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Recent eLetters

Displaying 11-20 letters out of 203 published

  1. Is skeletal flourosis?

    Thank you for this interesting report. Please check for skeletal fluorosis also given amount of tea consumed per day over so many years.

    Thank you

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  2. Re:A case of misdiagnosis: chronic fluoride intoxication?

    Dear Editor,

    I wish to draw attention to the following misdescription in my orginal letter (dated 28th Nov 2015). I had incorrectly stated that Amoxicillin was a fluoroquinolone. I had assumed that since Hong et al (2005) found a significant association between the use of this antibiotice and dental fluorosis that it must be a fluoroquinolone antibiotic. I was unaware that the letter had been published in the BMJ until yesterday and feel that to safeguard the integrity of scientific debate and promote constructive dialogue among the scientific community it is important to correct this for the record. I have corrected my letter and in doing do have explained how amolicillin enhances fluoride toxicity.

    Yours sincerely

    Declan Waugh

    A case of misdiagnosis: chronic fluoride intoxication? Lugg et al (2015) reported a case study of a 16 year old girl who presented with signs of chronic joint pain, dizziness and non-specific abdominal pains after consuming 3 cups per day of imported herbal green tea (as tea bags) for a period of 3 months [1]. There are a number of interesting points not addressed in the case study which physicians may not be aware of that are of clinical significance. Firstly, the description of the ailments which the subject presented with strongly suggest chronic fluoride intoxication. Hallanger et al (2007) reported that the clinical features associated with fluoride intoxication resulting from habitual tea consumption can include joint pain and gastrointestinal complaints and that fluoride toxicity is often overlooked by clinicians [2]. Despite the publication of a large number of reports addressing fluoride intoxication from habitual tea drinking [3] many health care professionals remain unaware of the risk of fluoride intoxication from tea and lack an understanding of the pathophysiology of fluoride toxicosis. The United States National Academy, National Research Council (2006) reported that excessive intake of fluoride will manifest itself in a musculoskeletal disease with associated symptoms including chronic joint pain and arthritic symptoms [4]. However, perhaps one the most detailed explanations of the pathophysiology of fluoride toxicosis is provided by Professor Alexander V. Akleyev [5]. In addition to musculoskeletal disorders, Akleyev reported that stage 2 fluorosis, the following symptoms are observed: subatrophic and atrophic rhinitis, pharyngitis, laryngitis, chronic conjunctivitis, retinal degeneration with visual impairment, hearing loss, increasing impairment of bronchial patency, and pulmonary insufficiency; mycrodial dystrophy with reduced contractility, chronic gastritis mainly with the reduction of secretory and acid forming function of the stomach, and chronic hepatitis with persistent liver failure; distinct astheno-vegetative syndrome, toxic polyneuritis and decrease in glucocorticoid function of adrenal cortex; and microhematuria and proteinura [4]. Kessabi et al (1986) also reported that acute hepatitis and degeneration in the liver develop following chronic fluoride intake [6]. Other studies have also found that fluoride toxicosis can induce hepatotoxicity and oxidative stress in humans [7-8] and animals [9]. In the case study described by Lugg and associates [1], the fluoride concentration in the tea samples ingested by the patient are unknown, as they were not tested. Chan et al (2013) reported high fluoride levels in tea infusions in the United Kingdom including green tea leaves which were found to contained up to 6.67mg/L when made with deionized water [10]. The European Food Safety Authority (EFSA) have reported that drinking just 2 cups of tea per day (with a fluoride content of 5mg/l), combined with an average consumption of fluoridated drinking water and use of fluoridated tap water in the preparation of food, but excluding all other sources (including solid foods, toothpaste and dental products), would provide a daily dietary intake of 6 mg per day [11]. The EFSA have established daily recommended intake levels (AI) and Tolerable Upper Intake Levels (ULs) for fluoride. For an adult female the AI is 2.9mg per day while the UL is 7mg per day [11-12]. Birmingham is the largest city in the England with artificially fluoridated water. Thus, the patient having consumed 3 cups of tea per day, is likely to have exceeded the recommended UL for fluoride, thereby increasing the risk of chronic fluoride intoxication. Secondly, Lugg and associates noted that the condition of the subject worsened following prescribing of amoxicillin [1]. While amoxicillin is not a fluoroquinolone, which like ciprofloxacin can significantly contribute to daily fluoride intake [13], amoxicillin has nevertheless been found to enhance the toxicity of fluoride [14]. The mechanism by which this appears to occur is by the ability of amoxicillin to increase cell permeability [15-16], thereby enhancing the absorption and activity of fluoride. This would perhaps explain why Hong et al (2005) reported that amoxicillin significantly increased the risk of fluorosis in children when compared with those who never used amoxicillin during the first year of life [17]. Thus, it is likely that administration of amoxicillin resulted in further contributing to chronic fluoride intoxication of the subject and a worsening of her condition. Thirdly, on cessation of the herbal tea and treatment with intravenous fluids and N-acetylcysteine, her condition resolved [1]. N-acetylcysteine is known to protect against fluoride-induced oxidative damage [18]. Overall, the evidence indicates the symptoms reported may be due fluoride toxicosis caused by high fluoride intake from tea, combined with other fluoride sources such as fluoridated drinking water and potentiated by the use of certain medications. There is a need for healthcare workers to be aware of the pathophysiology of fluoride toxicosis as well as dietary fluoride sources, particularly among habitual tea drinkers in communities with artificially fluoridated drinking water. Urinary or blood fluoride levels should be routinely monitored in patients with musculoskeletal and gastrointestinal disorders. Fasting serum fluoride concentrations ranging from 2.5 - 8.0 ?M/L can result in chronic fluoride intoxication and stage I and stage II skeletal fluorosis [19].

    [1] Lugg ST, Menezes DB, Gompertz S. Chinese green tea and acute hepatitis: a rare yet recurring theme. BMJ Case Rep 2015, doi:10.1136/ bcr -2014-208534 [2] Hallanger-Johnson JE, Kearns AE, Doran PM, Khoo TK., Wermers RA. Fluoride-related bone disease associated with habitual tea consumption. Mayo Clinic Proceedings 2007;82(6):719-24. [3] Yi J, Cao J. Tea and fluorosis. Journal of Fluorine Chemistry, 2008, 129: 76-81. [4] National Research Council, Review of Fluoride in Drinking Water, U.S. National Research Council 2006. [5] Neurological Disorders of Non-Radiation Nature, Fluorosis, In Chronic Radiation Syndrome, Alexander V. Akleyev, Spriner-Verlag Berlin Heidelberg 2014. ISBN 978-3-642-45116-4 [6] Kessabi M, Hamliri A. Experimental fluorosis in sheep: Alleviating effects of aluminum. Vet. Hum. Toxicol., 1986, 28: 300-304. [7] Michael M, Barot VV, Chinoy NJ. Investigations of Soft Tissue Functions In Fluorotic Individuals of North Gujarat. Fluoride 1996, Vol.29 No.2 63-71. [8] Medvedeva VN. Characteristics of the course of chronic hepatitis in workers coming in contact with flourine compounds. Gigiena Truda; Professional'nye Zabolevaniia, Jan 1985. pg 24-6 [9] AL-Harbia MS, Hamzaa RZ, Dwarya AA. Ameliorative effect of selenium and curcumin on sodium fluoride induced hepatotoxicity and oxidative stress in male mice. J Chem Pharma Res, 2014, 6(4):984-998. [10] Chan L, Mehra A, Saikat S, Lynch P. Human exposure assessment of fluoride from tea (Camellia sinensis L.) Food Res Internat. 2013; 51: 564- 570. [11] European Food Safety Authority, Scientific Opinion on Dietary Reference Values for fluoride, EFSA Panel on Dietetic Products, Nutrition, and Allergies: EFSA Journal. 2013;11(8):3332. [12] European Food Safety Authority, Scientific Opinion of the Panel on Dietetic Products, Nutrition, and Allergies (NDA) on the tolerable upper intake level of fluoride. The EFSA Journal. 2005, 192, 1-65. [13] Pradhan KM, Arora NK, Jena A, Susheela AK, Bhan MK. Safety of ciprofloxacin therapy in children: magnetic resonance images, body fluid levels of fluoride and linear growth. Acta Paediatr. 1995, 84:555-560. [14]Sahlberg C, Pavlic A, Ess A, Lukinmaa PL, Salmela E, Alaluusua S. Combined effect of amoxicillin and sodium fluoride on the structure of developing mouse enamel in vitro. Arch Oral Biol. 2013 Sep;58(9):1155-64. doi:10.1016/j.archoralbio.2013.03.007. Epub 2013 Apr 17. [15]Novo DJ, Perlmutter NG, Hunt RH, Shapiro HM. Multiparameter Flow Cytometric Analysis of Antibiotic Effects on Membrane Potential, Membrane Permeability, and Bacterial Counts of Staphylococcus aureus and Micrococcus luteus. Antimicrobial Agents and Chemotherapy. 2000;44(4):827- 834. [16] Khargharia S, Chakraborty AK., Bhattacharyya A, Manda T K. Disposition Kinetic of Amoxicillin in Healthy and Nephropathic Goats with Immunological and Residual Level in Blood and Tissues. J Drug Metab Toxicol S5:003. doi:10.4172/2157-7609.S5-003 [17] Hong L, Levy SM, Warren JJ, Dawson DV, Bergus GR, Wefel JS. Association of Amoxicillin Use During Early Childhood With Developmental Tooth Enamel Defects, Arch Pediatr Adolesc Med. 2005;159:943-948, 995-996. [18] Paw?owska-G?ral K, Kurzeja E, Stec M. N-acetylcysteine protects against fluoride-induced oxidative damage in primary rat hepatocytes. Toxicology in Vitro, December 2013, Volume 27, Issue 8, Pages 2279-2282. doi:10.1016/j.tiv.2013.09.019 [19] Xiang QY, Chen LS, Chen XD., Wang CS, et al. Serum Fluoride And Skeletal Fluorosis In Two Villages In Jiangsu Province, China. 178 Fluoride 2005;38(3):178-184

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  3. ICP complications

    There are several methods of measuring intracranial pressure (ICP). These include insertion of an ICP 'bolt' into brain parenchyma or subdurally through a small burr hole, direct placement of a pressure monitor under the dura following a craniotomy/craniectomy, or insertion of a drainage catheter into the ventricles allowing direct transduction of cerebrospinal fluid (CSF) pressure. The later is known as an external ventricular drain, a term often used synonymously with ventriculostomy. The high infection rates associated with ICP measurement that Lewis cites (Lozier et al, 2002) refer to ventriculostomy catheters and not ICP bolts or subdural monitors. The case study describes an "ICP bolt placed over the left frontal lobe", from this description it is not possible to ascertain the exact monitor used but it does not appear to describe an intraventricular catheter. Therefore, in the context of the case; it may be prudent to note that intraparenchymal or subdural ICP monitoring is recognised as having far lower infection rates and does not allow CSF drainage or sampling.

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  4. 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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  5. 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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  6. 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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  7. 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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  8. 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

    Conflict of Interest:

    None declared

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  9. 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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  10. 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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