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Clinically it is characterized by microangiopathic haemolytic anaemia, thrombocytopenia, renal and neurological involvement. It encompasses four entities: thrombotic thrombocytopenic purpura (TTP) due to ADAMTS13 enzyme activity deficiency, typical haemolytic uremic syndrome (HUS) due to enteric infection by Shiga toxin-producing <span class="elsevierStyleItalic">Escherichia coli</span>, atypical HUS as a consequence of deregulation of the alternative complement pathway, and lastly, TMA secondary to drugs and other clinical entities<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>. Without proper diagnosis and treatment, this type of pathology is associated with high morbidity and mortality<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>. We report the case of a patient with rifampicin-induced TMA.</p><p id="par0010" class="elsevierStylePara elsevierViewall">A 79-year-old woman with a history of rheumatoid arthritis on treatment with tocilizumab. Admitted for cavitary pneumonia due to <span class="elsevierStyleItalic">Mycobacterium avium intracellulare</span>. Treatment with ethambutol, rifampicin, clarithromycin and amikacin was started with good tolerance. After 72 h, symptoms of dyspnoea and fever began. Laboratory tests showed elevated white blood cells (20,000/mm<span class="elsevierStyleSup">3</span>), indirect bilirubin (5.4 mg/dL), LDH (941 U/L), and thrombocytopenia (18,000/mm<span class="elsevierStyleSup">3</span>). In this context, superinfection and consumption thrombocytopenia were suspected, so meropenem and levofloxacin were added to the treatment. Poor evolution with increased oxygen requirements, decreased haemoglobin 9.8 g/dL and progression of thrombocytopenia up to 2000/mm<span class="elsevierStyleSup">3</span>. A peripheral blood smear showed schistocytes and low haptoglobin, confirming intravascular haemolysis. Given the diagnostic impression of TTP, methylprednisolone was started, <span class="elsevierStyleItalic">Mycobacterium</span> treatment was discontinued, and the patient was admitted to the Critical Care Unit for plasmapheresis and respiratory support. The work-up was completed with an ADAMTS13 assay, levels of which were within the normal range (activity > 5–10%) which ruled out PTT, anti-ADAMTS13 antibodies were not determined. After 48 h of corticosteroids and two sessions of plasmapheresis, laboratory and clinical improvement, treatment for <span class="elsevierStyleItalic">Mycobacterium</span> was reintroduced and the haemolytic anaemia and thrombocytopenia recurred. Rifampicin-induced TMA was suspected given the described toxicity of the drug, with a score of nine in the Naranjo algorithm (establishes a definite relationship between the drug and the adverse event), so it was discontinued, maintaining clarithromycin, ethambutol and amikacin, with good progression and discharge.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Awareness of drug-induced TMAs is essential, as they are life-threatening and rapidly progressive disorders<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a>. Typically, the distinction between these entities was based on clinical criteria. However, the wide clinical overlap has led to the need for Shiga toxin detection (diagnostic of typical HUS) and the determination of ADAMTS13 activity. Thus, levels below 5–10% evidence a case of TTP, and non-low levels of ADAMTS13 will guide the diagnosis towards atypical HUS and secondary TMA. This is the first case described in the literature of rifampicin-induced TMA, given the temporal relationship and the absence of other triggers (systematic search in PubMed for articles published between 2012 and 2022 on thrombotic microangiopathy. The search combined the terms “<span class="elsevierStyleItalic">thrombotic microangiopathies</span>”, “<span class="elsevierStyleItalic">rifampicin</span>”, “<span class="elsevierStyleItalic">atypical haemolytic uremic syndrome</span>”, “<span class="elsevierStyleItalic">induced thrombocytopenia</span>” and “<span class="elsevierStyleItalic">thrombotic thrombocytopenic purpura</span>”). There are several mechanisms by which drugs cause these adverse effects<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a>, acute immune-mediated reactions or toxic reactions. Treatment is based on targeting the underlying cause, thereby reversing the thrombocytopenia within seven to 10 days. Treatment with corticosteroids, immunoglobulins, plasmapheresis or platelet transfusion<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> is necessary in patients with platelet counts <10,000–20,000/mm<span class="elsevierStyleSup">3</span>.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0020" class="elsevierStylePara elsevierViewall">This paper has not received any type of funding.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interests</span><p id="par0025" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Funding" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Conflict of interests" ] 2 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Síndrome hemolítico urémico atípico" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "M. Blasco Pelicano" 1 => "S. Rodríguez De Córdoba" 2 => "J.M. Campistol Plana" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.medcli.2014.08.006" "Revista" => array:6 [ "tituloSerie" => "Med Clin (Barc)" "fecha" => "2015" "volumen" => "145" "paginaInicial" => "438" "paginaFinal" => "445" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25433773" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Diagnostic and therapeutic guidelines of thrombotic microangiopathies of the Spanish Apheresis Group" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "E. Contreras" 1 => "J. De La Rubia" 2 => "J. Del Río-Garma" 3 => "M. Díaz-Ricart" 4 => "J.M. García-Gala" 5 => "M. Lozano" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Med Clin (Barc)" "fecha" => "2015" "volumen" => "144" "paginaInicial" => "331.e1" "paginaFinal" => "331.e13" ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0015" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Syndromes of thrombotic microangiopathy" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "J.N. George" 1 => "C.M. Nester" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1056/NEJMra1312353" "Revista" => array:6 [ "tituloSerie" => "N Engl J Med" "fecha" => "2014" "volumen" => "371" "paginaInicial" => "654" "paginaFinal" => "666" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25119611" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0020" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Rifampin induced thrombotic thrombocytopenic purpura" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "H. Hamad" 1 => "K.K. Sahu" 2 => "S. Dunn" 3 => "L. Milla" 4 => "A. Caffery" 5 => "N. Islam" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s12288-019-01249-9" "Revista" => array:6 [ "tituloSerie" => "Indian J Hematol Blood Transfus" "fecha" => "2020" "volumen" => "36" "paginaInicial" => "575" "paginaFinal" => "577" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/32647438" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0025" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Trombocitopenia grave inducida por levofloxacino" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "C. Sanclemente-Ansó" 1 => "K. Mojica-Poveda" 2 => "C. Capdevila-Aguilera" 3 => "R. Pujol-Farriols" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.regg.2012.02.011" "Revista" => array:6 [ "tituloSerie" => "Rev Esp Geriatr Gerontol" "fecha" => "2012" "volumen" => "47" "paginaInicial" => "180" "paginaFinal" => "181" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/22682015" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000015900000011/v2_202301310812/S2387020622005290/v2_202301310812/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000015900000011/v2_202301310812/S2387020622005290/v2_202301310812/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020622005290?idApp=UINPBA00004N" ]
