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Blood Aug 2022
Topics: Humans; Prevalence; Purpura, Thrombotic Thrombocytopenic; Stroke
PubMed: 35980682
DOI: 10.1182/blood.2022016942 -
Internal Medicine (Tokyo, Japan) Nov 2021Drug-induced thrombocytopenia occurs through immune-mediated platelet destruction, and its management is challenging during tuberculosis treatment. Although rifampicin...
Drug-induced thrombocytopenia occurs through immune-mediated platelet destruction, and its management is challenging during tuberculosis treatment. Although rifampicin is the most common drug causing thrombocytopenia, isoniazid can also cause thrombocytopenia. We herein report a 75-year-old man who developed thrombocytopenia during tuberculosis treatment. Platelet-associated immunoglobulin G and a drug-induced lymphocyte stimulation test for isoniazid were positive; no other causes of thrombocytopenia were identified. The patient was diagnosed with isoniazid-induced immune thrombocytopenia, and the platelet count normalized after isoniazid discontinuation. We describe the immunological mechanism of thrombocytosis due to isoniazid, an uncommon cause of thrombocytopenia that physicians should be aware exists.
Topics: Aged; Humans; Isoniazid; Male; Platelet Count; Purpura, Thrombocytopenic, Idiopathic; Rifampin; Thrombocytopenia
PubMed: 34053983
DOI: 10.2169/internalmedicine.6520-20 -
Blood Jun 2023
Topics: Humans; Prospective Studies; Purpura, Thrombocytopenic, Idiopathic; Receptors, Thrombopoietin
PubMed: 37289475
DOI: 10.1182/blood.2023020243 -
Blood Jun 2021
Topics: ADAMTS13 Protein; Humans; Purpura, Thrombotic Thrombocytopenic
PubMed: 34165543
DOI: 10.1182/blood.2021011265 -
CMAJ : Canadian Medical Association... Jul 2021
Topics: Humans; Purpura, Thrombocytopenic, Idiopathic; Thrombocytopenia; Thrombosis; Vaccines
PubMed: 34226274
DOI: 10.1503/cmaj.210882-f -
Haematologica Feb 2023
Topics: Humans; Purpura, Thrombotic Thrombocytopenic
PubMed: 35488359
DOI: 10.3324/haematol.2022.281095 -
Tidsskrift For Den Norske Laegeforening... Apr 2024
Topics: Humans; Purpura; Male
PubMed: 38651721
DOI: 10.4045/tidsskr.23.0604 -
International Journal of Molecular... Apr 2022Since the discovery of camelid heavy-chain antibodies in 1993, there has been tremendous excitement for these antibody domains (VHHs/sdAbs/nanobodies) as research tools,... (Review)
Review
Since the discovery of camelid heavy-chain antibodies in 1993, there has been tremendous excitement for these antibody domains (VHHs/sdAbs/nanobodies) as research tools, diagnostics, and therapeutics. Commercially, several patents were granted to pioneering research groups in Belgium and the Netherlands between 1996-2001. Ablynx was established in 2001 with the aim of exploring the therapeutic applications and development of nanobody drugs. Extensive efforts over two decades at Ablynx led to the first approved nanobody drug, caplacizumab (Cablivi) by the EMA and FDA (2018-2019) for the treatment of rare blood clotting disorders in adults with acquired thrombotic thrombocytopenic purpura (TPP). The relatively long development time between camelid sdAb discovery and their entry into the market reflects the novelty of the approach, together with intellectual property restrictions and freedom-to-operate issues. The approval of the first sdAb drug, together with the expiration of key patents, may open a new horizon for the emergence of camelid sdAbs as mainstream biotherapeutics in the years to come. It remains to be seen if nanobody-based drugs will be cheaper than traditional antibodies. In this review, I provide critical perspectives on camelid sdAbs and present the promises and challenges to their widespread adoption as diagnostic and therapeutic agents.
Topics: Belgium; Humans; Immunoglobulin Heavy Chains; Netherlands; Purpura, Thrombotic Thrombocytopenic; Single-Domain Antibodies
PubMed: 35563400
DOI: 10.3390/ijms23095009 -
Indian Journal of Pharmacology 2020
Topics: Antitubercular Agents; Female; Humans; Purpura, Thrombocytopenic, Idiopathic; Tuberculosis; Young Adult
PubMed: 33283778
DOI: 10.4103/ijp.IJP_365_20 -
Blood Advances Feb 2022Immune thrombotic thrombocytopenic purpura (iTTP) is a life-threatening thrombotic microangiopathy. It is caused by a severe ADAMTS13 (a disintegrin and metalloprotease...
Immune thrombotic thrombocytopenic purpura (iTTP) is a life-threatening thrombotic microangiopathy. It is caused by a severe ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 motifs, 13) deficiency due to circulating autoantibodies, and is associated with significant morbidity and mortality. Current treatment options include plasma exchange, immunosuppression, and caplacizumab. When remission is achieved, the risk of relapse is high, especially in patients with persistent ADAMTS13 deficiency. We report the eradication of persistent ADAMTS13 inhibitory autoantibodies and restoration of normal ADAMTS13 activity using the anti-CD38 antibody daratumumab in two patients with iTTP. One patient had a frequently relapsing course, and the other a treatment-refractory first episode. There were no relevant adverse drug reactions.
Topics: Antibodies, Monoclonal; Autoantibodies; Humans; Purpura, Thrombocytopenic, Idiopathic; Purpura, Thrombotic Thrombocytopenic; Recurrence
PubMed: 34551063
DOI: 10.1182/bloodadvances.2021005124