Peripheral Gangrene, a Rare Side Effect of Methergine, Secondary to Antiphospholipid Antibody Syndrome: Case Report

Author(s):  
Major Anjali Rani ◽  
Preeti Vashistha ◽  
Mayank Sharma ◽  
Amrita Singh
2001 ◽  
Vol 77 (6) ◽  
pp. 517-21
Author(s):  
Célia S. Macedo ◽  
Roberta S. Martinez ◽  
Márcia C. Riyuzo ◽  
Herculano D. Bastos

2019 ◽  
Vol 26 (4) ◽  
pp. 1032-1036
Author(s):  
So Yi Lam ◽  
Chung-Shien Lee ◽  
Sandhya Sharma ◽  
Kit Cheng

Introduction Anti-angiogenic treatment in adjunct with chemotherapy is widely used for the treatment of various cancers. These agents inhibit vascular endothelial growth factor (VEGF) signaling thereby inhibiting tumor proliferation and invasion. Dysphonia, or voice changes, has been documented, but is an underreported side effect of anti-angiogenic agents. We report a case of intermittent dysphonia in a patient with metastatic, platinum-refractory ovarian cancer treated with bevacizumab. Case report A 48-year-old female with high grade mixed type ovarian adenocarcinoma and concurrent left sided breast cancer was transitioned to palliative therapy with gemcitabine-bevacizumab for her ovarian cancer. At a follow-up visit after three cycles of the new therapy, the patient complained of intermittent changes in her voice, describing periods of hoarseness or softness in her voice after the chemotherapy—sometimes to the point that her voice was inaudible. Management and outcome: A new pelvic thrombus was discovered upon assessment of the patient’s disease. Bevacizumab was held and she was referred to ear, nose, and throat evaluation for dysphonia. Laryngoscopic examination showed normal vocal cord, with normal movements and no lesion or necrosis. During subsequent follow-up, the patient reported improvement in her voice with no additional dysphonia. Discussion Vocal adverse effects of anti-VEGF agents have been documented in landmark trials and case reports; however, clinicians are often unaware of this rare side effect. Although VEGF-induced dysphonia may be rare and may not impede the patient’s quality of life in some cases, it is critical to acknowledge and not underestimate this adverse effect.


Lupus ◽  
2016 ◽  
Vol 26 (7) ◽  
pp. 777-782 ◽  
Author(s):  
X-J Zhou ◽  
M Chen ◽  
S-X Wang ◽  
F-D Zhou ◽  
M-H Zhao

Background Microvascular manifestations of antiphospholipid antibody syndrome in the kidneys include acute renal failure, thrombotic microangiopathy and hypertension. Therapy has been largely empiric. Case report A 49-year-old Chinese man presented with anuric acute renal failure without abundant proteinuria and heavy haematuria, but markedly low levels of urinary sodium, potassium and chlorine upon admission. On day 1 of hospitalization, his thrombocytopenia, anaemia and renal failure showed rapid progression. The presence of lupus anticoagulant and vascular ischaemia of the small vessels in renal arteriography were also observed. Anticoagulants, continuous renal replacement therapy, glucocorticoids and six sessions of plasma exchange were started. After the fourth plasma exchange (on day 20), his urine output increased and began to normalize. On day 25, haemodialysis was stopped and his general condition gradually improved. A renal biopsy was subsequently performed, and the histopathological diagnosis was thrombotic microangiopathy due to antiphospholipid antibody syndrome. A further 3-year follow-up showed that his haemoglobin level, platelet count and serum creatinine were within the normal range, with stable blood pressure. Conclusion Treatment modalities such as anticoagulation, immunosuppression and plasma exchange are likely to be necessary when severe acute renal failure combined with thrombotic microangiopathy present in nephropathy of antiphospholipid antibody syndrome.


2020 ◽  
pp. 107815522093549
Author(s):  
Gizem Yassa ◽  
Abdur R Shakir ◽  
Kuppuswamy Jagarlamudi ◽  
Ahmet E Yassa

Introduction Immune thrombocytopenia is an autoimmune disorder associated with increased thrombocyte destruction and impaired production in the bone marrow. Proposed mechanisms include an antibody or autoreactive T-cell-associated autoimmunity and thrombopoietin deficiency among others. Clinical manifestations are predominantly mucocutaneous hemorrhages including petechiae, purpura, mucosal bleeding in the urinary or the gastrointestinal tracts, menorrhagia, and epistaxis. The purpose of the treatment is to prevent bleeding rather than normalizing the platelet counts. First-line treatments include corticosteroids ± intravenous immunoglobulin and Anti-D which mainly decrease antibody-mediated platelet destruction and increase the number of peripheral Tregs. Second-line and subsequent therapies include splenectomy, chimeric anti-CD20 antibody (rituximab), which eliminates B cells and act as an immunomodulatory agent, and Thrombopoietin receptor agonists (romiplostim), which promote platelet production. Case report We describe a 40-year-old male patient diagnosed with immune thrombocytopenia that was refractory to first-line corticosteroid and intravenous immunoglobulin and second-line romiplostim monotherapy treatments. Management and outcome: The patient was given the romiplostim and rituximab combination which not only successfully treated thrombocytopenia but also resulted in grade 3 bone pains and the patient’s subsequent refusal to continue therapy. Discussion Common adverse effects of rituximab are infusion reactions and prolonged immunosuppression; those of romiplostim include thrombosis, headaches, arthralgia–myalgia, and gastrointestinal symptoms. This case shows that romiplostim has not caused any discernible side effects when given alone, while combination with rituximab resulted in severe bone and joint pains. We hypothesize that this combination regimen shows a synergistic effect both in terms of efficacy and adverse-effect probability and/or severity.


2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Hava Üsküdar Teke ◽  
Olga Meltem Akay ◽  
Deniz Gören Şahin ◽  
Mustafa Karagülle ◽  
Eren Gündüz ◽  
...  

Pleural effusion, as a side effect of tyrosine kinases, may be seen as most commonly associated with dasatinib and very rarely seen with nilotinib. In this report we present a chronic phase of CML case that was treated with nilotinib due to imatinib (Gleevec) allergy and had pleural effusion with nilotinib at 5th year of treatment. If pleural effusion develops in patients taking nilotinib and if this effusion is exudative and lymphocyte predominant, after ruling out pulmonary and cardiac etiologies, it must be associated with nilotinib; according to stage of effusion drug should be discontinued and/or steroid should be started and/or surgery should be performed.


2018 ◽  
Vol 9 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Augusto Ferreira Correia ◽  
Dinaldo Cavalcanti Oliveira ◽  
Marcio Sanctos

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