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Visceral leishmaniasis: an unusual cause of isolated lymphadenopathy
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  • Published on:
    Ref: bcr-2021-242073.R2 - Very Late Onset Friedreich’s Ataxia with rapid course mimicking as Possible Multiple System Atrophy Cerebellar Type. Rapid Response from Dr. Stefan M. Pulst, Professor & Chair, Neurology, University of Utah
    • Tushar Vidhale, Assistant Professor Grant Government Medical College and JJ Group of Hospitals, Mumbai

    Respected Editor and Dr. Pulst,

    Thank you for your interest in our case. We agree with your comment that Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by bi-allelic expansion of an intronic GAA repeat in the frataxin (FXN) gene, but our patient had eight GAA repeats on allele-1 and 37 repeats (pre-mutated allele) on allele-2. The pre-mutated allele can be responsible for the disease, in
    rare cases, by causing somatic expansion or pre-mutation in cell populations. But this occurs only when in the setting of the second allele in the clear pathogenic range of expansion. This intronic GAA expansion further silences the FXN gene, resulting in pathologically suppressed levels of the frataxin protein. As per the respected reader, even though the patient had the probability of compound
    heterozygous mutation with a pathogenic point mutation in one allele, the second allele would not be pathogenic at 37 GAA repeats.

    Usually, individuals with ataxia who are heterozygous for an expanded GAA repeat (> 66) may contain a separate loss-of-function mutation in the FXN gene copy over the allele with normal GAA repeat length. In the relevant clinical context, these patients should be considered to have Friedreich ataxia. [1] However, in populations where the prevalence of Friedreich ataxia carriers is high, such an
    individual may have a different disorder responsible for ataxia apart from being a carrier for Fr...

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    Conflict of Interest:
    None declared.
  • Published on:
    Not Visceral, but Localized Leishmanial Lymphadenopathy
    • Juan-Victor San Martin, Infectious Diseases (Internal Medicine) Hospital Universitario de Fuenlabrada
    • Other Contributors:
      • Jose-Manuel Ruiz-Giardin, Infectious Diseases (Internal Medicine)

    Dear Editor:
    We have read with interest this case, but we do not agree with the authors about considering this case as a visceral leishmaniasis (VL). This is a typical case of localized leishmanial Lymphadenopathy (LLL), as we and others described in several series of cases (1,2). This not-well known form of presentation of leishmaniasis is more common in Middle-East region, caused by dermatotropic strains like L. tropica or L. major, but isolated cases are described in Mediterranean region caused by L. infantum, as probably this case.
    In last decade, we suffered in Southern urban cities of Madrid, mainly Fuenlabrada, an important outbreak of leishmaniasis. More than 1000 cases of leishmaniasis were reported, and we could describe several cases of LLL (2).
    LLL is a form of presentation of leishmaniasis in patients without cellular immunosuppression, which presented with lymphadenopathy as the only form of presentation, and without systemic manifestations (no fever, no splenomegaly, no kytopenias, and normal acute phase reactants). Some LLL patients can refer lesions of cutaneous leishmaniasis (CL) near the adenopathy that had been previously spontaneously resolved or not, showing adenopathies as a local inflammatory rather than a systemic disease. Median duration of the adenopathy was 3 months in our patients. None of these patients, some of them without treatment, progressed to VL.
    We think it is important to distinguish LLL from VL because of crit...

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    Conflict of Interest:
    None declared.