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Updated: Nov 8, 2025

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
Published on: May 1, 2015
Bleeding Diathesis in Multiple Myeloma: A Rare Presentation of a Dreadful Emergency With Management Nightmare
Sabih Rahman1, Sindhusha Veeraballi2, Kok Hoe Chan1
1Internal Medicine, Saint Michael's Medical Center, Newark, USA.
Abstract:
Multiple myeloma is a neoplastic disorder of plasma cells. An abnormal coagulation profile, though commonly seen in multiple myeloma, can rarely manifest as life-threatening hemorrhagic complications. Bleeding tendencies in multiple myeloma can be explained by a variety of mechanisms such as dysfibrinogenemia, paraprotein-induced platelet dysfunction, shortened platelet survival, damage to the vascular endothelium, and acquired von-Willebrand syndrome. Herein, we report a 61-year-old female who presented with the signs and symptoms of hemorrhagic shock with multiple myeloma, which remained refractory to a massive transfusion protocol. Her condition stabilized when she was started on dexamethasone and antifibrinolytic infusion targeting acquired dysfibrinogenemia. To the best of our knowledge, hemorrhagic shock secondary to dysfibrinogenemia is an unusual phenomenon in multiple myeloma.
Insights
Multiple myeloma can cause severe bleeding due to dysfibrinogenemia, a rare complication. This case report highlights successful treatment with dexamethasone and antifibrinolytic therapy for hemorrhagic shock in a multiple myeloma patient.
Area of Science:
- Hematology
- Oncology
Background:
- Multiple myeloma, a plasma cell neoplasm, frequently presents with coagulation abnormalities.
- Hemorrhagic complications, though uncommon, can be severe and life-threatening in multiple myeloma patients.
- Potential mechanisms include dysfibrinogenemia, paraprotein effects on platelets, and acquired von-Willebrand syndrome.
Observation:
- A 61-year-old female with multiple myeloma experienced hemorrhagic shock.
- The patient's condition was refractory to massive transfusion protocols.
- Acquired dysfibrinogenemia was identified as a contributing factor.
Findings:
- Treatment with dexamethasone and antifibrinolytic infusion targeting dysfibrinogenemia led to clinical stabilization.
- This case illustrates an unusual presentation of hemorrhagic shock secondary to dysfibrinogenemia in multiple myeloma.
Implications:
- Highlights the importance of recognizing and managing rare bleeding complications in multiple myeloma.
- Suggests that antifibrinolytic therapy may be beneficial in specific cases of dysfibrinogenemia-related bleeding in multiple myeloma.
- Underscores the need for tailored treatment strategies for complex hemostatic disorders in plasma cell neoplasms.
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