Recent eLetters

Displaying 11-20 letters out of 128 published

  1. Inadequate surgical procedure

    In ankylosing spine there are unique biomechanical conditions which any spine surgeon has to know. Rules should be obeyed, otherwise the implanted screw-rod-system will not lead to successful treatment. Often revision surgery is necessary.

    The authors very well describe the systemtic pharmacological therapy that diminuished inflammation and helped the patient to recover.

    But in a spine surgeon's view the surgical procedure was inadequate: An Andersson lesion is a sign of severe instability. This was recognized by the surgeon because he tried to fix both ends of the vertebral column, that has the appearance of a "bamboo spine" (shown image b). But he has chosen a too short, bisegmental instrumentation. There is a lot of evidence, that this type of instability can't be restored by this surgical strategy (see literature below).

    The surgical principles in Andersson lesion seem to be the same as in fractures in ankylosing spine.

    The persisting postoperative pain can also be explained as a persisting instability.

    The therapy of Andersson lesion has to include both: First of all adequate stabilization and second adequate pharmacological inhibiton of inflammation.

    Literature: - Caron T, Bransford R, Nguyen Q et al (2010) Spine fractures in patients with ankylosing spinal disorders. Spine (Phila Pa 1976) 35:E458-464 - Hitchon PW, From AM, Brenton MD et al (2002) Fractures of the thoracolumbar spine complicating ankylosing spondylitis. J Neurosurg 97:218-222

    Best regards A.T. Mameghani, Basel, Switzerland

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  2. Giant cavernous carotid artery aneurysm mimicking a fungal granuloma and presenting with massive epistaxis

    It very important to be knowledgable regarding UNUSUAL causes of any clinical presentation. Epistaxis being a very common symptom presenting in varying degrees and forms maybe not taken seriously at times. This could lead to missing a vital diagnosis. I like this article as it has made me aware of another possible cause of epsitaxis which will make us more vigilant when managing these cases.

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    Hi, I am a prosthodontist and I deal with the fabrication of complete dentures. Although the article 'Radiological diagnosis of a small bowel perforation secondary to toothpick ingestion' is not related to our specialization yet it seems to be very useful for us. In this article an edentulous patient unknowingly ingested a tooth pick which perforated his small bowel and caused pain. In the learning points of this article it is told that one of the risk factors for ingestion of a toothpick includes loss of palatal sensation due to worn dentures. This information may be quite helpful for the edentulous patients wearing dentures. For the first time when denture is going to be delivered, we give some oral and written instructions to the patient regarding chewing with dentures, maintenance of hygiene of dentures, speaking with dentures, initial excessive salivation etc. Now we have decided to add a new point to this list "DO NOT TAKE UNEATABLE OBJECTS LIKE TOOTH PICK INTO THE MOUTH" to avoid accidental unknowing ingestion of these objects when dentures are placed into the mouth.

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  4. A really unique one !

    - The first of its type in Egypt. - very remarkable one among very few studies about HSV. - As a general director of the clinical pharmacy director of the fellowship it was very useful for my students in the hepatology and tropical medicine institute .

    Conflict of Interest:

    - General manager of the Clinical pharmacy fellowship at the national hepatology and tropical medicine research institute

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  5. Crohn's disease or TB - the perennial question and diagnostic pitfalls

    As TB is relatively more often seen in our part of the world, many a times we depend on our clinical sense and start Anti TB therapy empirically. Many of these patients are not economically well and cannot afford expensive and costly investigations. Tuberculosis can mimick many other diseases, and one has to be all the time suspicious and consider TB in the differential diagnosis when patient fails to improve.

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  6. Subacute liver failure secondary to black cohosh leading to liver transplantation:

    Letter to the Editor

    Subacute liver failure secondary to black cohosh leading to liver transplantation: A challenging interpretation

    Rolf Teschke Department of Internal Medicine II, Division of Gastroenterology and Hepatology, Klinikum Hanau, Academic Teaching Hospital of the Medical Faculty of the Goethe University rankfurt/ Main, Germany

    Correspondence to:

    SUMMARY Causality assessment in cases of suspected herb induced liver injury requires clear identification of the incriminated herbal product, otherwise a causal association cannot be established for a particular herb. In addition, herbs may erroneously be used for treatment of misinterpreted and unspecific prodromi of acute liver diseases, which excludes causality attribution for the incriminated herb.

    The report of Lim et al.1 provides a challenging interpretation for two cases of herb induced liver injury (HILI) by black cohosh (BC) and raises a number of questions related to case presentation, product identification, and causality assessment. Discussing these issues, important clinical lessons are to be learnt to reach at a valid diagnosis.

    The 60-year old woman (case 1) had a medical history of hypothyroidism managed by levothyroxine 100 ?g daily and migraine treated by propranolol 20 mg daily.1 She experienced symptoms considered by her as menopause-related, uses black cohosh (BC) for two weeks, and required a liver transplant due to subacute liver failure. However, the past medical history is otherwise poorly documented but essential for assessing causality in suspected herb induced liver injury (HILI). In this patient with 60 years of age, the last menstrual date is clinically important but this actual question neither was addressed nor answered presently.1 Menopausal symptoms are multifaceted,2 need specifications, and require clear differentiation from migraine symptoms and other ones related to diseases of various organs including the liver. Perceived as menopausal and likely being misinterpreted, the unspecified symptoms could well have been attributed to unspecific prodromi of an emerging acute liver disease, a diagnosis easily missed in its initial course. BC may be helpful for treatment of menopausal symptoms but not of incipient acute liver disease. Considering the rarity of assumed menopausal symptoms in a 60-year old patient, assessment of the time course and specification of previous menopausal symptoms of the would have assisted to arrive at the correct diagnosis.

    Other shortcomings include information gaps with lacking results of laboratory values at first presentation to her general practitioner and subsequently until admission.1 In addition, dates are missing on which BC, propranolol, and levothyroxine were discontinued. There are also no data on alanine aminotransferase (ALT) activities at admission and on liver values following admission until liver transplantation three weeks later, hampering a valid assessment of dechallenge features.

    The BC product used in this case remained unnamed and undefined regarding ingredients and possible warnings, which precluded valid causality assessment. In particular, there is uncertainty whether BC was consumed as a licensed drug or unlicensed herbal mixture with potentially hepatotoxic herbal ingredients unrelated to BC. Authentication of the product and daily dose were not reported, leaving the question of adulterants, herbal misidentification, impurities, and daily overdose.

    Credit is given1 to Bernal et al.,3 another group of King's College Hospital, who described the complexity and challenging issues of acute liver failure, with unknown causes in up to 38% of cases despite thorough investigations. In reference to cases with seronegative liver failure described in the literature, clinical features and associated haematological abnormalities can suggest viral infection, but serological testing for established and putative hepatotropic viruses can be negative. In the report under discussion,1 methodological details for parameters used for individual serological testing for viruses were not provided. Uncommon but well documented viral causes of acute liver failure include varicella zoster virus and parvovirus B193 that were not considered in the present case report.1

    Lim et al.1 presented a second case of unknown age with assumed HILI by an unidentified BC product. Information gaps included not only unknown age and unnamed product lacking authentication, but also undeclared indication for use and unknown daily dose. Undefined symptoms appeared two weeks after cessation of the product that had been used for 6 weeks, and admission was 4 weeks after symptoms had appeared. Exclusion of alternative causes was fragmentary. Following product cessation, initial ALT activities decreased from 1119 to 339 U/L over 9 days and then peaked at 7304 U/L 7 days later for unknown reasons. A recurrent ALT increase speaks against the role of the incriminated product.4

    Considering available and missing data in the two cases,1 causality for the two unidentified products was possible in the first case and excluded in the other one (Table), using the Council for International Organizations of Medical Sciences (CIOMS) scale4 as described in detail before.5 Lim et al.1 provided for the first case a total score, which signified the lowest level of a probable causality without presenting individual scores for each item of the CIOMS scale to be used for further evaluation; of unknown reasons, CIOMS-based causality for the second case was not provided.

    Lim et al.1 refer to the literature quoting 3 reports6-8 with assumed BC hepatotoxicity, but there was lack of causality upon further CIOMS based evaluation in these reported cases9,10 as well in other cases.9-12 It has also been argued that using the WHO method 14 out of 21 spontaneous reports of the Medicines and Healthcare products Regulatory Agency (MHRA) were shown to support a relation between BC and liver damage, but levels of causality were not communicated.1 Most of these spontaneous MHRA cases likely had been analyzed by the European Medicines Agency (EMA), but there was lack of causality for BC as assessed with the CIOMS scale,13 which is liver specific and validated for hepatotoxicity.14 The WHO method used by MHRA is not liver specific, not validated for hepatotoxicity, and therefore obsolete for assessing hepatotoxicity cases.15 Finally, there is also no evidence for BC hepatotoxicity by metaanalysis of randomized controlled clinical trials.16

    In conclusion, to assess cases of suspected HILI we need good quality of case data and liver specific assessment tools such as the CIOMS scale, in addition to thorough clinical evaluation and clear product identification. If these conditions are not fulfilled, we are left with more questions than answers are given.

    Learning points ? Causality attribution for a herb in cases of assumed herb induced liver injury requires clear

    identification of the incriminated herbal product used by the patient and information of the

    daily dose. ? Unspecific prodromi of acute liver disease may be misinterpreted and erroneously be

    treated by herbal products, offsetting causality attribution for the herb under discussion. ? A careful case analysis is mandatory, which includes the use of a liver specific causality

    assessment method such as the CIOMS scale, providing transparency by listing each

    individual and scored item of the scale rather than a total score that lacks transparency.

    Contributor Rolf Teschke Competing interests None.

    REFERENCES 1. Lim TY, Considine A, Quaglia A, et al. Case report: Subacute liver failure secondary to black cohosh leading to liver transplantation. BMJ 2013. DOI : 10.1136/bcr-2013-009325 2. Nelson HD. Menopause. Lancet 2008; 371: 760-70 3. Bernal W, Auzinger G, Dhawan A, et al. Acute liver failure. Lancet 2010; 376: 190-201 4. Danan G, B?nichou C. Causality assessment of adverse reactions to drugs - I. A novel method based on the conclusions of international consensus meetings: application to drug-induced liver injuries. J Clin Epidemiol 1993; 46:1323 -30 5. Teschke R, Frenzel C, Schulze J, et al. Herbal hepatotoxicity: challenges and pitfalls of causality assessment methods. World J Gastroenterol 2013; 19: 2864-82 6. Whiting PW, Clouston A, Kerlin P. Black cohosh and other herbal remedies associated with acute hepatitis. Med J Aust 2002; 177: 432-5 7. Lontos S, Jones RM, Angus PW, et al. Acute liver failure associated with the use of herbal preparations containing black cohosh. Med J Aust 2003; 179: 390-1 8. Levitsky J, Alli TA, Wisecarver J, et al. Fulminant liver failure associated with the use of black cohosh. Dig Dis Sci 2005; 50: 538-9 9. Teschke R, Schwarzenboeck A. Suspected hepatotoxicity by cimicifugae racemosae rhizoma (black cohosh, root): critical analysis and structured causality assessment. Phytomedicine 2009; 16: 72-84 10. Teschke R, Bahre R, Fuchs J, et al. Black cohosh hepatotoxicity: quantitative causality evaluation in nine suspected cases. Menopause 2009; 16: 956-65 11. Teschke R, Schmidt-Taenzer W, Wolff A. Spontaneous reports of assumed herbal hepatotoxicity by black cohosh: Is the liver unspecific Naranjo scale precise enough to ascertain causality? Pharmacoepidemiol Drug Saf 2011; 20: 567-82 12. Teschke R. Black cohosh and suspected hepatotoxicity - inconsistencies, confounding variables, and prospective use of a diagnostic causality algorithm: A critical review. Menopause 2010; 17: 426 -40 13. EMA (European Medicines Agency): Assessment of case reports connected to herbal medicinal products containing cimicifugae racemosae rhizoma (black cohosh, root). Issued May 8, 2007. Available at: _HMPC_assessment_report/2010/02/WC500074167.pdf Accessed 14 July 2013 14. B?nichou C, Danan G, Flahault A. Causality assessment of adverse reactions to drugs - II. An original model for validation of drug causality assessment methods: case reports with positive rechallenge. J Clin Epidemiol 1993; 46: 1331-6 15. Teschke R, Eickhoff A, Wolff A, et al. Herbal hepatotoxicity and WHO global introspection method. Ann Hepatol 2013; 12: 11-21 16. Naser B, Schnitker J, Minkin MJ, et al. Hepatotoxicity suspected by black cohosh: No evidence by metaanalysis of randomized controlled clinical trials for isopropanolic black cohosh extract. Menopause 2011; 18: 366-75

    Table: Case scoring with the CIOMS scale

    Items for hepatocellular injury Possible Score Patient 1 Score Patient 2 Score Time to onset from the beginning of the herb

    5-90 days (rechallenge: 1-15 days) +2 +2

    < 5 or > 90 days (rechallenge: > 15 days) +1

    Alternative assessment: Time to onset from cessation of the herb

    ? 15 days (except for slowly metabolized chemicals: > 15 days) +1 +1 Course of ALT after cessation of the herb

    Percentage difference between ALT peak and N

    Decrease ? 50% within 8 days +3

    Decrease ? 50% within 30 days +2

    No information or continued herb use 0 0

    Decrease ? 50% after day 30 0

    Decrease < 50% after day 30, or recurrent increase -2 -2 Risk factors

    Alcohol use (drinks/day: > 2 for women, > 3 for men) +1

    Alcohol use (drinks/day: ? 2 for women, ? 3 for men) 0 0

    Age ? 55 years +1 +1

    Age < 55 years 0 Concomitant drug(s) or herbs(s)

    None, or no information 0

    Concomitant drug or herb with incompatible time to onset 0

    Concomitant drug or herb with compatible or suggestive time to onset -1 -1

    Concomitant drug or herb known as hepatotoxin and with compatible or

    suggestive time to onset -2

    Concomitant drug or herb with evidence for its role in this case (positive

    re-challenge or validated test) -3 Search for non herb causes

    Group I (6 causes)

    Anti-HAV IgM - -

    HBsAg, anti-HBc IgM, HBV-DNA - -

    Anti-HCV, HCV-RNA - -

    Hepatobiliary sonograph /colour Doppler sonography of liver

    vessels/endosonography/CT/MRC -

    Alcoholism (AST/ALT ? 2)

    Acute recent hypotension history (particularly if underlying heart

    disease present) -

    Group II (6 causes) -

    Complications of underlying disease(s) such as sepsis, autoimmune

    hepatitis, chronic hepatitis B or C, primary biliary cirrhosis or sclerosing

    cholangitis, genetic liver diseases -

    Infection suggested by PCR and titer change for

    CMV (anti-CMV IgM, anti-CMV IgG)


    EBV (anti-EBV IgM, anti-EBV IgG) -

    HEV (anti-HEV IgM, anti-HEV IgG) -

    HSV (anti-HSV IgM, anti-HSV IgG) -

    VZV (anti-VZV IgM, anti-VZV IgG)

    Evaluation of groups I and II

    All causes groups I and II reasonably ruled out +2

    The 6 causes of group I ruled out +1

    5 or 4 causes of group I ruled out 0 0

    < 4 causes of group I ruled out -2 -2

    Non-drug/herb cause highly probable -3 Previous information on hepatotoxicity of the herb

    Reaction labelled in the product characteristics +2

    Reaction published but unlabelled +1 +1 +1

    Reaction unknown 0 Response to re-administration

    Doubling of ALT with the herb alone, provided ALT< 5N before re- exposure +3

    Doubling of ALT with the drug(s) and herb(s) already given at the time of

    first reaction +1

    Increase in ALT but < N under the same conditions as for the first

    administration -2

    Other situations 0 Total score for patient +3 -2

    CIOMS based causality assessment for the two cases of the report of Lim et al.1 The compilation of individual items is derived from the updated CIOMS scale,5 which is based on the original CIOMS scale.4 The - sign indicates that the parameter was assessed with a negative result. Abbreviations: ALT, Alanine aminotransferase; AST, Aspartate aminotransferase; CIOMS, Council for International Organizations of Medical Sciences; CMV, Cytomegalovirus; CT, Computed tomography; EBV, Epstein-Barr virus; HAV, Hepatitis A virus; HBc, Hepatitis B core; HBsAg, Hepatitis B surface antigen; HBV, Hepatitis B virus; HCV, Hepatitis C virus; HEV, Hepatitis E virus; HSV, Herpes simplex virus; MRC, Magnetic resonance cholangiography; N, upper limit of normal; VZV, Varicella zoster virus. Total score and resulting causality grading: ? 0, excluded; 1-2, unlikely; 3-5, possible; 6-8, probable; ? 9, highly probable.

    Conflict of Interest:

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  7. The clitoral or female priapism is not caused from arousal, it is a more accurate term than persistent genital arousal disorder (PGAD) or Restless genital syndrome.

    In 2013 Gadit stated "A 54-year-old woman presented to a community- based psychiatric clinic with unique problem of persistent genital arousal disorder. ... this case has become a clinical challenge in terms of treatment" [1]. The clitoris is an external organ ("internal" clitoris does not exist) and has three erectile tissue parts, in the free part of the organ, is composed of the body and the glans located inside of the prepuce; the hidden part of the clitoris are the roots or crura, they are covered by the ischiocavernosus muscles. Their contraction results in a surge of blood in the crura toward the corpora cavernosa of the clitoris and compression of the deep dorsal veins, contributing to erection of the clitoris. Studies by Dickinson, in 1949, identified a small number of reports showing that pronounced erection can occur. In fact, as in males, in females, it is possible to have the priapism of the clitoris, a rare condition associated with prolonged painful erection of the corpora cavernosa lasting for more than 6 hr and unassociated with sexual arousal, not associated with sexual stimulation. It causes engorgement, swelling, pain of the clitoris and of its immediate adjacent area [2-4]. Female priapism treatment depends on aetiology. The cause of priapism, in male and female, is impaired outflow of blood from the corpora cavernosa because of venous obstruction or because of failure of the alpha- adrenergic relaxation system. ''Most reported cases of female priapism describe the association with the use of antidepressant and other psychotropic drugs, all with alphaadrenergic blocking potential, such as trazodone, buproprion citalopram and nefazodone. Treatment consisted of discontinuing the offending medication or providing symptomatic pain relief. Serious permanent damage where treatment has been delayed has been reported in men but not in women. Furthermore, the association between congenital clitoromegaly and priapism has also not been reported previously. With this concern in mind, we felt justified to resort to management options described for male priapism but hitherto not for female priapism, i.e. the direct injection with epinephrine and heparin, followed by aspiration to provide immediate decompression''[4,5]. The etiology of PGAD is not completely understood, it is described as spontaneous, intrusive, and unwanted genital arousal in the absence of sexual interest and desire. PGAD definition is equal to that of clitoral/female priapism. PGAD is not a newly recognized condition. In addition, if the "genital arousal" is unwanted, why to use "arousal"? This term could suggests that women should, may end up feeling "abnormal" from sexuality viewpoint. Restless Genital Syndrome includes restless legs and/or overactive bladder, and it may include PGAD: it cannot be defined how PGAD. The term clitoral, or female, priapism is a more accurate term than persistent genital arousal disorder or Restless genital syndrome. Treatment described for male priapism must be divulged to the sexual medicine experts [4,5]: it must be a therapy also for clitoral/female priapism. Sexologists and sexual medicine experts use questionnaires for the prevalence, etiology, diagnosis and treatment of female sexual dysfunctions (FSD). Female Sexual Function Index (FSFI) questionnaire is the most widely used scale to assess sexual dysfunction in women. Physiologically the FSFI questionnaire does not provide an assessment of female sexual function, but primarily assesses vaginal intercourse: many questions seem to assess the degree of lubrication and ease of penetration, while very little attention is paid to clitoral sensation. Questionnaires for women's sexual function must mainly assess the presence or absence of orgasm with masturbation and in the questions there must not be the words "intercourse" and "satisfaction"[6]. As a matter of fact female sexual dysfunctions are popular because they are based on something that doesn't exist, i.e. the vaginal orgasm[2,3,6]. Clitoral/female priapism is not a sexological disease, but a gynecological/urological disease. I warn colleagues to maintain a high level of professionalism and not to be use nonmedical or not scientific definition, terms and questionnaires.


    [1] Gadit A. Persistent genital arousal disorder: a clinical challenge. BMJ Case Rep. May 21; 2013. doi:10.1136/bcr-2013-009098

    [2] Puppo V. Anatomy and Physiology of the Clitoris, Vestibular Bulbs, and Labia Minora With a Review of the Female Orgasm and the Prevention of Female Sexual Dysfunction. Clin Anat 2013; 26: 134-52.

    [3]Puppo V. Embryology and anatomy of the vulva: The female orgasm and women's sexual health. Eur J Obstet Gynecol Reprod Biol 2011; 154:3-8.

    [4] Arntzen BW, de Boer CN. Priapism of the clitoris. BJOG 2006; 113: 742-43.

    [5] Montague DK, Jarow J, Broderick GA, Dmochowski RR, Heaton JP, Lue TF, et al. American Urological Association guideline on the management of priapism. J Urol 2003; 170(4 Pt 1): 1318-24.

    [6] Puppo V. Female sexual function index (FSFI) does not assess female sexual function. Acta Obstet Gynecol Scand 2012; 91:759.

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  8. Drugs of Abuse including Newer Stimulants: the NPIS data.

    The potential value of NPIS data for surveillance has increasingly been recognised by official government bodies.1

    During the year 2011/12, the NPIS answered telephone enquiries relating to drugs of abuse, constituting 2.6% of the overall telephone workload. Over the same period there were accesses to drugs of abuse monographs on TOXBASE, representing 4.0% of the total TOXBASE activity. As with all NPIS activity data, these figures are not a direct measure of the frequency of toxicity or hospital admission with drugs of abuse, but give an indirect indication of the substances being encountered by the NHS clinicians. It should be noted that analytical confirmation of exposure is rarely available and the statistics reported here reflect what has been reported as being taken by the recreational drug users involved.

    Cocaine, amphetamines, MDMA ('ecstasy'), heroin, cannabis, methadone, mephedrone and ketamine all feature in the top ten telephone enquiries and TOXBASE accesses for drugs of abuse.

    The NPIS continues to monitor activity relating to newer recreational drugs. Those most frequently involved in telephone enquiries over the last three years have been mephedrone, 'legal highs' (not otherwise specified), naphyrone, methcathinone, 6-APB, 'Ivory Wave' products (not otherwise specified, but reported to contain desoxypipradrol) and methoxetamine.

    For mephedrone 2 the previously reported substantial reduction in enquiry numbers following legal control in April 2010 has been maintained for telephone enquiries, although there has been a small increase in TOXBASE hits over the last year. Reductions in activity following legal control have also been maintained for 'Ivory Wave' products and naphyrone. On the advice of the Advisory Council on Misuse of Drugs (ACMD), ketamine analogue methoxetamine ('mexxy'or 'MXE') was subject to a Temporary Drug Class Order coming into effect on 5 April 2012. The impact of this on enquiries to the NPIS will continue to be monitored.

    During the year 2011/12 the NPIS has developed its working relationship with the UK Focal Point Early Warning System (EWS) on new psychoactive substances or 'legal highs', which is managed by the Department of Health. Data were provided on NPIS activity relating to methoxetamine and this formed some of the evidence provided to the ACMD and the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA). Further discussions with the UK Focal Point EWS are planned with a view to developing a chapter for the exchange of data and information, but, in the meantime, the NPIS has been listed by the EMCDDA as part of the UK early warning system national profile.



    2. James D, Adams R, Spears R, Cooper G et al. Clinical characteristics of mephedrone toxicity reported to the UK National Poisons Information Service. Emerg Med J 2011; 28(8): 686-9.

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  9. XDR-TB: The name is not enough!

    Dear Sir,

    We read with interest the case report "Extensively drug resistant tuberculosis in a 7-year-old child with interferon-gamma and interleukin- 12 deficiency" by Kulkarni et al [1]. The reports of XDR-TB hold an important epidemiological implication and need to be defined accurately. We would like to clarify the definition used for extensively drug resistant tuberculosis (XDR-TB) in the report.

    The case presented above reported the drug resistance pattern of the M. tuberculosis isolate for the second line anti-tuberculosis drugs to be: sensitive to para-aminosalicylic acid, ofloxacin and kanamycin but resistant to amikacin, cycloserine and ethionamide. The isolate cannot be labeled as XDR-TB based on the above sensitivity pattern as it was sensitive to ofloxacin. XDR-TB is correctly defined as MDR-TB plus resistance to a fluoroquinolone and at least one second-line injectable agent: amikacin, kanamycin and/or capreomycin [2], based on which it is necessary for the MDR-TB isolate to be resistant to a fluroquinolone to be termed as a XDR-TB, which is not present in the present case. Hence, the isolate may be termed as MDR-TB at best, and not XDR-TB.

    The risk factors for acquisition of extensive drug resistance in TB include inappropriate use of second-line drugs in a patient for whom first -line drugs are failing [3]. This child was treated with the first line anti-tuberculosis drugs earlier, but had no exposure to the second line drugs, which does not make a strong case of the acquisition of resistance to second line drugs. The global threat of XDR tuberculosis has great significance for the public health field, as the the existence of XDR-TB is a reflection of weaknesses in tuberculosis management programmes [3]. Moreover, there is a need for universal definitions for the various degrees of antimicrobial resistance in bacteria [4], and international norms should be used to avoid confusion in the medical literature.


    1. Kulkarni K, Singh M, Soneja P, Mathew J, Marwaha RK. Extensively drug resistant tuberculosis in a 7-year-old child with interferon-gamma and interleukin-12 deficiency. BMJ Case Rep. 2009;2009. pii: bcr06.2008.0293.

    2. World Health Organization: Multidrug and extensively drug- resistant TB (M/XDR-TB): 2010 global report on surveillance and response. [Available:]. Accessed 22 January, 2012.

    3. Raviglone MD, Smith IM. XDR Tuberculosis - Implications for Global Public Health. N Engl J Med 2007;356:656-659.

    4. Falagas ME, Karageorgopoulos DE. Pandrug resistance (PDR), extensive drug resistance (XDR), and multidrug resistance (MDR) among Gram -negative bacilli: need for international harmonization in terminology. Clin Infect Dis. 2008;46:1121-2;author reply 1122.

    Conflict of Interest:

    None declared

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  10. Use a felt tip pen and an alcohol pad to stain the skin prior to dermoscopy

    I have found using a "Sharpie" marker over the site, then cleaning it off with an alcohol pad, (a method described in Habiff's Dermatology to stain burrows), makes the "delta wing pattern" which can be subtle, obvious. I use a usb polarizing dermatoscope and a laptop at bedside to diagnose and show the patient multiple linear aggregations of the delta patterns and find this method useful in my every day practice. The procedure takes 1-2 minutes. I am a family practice doctor in an urgent care setting. The dermatoscope I use is less than $300 online.

    Conflict of Interest:

    None declared

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