Evaluation and Management of Drug‐Induced Thrombocytopenia in the Acutely Ill Patient

Wazny, Lori D; Ariano, Robert E.

doi:10.1592/phco.20.4.292.34883

Cited by 68 publications

(41 citation statements)

References 88 publications

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“…Non-immune thrombocytopenia caused by drugs results from a loss of cellularity within the bone marrow and an impairment of megakaryocyte proliferation and maturation, thereby leading to a decrease in platelet production. The myelosuppression is dose-dependent and often occurs slowly over the course of several weeks [6]. Chemotherapeutic compounds, including antimetabolites, cytotoxic agents, and alkylating agents are directly toxic to hematopoietic cells.…”

Section: Non-immune Suppression Of Platelet Productionmentioning

confidence: 99%

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Arnold

Nazi

Warkentin

et al. 2013

Transfusion Medicine Reviews

151

144

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Drug-induced immune thrombocytopenia (DITP) is a challenging clinical problem that is underrecognized, difficult to diagnose and associated with severe bleeding complications. DITP may be caused by classic drug-dependent platelet antibodies (eg, quinine); haptens (eg, penicillin); fibandependent antibodies (eg, tirofiban); monoclonal antibodies (eg, abciximab); autoantibody formation (eg, gold); and immune complex formation (eg, heparin). A thorough clinical history is essential in establishing the diagnosis of DITP and should include exposures to prescription medications, herbal preparations and even certain foods and beverages. Clinical and laboratory criteria have been established to determine the likelihood of a drug being the cause of thrombocytopenia, but these criteria can only be applied retrospectively. The most commonly implicated drugs include quinine, quinidine, trimethoprim/sulfamethoxazole and vancomycin. We propose a practical approach to the diagnosis of the patient with suspected DITP. Key features are: the presence of severe thrombocytopenia (platelet nadir <20 × 10 9 /L); bleeding complications; onset 5 to 10 days after first drug exposure, or within hours of subsequent exposures or after first exposure to fibans or abciximab; and exposure to drugs that have been previously implicated in DITP reactions. Treatment involves stopping the drug(s), administering platelet transfusions or other therapies if bleeding is present and counselling on future drug avoidance. The diagnosis can be confirmed by a positive drug re-challenge, which is often impractical, or by demonstrating drug-dependent platelet reactive antibodies in vitro. Current test methods, which are mostly flow cytometry-based, must show drug-dependence, immunoglobulin binding, platelet specificity and *

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Section: Non-immune Suppression Of Platelet Productionmentioning

confidence: 99%

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Arnold

Nazi

Warkentin

et al. 2013

Transfusion Medicine Reviews

151

144

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“…The evaluated clinically defined reduced platelet counts included three clinically relevant cutoffs: Յ100,000 cells/mm 3 , Յ50,000 cells/mm 3 , and Յ20,000 cells/mm 3 . These absolute platelet thresholds were evaluated because they, particularly the latter two, have been implicated as carrying an increased risk for spontaneous bleeding (14)(15)(16)(17)(18). In addition, decreases of Յ50% from baseline in patients with normal baseline platelet counts were evaluated because the occurrence of this endpoint has been identified as a meaningful exposure-response reducedplatelet-count outcome (19)(20)(21).…”

Section: Phase 3 Absssi Clinical Trials Establish-1 and Establish-2mentioning

confidence: 99%

Platelet Profile in Patients with Acute Bacterial Skin and Skin Structure Infections Receiving Tedizolid or Linezolid: Findings from the Phase 3 ESTABLISH Clinical Trials

Lodise

Fang

Minassian

et al. 2014

Antimicrob Agents Chemother

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c Tedizolid, the active moiety of tedizolid phosphate, is a recently approved oxazolidinone antibacterial with activity against a wide range of Gram-positive pathogens, including resistant strains such as methicillin-resistant Staphylococcus aureus. To date, 6 days of 200 mg tedizolid once daily has been shown to be noninferior to 10 days of 600 mg linezolid twice daily in two randomized, double-blind phase 3 trials (ESTABLISH-1 and ESTABLISH-2) for the treatment of patients with acute bacterial skin and skin structure infections (ABSSSIs). The intent of this study was to characterize the platelet profiles of patients receiving tedizolid relative to linezolid over the course of treatment using pooled data from these two trials. The occurrences of clinically defined and statistical analysis plan-specified reduced platelet counts were assessed at the study days 7 to 9 visit, the study days 11 to 13 visit, and the posttherapy evaluation (PTE) visit. At the study days 7 to 9 visit, incidences of reduced platelet counts were low and largely similar between the groups. The only notable difference was a lower incidence of thrombocytopenia (platelet counts, <150,000 cells/mm 3 ) among patients who received tedizolid (3.2%) relative to those who received linezolid (5.6%). At the study days 11 to 13 visit, patients who received tedizolid had lower incidences of platelet counts of <150,000 cells/mm 3 (؊5.9%), <112,500 cells/mm 3 (؊2.4%), and <100,000 cells/mm 3 (؊1.9%) than patients in the linezolid group. Similar differences were noted at the PTE visit. Findings across the two phase 3 ABSSSI trials suggest that 6 days of 200 mg tedizolid daily confers a low potential for reduced platelet counts among patients with ABSSSIs. (The ESTABLISH-1 and ESTABLISH-2 trials have been registered at ClinicalTrials.gov under registration numbers NCT01170221 and NCT01421511, respectively.)

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“…In addition, a variety of studies have shown that the immunologic activity of the drugs is specifically due to their single active pharmacologic components; in fact, cross-reactivity is absent even between thrombocytopenic drugs, such as quinidine and sulfamethoxazole. 11,12,15 The latter is one of the most frequent drug implicated in thrombocytopenia; it belongs to the class of sulfonamides, which also include sulpha-drugs. 16 The chemical structure of these compounds contains a group constituted by an atom of sulfur with valence 6 and double oxidation (S-O 2 ) and a link with an amino-nitrogen atom (NH 2 ); their general formula is R-SO 2 -NH 2 , with R representing an aromatic group.…”

Section: Discussionmentioning

confidence: 99%

Thrombocytopenia induced by a taurine-containing energy drink: an adverse reaction to herbal medicine

et al. 2014

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Thrombocytopenia is a well-recognized adverse effect of many drugs. The association of thrombocytopenia with herbal remedies, nutritional supplements, foods and beverages, complementary or alternative medicines, has been rarely described. There are reports of thrombocytopenia caused by quinine-containing beverages, cow's milk, cranberry juice, Jui, a Chinese herbal tea, Lupinus termis bean and tahini. A definite evidence of a causal association with thrombocytopenia is warranted; nevertheless not always there is provided probable or possible evidence in the association with thrombocytopenia. We report the first case, to our knowledge, of thrombocytopenia induced by taurine, present in an energy drink prescribed to our patient as tonic treatment.

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Evaluation and Management of Drug‐Induced Thrombocytopenia in the Acutely Ill Patient

Cited by 68 publications

References 88 publications

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Platelet Profile in Patients with Acute Bacterial Skin and Skin Structure Infections Receiving Tedizolid or Linezolid: Findings from the Phase 3 ESTABLISH Clinical Trials

Thrombocytopenia induced by a taurine-containing energy drink: an adverse reaction to herbal medicine

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