significant discomfort from abdominal distension.

    As you mentioned in your review there is now extensive literature on the success of up to continuous long-term mouthpiece IPPV in regimens of noninvasive ventilatory support but it should certainly not be viewed as a novelty considering its description in 1953 and its use by 257 patients described in 1993. Rather, the challenge is to break the paradigm that tracheostomy is required for ventilatory support for people with NMD or spinal cord injury.8 Current obstacles to implementing this management strategy today include abundance of nuisance alarms on commercial ventilators without mouthpiece ventilation modes and reimbursement for this type of "novel" care.9,10 Most importantly, continued lack of physician familiarity directly contributes to candidates missing out on this potential option to their long-term care.

    References

    1. Affeldt J. Round Table Conference on Poliomyelitis Equipment; Roosevelt Hotel, New York City; May 28-29, 1953. Sponsored by the National Foundation for Infantile Paralysis, Inc.

    2. Bach JR, Tuccio MC. Respiratory physical medicine: Physiatry's neglected discipline. Am J Phys Med Rehabil 2011;90(2):169-174.

    3. Garuti G. et al. Open circuit mouthpiece ventilation: Concise clinical review. Rev Port Pneumol. 2014;20(4):211-18.

    4. Gilgoff IS. The Breath of Life: the Role of the Ventilator in Managing Life-Threatening Illnesses. Lanham, MD: Scarecrow Press; 2001.

    5. Copyright Office, The Library of Congress. Catalog of Copyright Entries, Third Series: 1953: July-December. Vol 7. Washington;1954.

    6. Kacmarek RM. The Mechanical Ventilator: Past, Present, and Future. Respir Care 2011;56(8):1170-80.

    7. Bach JR, Mehta AD. Respiratory muscle aids to avert respiratory failure and tracheostomy: a new patient management paradigm. Journal of Neurorestoratology. 2014;2:25-35.

    8. Bach JR, Alba A. Intermittent positive pressure ventilation via the mouth as an alternative to tracheostomy for 257 ventilator users. Chest 1993;103:174-82.

    9. Khirani S, Ramirez A, Delord V, et al. Evaluation of ventilators for mouthpiece ventilation in neuromuscular disease. Respir Care 2014;59:1329-37

    10. Carlucci A, Mattei A, Rossi V, Gregoretti C. Ventilator settings to avoid nuisance alarms during mouthpiece ventilation. RespCare 2015;61(4):2-6.

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