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

UNLABELLED

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.