Augmentin Induced Thrombocytosis: A Maiden Case Series

Balaji, O; Amita, Dita; Patil, Navin

doi:10.22159/ajpcr.2017.v10i5.17119

Cited by 3 publications

(2 citation statements)

References 3 publications

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“…15 To improve the application of the data to the Naranjo probability scale, adaptations were made by adding thrombocytosis-specific criteria to improve the grading of case reports for causality, as seen in Table 2. For the purpose of this review, reports of suspected thrombocytosis were systematically assessed for causality (Table 3 16-45 ). The following criteria will be utilized to assess causality of a drug by case report: number of cases described by independent investigators and the Naranjo score associated with causality.…”

Section: Methodsmentioning

confidence: 99%

“…A significant number of antibiotics have been implicated in the development of thrombocytosis. [18][19][20][21]26,34,39,44 We have identified 10 cases of thrombocytosis attributed to antibiotics, from 8 different investigators with at least 1 case >5 on the Naranjo assessment score. This is good evidence that, as a class, antibiotics would be considered causative in the development of thrombocytosis.…”

Section: Antibioticsmentioning

confidence: 99%

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A Review and Assessment of Drug-Induced Thrombocytosis

Thompson

2018

Ann Pharmacother

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Objectives: The purpose of this article is to review the current literature on drug-induced thrombocytosis with the goal of critically assessing causality and providing a comprehensive review of the topic. Thrombopoietic growth factors, such as thrombopoietin-receptor agonists (romiplostim and eltrombopag) and erythropoietin are not included in our review. Data Sources: The literature search included published articles limited to the English language and humans in MEDLINE, EMBASE, and Web of Science databases. MEDLINE/PubMed (1966 to September 2018) was searched using the MeSH terms thrombocytosis/chemically-induced and thrombocytosis/etiology. EMBASE (1980 to September 2018) was searched using the EMTAGS thrombocytosis/side effect. Web of Science (1970 to September 2018) was searched using the search term thrombocytosis. References of all relevant articles were reviewed for additional citations and information. Study Selection and Data Extraction: Review articles, clinical trials, background data, case series, and case reports of drug-induced thrombocytosis were collected, and case reports were assessed for causality using a modified Naranjo nomogram. Data Synthesis: Drug-induced thrombocytosis, a form of reactive thrombocytosis cannot be easily differentiated from more common etiologies of reactive thrombocytosis. In all, 43 case reports of drug-induced thrombocytosis from a wide variety of drugs and drug classes were reviewed using a modified Naranjo probability scale that included criteria specific for thrombocytosis. Conclusions: Drug-induced thrombocytosis is a relatively rare adverse drug reaction. The strongest evidence of causality supports low-molecular-weight heparins and neonatal drug withdrawal. Weaker evidence exists for all-trans retinoic acid, antibiotics, clozapine, epinephrine, gemcitabine, and vinca alkaloids.

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Section: Methodsmentioning

confidence: 99%

Section: Antibioticsmentioning

confidence: 99%

A Review and Assessment of Drug-Induced Thrombocytosis

Thompson

2018

Ann Pharmacother

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Amoxicillin/clavulanic-acid

2017

Reactions Weekly

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Previous studies have demonstrated that Nocardia brasiliensis is susceptible to amoxicillin-clavulanic acid and that its I8-lactamases are inhibited in vitro by, clavulanic acid. A cardiac transplant patient with disseminated infection caused by N. brasiliensis was treated with this drug combination with good response, but relapsed while still on therapy. The relapse isolate was found to be identical to the initial isolate by using genomic DNA restriction fragment patterns obtained by pulsed field gel electrophoresis, but it was resistant to amoxicillin-clavulanic acid. On isoelectric focusing, the ,I-lactamase from the relapse isolate exhibited a shift in the isoelectric point (pl) of its major band from 5.10 to 5.04 compared with the enzyme from the pretreatment isolate. As determined by using values of the amount of ,-lactamase inhibitor necessary to give 50 5% inhibition of P-lactamase-mediated hydrolysis of 50 FM nitrocefin, the I8-lactamase of the relapse isolate was also 200-fold more resistant than the enzyme from the pretreatment isolate to clavulanic acid and was more resistant to sulbactam, tazobactam, cloxacillin, and imipenem. The I-lactamase of the relapse isolate exhibited a 10-fold decrease in hydrolytic activity for cephaloridine and other hydrolyzable cephalosporins compared with that for nitrocefin. Acquired resistance to amoxicillin-clavulanic acid in this isolate of N. brasiliensis appears to have resulted from a mutational change affecting the inhibitor and active site(s) in the

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Secondary thrombocythemia with ST-segment elevation myocardial infarction as the first manifestation: a case report

Hou

Zhao

et al. 2023

Annals of Medicine &Amp; Surgery

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Introduction: Secondary thrombocythemia (ST), also called reactive thrombocytosis, is caused by a disorder that triggers increased production by normal platelet-forming cells and is characterized by the abnormally increased number of platelet and megakaryocytes in the bone marrow. Previous reports have found complications from malignant tumors, chronic inflammation, acute inflammation, acute hemorrhage, splenectomy, etc. to be the common causes of ST. However, reports of secondary thrombocytosis caused by antibiotics are limited and there are no reports of secondary thrombocytosis with acute myocardial infarction as the first presentation. If the patient is at high risk of thrombosis, intensive antithrombotic therapy is required. To raise clinicians’ awareness of drug-induced secondary thrombocytosis and to enhance antithrombotic therapy for high-risk patients, this article presented a case of drug-induced secondary thrombocytosis with acute ST-segment elevation myocardial infarction as the primary manifestation. Case presentation: An 80-year-old woman was admitted with cardiogenic shock due to post-activity chest pain. She was started on aspirin and clopidogrel antiplatelet therapy, then replaced aspirin with indolibuprofen, which has relatively few side effects. There was no significant decrease in platelet counts during treatment. Clinical discussion: Secondary thrombocythemia, characterized by nonspecific symptoms, is difficult to diagnose. Secondary thrombocytosis with acute myocardial infarction as the first symptom is uncommon, but is very urgent and associated with a poor prognosis. What’s more, cause-specific treatment counts for secondary thrombocythemia. Therefore it is important to search for the causal factor of secondary thrombocytosis. Secondary thrombocytosis caused by cephalosporins is rare. There is a need to arouse the attention of clinicians to the ST caused by cephalosporins and to provide a guide of treatment to these patients. Conclusion: After a thorough analysis of the pertinent literature, we discovered that several retrospective studies demonstrated the effectiveness of cytoreductive therapy in significantly reducing platelet counts. Based on this finding, we prescribed hydroxyurea to our patient, which led to a gradual decrease in platelet count and ultimately resulted in a return to normal levels.

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Augmentin Induced Thrombocytosis: A Maiden Case Series

Cited by 3 publications

References 3 publications

A Review and Assessment of Drug-Induced Thrombocytosis

A Review and Assessment of Drug-Induced Thrombocytosis

Amoxicillin/clavulanic-acid

Secondary thrombocythemia with ST-segment elevation myocardial infarction as the first manifestation: a case report

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