scholarly journals First diagnosis of thrombotic thrombocytopenic purpura after SARS-CoV-2 vaccine – case report

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Bilgin Osmanodja ◽  
Adrian Schreiber ◽  
Eva Schrezenmeier ◽  
Evelyn Seelow
Keyword(s):  
Acute Kidney Injury ◽  
Differential Diagnosis ◽  
Platelet Count ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Reference Range ◽  
Kidney Injury ◽  
Thrombocytopenic Purpura ◽  
Important Differential Diagnosis ◽  
First Case ◽  
Low Platelet Count

Abstract Background We report a case of a 25-year-old male patient, who developed acquired thrombotic thrombocytopenic purpura (aTTP) after receiving a first dose of mRNA-based SARS-CoV-2 vaccine Spikevax (mRNA-1273, Moderna Biotech, USA). While this is the first case in literature describing a case of aTTP after receiving the Spikevax vaccine, there are two other cases after mRNA-based Covid-19 vaccine and two after adenoviral SARS-CoV-2 vaccine. Case presentation The patient presented with persisting malaise, fever, headache, word-finding difficulties, nausea, vomiting, petechial bleeding, and hematuria 13 days after receiving a first dose of vaccination. Laboratory testing showed low platelet count, Coombs-negative hemolytic anemia, and mild acute kidney injury. We excluded vaccine induced immune thrombotic thrombocytopenia (VITT) as another important differential diagnosis and the final diagnosis was established after ADAMTS-13 (A Disintegrin And Metalloproteinase with a ThromboSpondin type 1 motif, member 13) activity was found to be < 1% (reference range > 40%) and ADAMTS-13 antibodies being 72.2 IU/L (reference range < 12 IU/L). We initiated empiric therapy of plasmapheresis and corticosteroids on admission and started caplacizumab the day after. The patient’s thrombocyte count normalized 3 days after admission, hemolysis and acute kidney injury resolved after 2 weeks. The patient received 2 doses of rituximab (1 g each) after the diagnosis of immune TTP was established. One month after the initial presentation, the patient is in good overall condition, but still receives daily caplacizumab due to ADAMTS-13 activity of < 1%. Conclusions Low platelet count after vaccination against SARS-CoV-2 has gained attraction after vaccine-induced immune thrombotic thrombocytopenia (VITT) has been described as a rare but severe complication of adenoviral-based vaccines. Thrombotic thrombocytopenic purpura (TTP) is an important differential diagnosis, but there are only few reports of TTP following SARS-CoV-2 vaccination. Despite pathophysiological and clinical differences of both entities, diagnostic uncertainty can result in the acute setting, since they share main symptoms such as headache and neurological alterations in addition to thrombocytopenia. In difference to other cases reported, this patient developed first symptoms of TTP as early as 4 days after vaccination, which suggests that vaccination merely acted as trigger for occult TTP, instead of truly inducing an autoimmunological process.

Cetuximab-induced thrombotic thrombocytopenic purpura in a patient with a resected squamous cell carcinoma of the lip

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14155-14155
Author(s):  
F. Rosen ◽  
T. Lad ◽  
M. Telfer ◽  
R. Catchatourian ◽  
B. Yim ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Platelet Count ◽  
Cell Carcinoma ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Squamous Cell ◽  
Egf Receptor ◽  
Endothelial Damage ◽  
Thrombocytopenic Purpura ◽  
Normal Peripheral Blood ◽  
First Case

14155 Background: Chemotherapy-associated thrombotic thrombocytopenic purpura (TTP) has been described in the literature. However Cetuximab, a monoclonal antibody targeted to the EGF receptor, has not yet been associated with TTP. We report a case of an 85 year old woman with a resected squamous cell carcinoma of the lip who developed TTP after receiving cetuximab. Methods: A day after receiving Cetuximab, as part of an adjuvant concurrent cetuximab-radiotherapy regimen, the patient presented with gingival bleeding and confusion without fever but with significant petechial rash and jaundice.. Hemoglobin level was 6.9 g/dL WBC 3.9 k/uL Platelet count 4 k/uL Lactate dehydrogenase 1350 U/L Indirect bilirubin 3.8 mg/dL Haptoglobulin < 6 mg/dL Reticulocyte count 4.4 %. Serum creatinine, ANA, coagulation profile, coomb‘s test were normal. Peripheral blood smear showed 3+ schistocytes. TTP was diagnosed and daily plasmapheresis was initiated. TTP resolved after 8 sessions of plasmapheresis with platelet count increasing to 446 k/uL and sustained. Results: Competing etiologies for our patient’s TTP were cancer and cetuximab. Most reported cases of cancer-associated TTP occurred in patients with metastatic adenocarcinoma. Our patient had a non-metastatic resected squamous cell carcinoma with only residual microscopic disease. Since TTP developed closely following cetuximab administration and resolved with plasmapheresis after stopping cetuximab, we concluded that its development was most likely secondary to cetuximab or to antibody developed to it. Possible mechanisms for cetuximab-induced TTP are direct endothelial damage by cetuximab leading to platelet activation and aggregation or inhibition of metalloproteinase, resulting in accumulation of Ultra-large VWF multimers. Conclusions: Targeted-therapy is emerging as an effective treatment modality in medical-oncology. Further clinical experience is needed to ascertain the full extent of potentially fatal adverse events. To our knowledge this is the first case of cetuximab-induced TTP. No significant financial relationships to disclose.

Platelet transfusion and catheter insertion for plasma exchange in patients with thrombotic thrombocytopenic purpura and a low platelet count

Transfusion ◽  
2015 ◽  
Vol 55 (7) ◽  
pp. 1798-1802 ◽  
Author(s):  
Etienne Riviere ◽  
Mélanie Saint-Léger ◽  
Chloé James ◽  
Yahsou Delmas ◽  
Benjamin Clouzeau ◽  
...  
Keyword(s):  
Platelet Count ◽  
Plasma Exchange ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Platelet Transfusion ◽  
Catheter Insertion ◽  
Thrombocytopenic Purpura ◽  
Low Platelet Count

scholarly journals Coagulopathy in Acute Puumala Hantavirus Infection

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1553
Author(s):  
Sirpa Koskela ◽  
Satu Mäkelä ◽  
Tomas Strandin ◽  
Antti Vaheri ◽  
Tuula Outinen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Platelet Count ◽  
Disseminated Intravascular Coagulation ◽  
Inflammatory Mediators ◽  
Kidney Injury ◽  
Hemorrhagic Fever ◽  
Endothelial Activation ◽  
Hantavirus Infection ◽  
Increased Risk ◽  
Low Platelet Count

Puumala hantavirus (PUUV) causes a hemorrhagic fever with renal syndrome (HFRS), also called nephropathia epidemica (NE), which is mainly endemic in Europe and Russia. The clinical features include a low platelet count, altered coagulation, endothelial activation, and acute kidney injury (AKI). Multiple connections between coagulation pathways and inflammatory mediators, as well as complement and kallikrein–kinin systems, have been reported. The bleeding symptoms are usually mild. PUUV-infected patients also have an increased risk for disseminated intravascular coagulation (DIC) and thrombosis.

The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura

2015 ◽  
Author(s):  
Marina Noris ◽  
Tim Goodship
Keyword(s):  
Acute Kidney Injury ◽  
Plasma Exchange ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Haemolytic Uraemic Syndrome ◽  
Renal Involvement ◽  
Kidney Injury ◽  
Fresh Frozen Plasma ◽  
Thrombocytopenic Purpura ◽  
Geographical Variations ◽  
Fresh Frozen

The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.

scholarly journals P73 A rare case: Thrombotic thrombocytopenic purpura presenting with acute kidney injury

2019 ◽  
Author(s):  
Gamze Seval Şahin ◽  
Beltinge Demircioğlu Kılıç ◽  
Mithat Büyükçelik ◽  
Sinan Akbayram
Keyword(s):  
Acute Kidney Injury ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Rare Case ◽  
Kidney Injury ◽  
Thrombocytopenic Purpura

scholarly journals Heparin-induced thrombocytopenia as a cause of prolonged low platelet count in patient with thrombotic thrombocytopenic purpura treated with plasmapheresis

2017 ◽  
Vol 64 (2) ◽  
Author(s):  
Agata Winiarska ◽  
Norbert Kwella ◽  
Tomasz Stompór
Keyword(s):  
Platelet Count ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Low Molecular Weight Heparin ◽  
Careful Analysis ◽  
Low Molecular Weight ◽  
Thrombotic Microangiopathies ◽  
Thrombocytopenic Purpura ◽  
Heparin Induced Thrombocytopenia ◽  
Low Platelet Count ◽  
Functional Deficiency

Thrombotic thrombocytopenic purpura (TTP) is a rare disorder belonging to thrombotic microangiopathies (TMA) and is caused by functional deficiency of metalloproteinase ADAMTS-13. Plasma exchange (PE) remains the treatment of choice in this disease. Here were describe the case of patient who apparently recovered from TTP following multiple sessions of PE, but remained thrombocytopenic. Careful analysis revealed the development of heparin-induced thrombocytopenia (HIT) that precluded platelet count (PLT) normalization. Full normalization of PLT followed discontinuation of PE and low-molecular weight heparin.

Thrombotic Thrombocytopenic Purpura: Mechanism for Effectiveness of Plasmapheresis

1979 ◽  
Author(s):  
J. G. Kelton ◽  
P. B. Neame ◽  
I. Walker ◽  
A. G. Turpie ◽  
J. McBride ◽  
...  
Keyword(s):  
Platelet Count ◽  
Thrombotic Thrombocytopenic Purpura ◽  
The Other ◽  
Unknown Etiology ◽  
Normal Range ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura ◽  
Serious Illness ◽  
Normal Platelet ◽  
Very High

Thrombotic thrombocytopenic purpura (TTP) is a rare but serious illness of unknown etiology. Treatment by plasmapheresis has been reported to be effective but the mechanism for benefit is unknown. We have investigated the effect of plasmapheresis in 2 patients with TTP by quantitating platelet associated IgG (PAIgG) levels prior to and following plasmapheresis. Both patients had very high levels of PAIgG at presentation (90 and A8 fg IgG/platelet respectively, normal 0-5). in both, the PAIgG levels progressively fell to within the normal range and the platelet count rose following plasmapheresis. One patient remained in remission with normal platelet counts and PAIgG levels. The other relapsed after plasmapheresis and the PAIgG level rose prior to the fall in platelet count. Plasmapheresis was repeated and resulted in normalization of both the platelet count and PAIgG level. It is suggested that plasmapheresis removes antiplatelet antibody or immune complexes which may be of etiological importance in this illness.

Acute kidney injury and nephrotic syndrome associated with eltrombopag therapy in chronic idiopathic thrombocytopenic purpura

2021 ◽  
Vol 14 (4) ◽  
pp. e241462
Author(s):  
Suchi Anindita Ghosh ◽  
Jean Patrick ◽  
Kyaw Zin Maw
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Nephrotic Syndrome ◽  
Idiopathic Thrombocytopenic Purpura ◽  
Kidney Injury ◽  
High Dose ◽  
Chronic Idiopathic Thrombocytopenic Purpura ◽  
Thrombocytopenic Purpura ◽  
Antibody Screen ◽  
Auto Antibody

A 77-year-old man was admitted with severe acute kidney injury and nephrotic syndrome. He was started on eltrombopag for chronic idiopathic thrombocytopenic purpura 6 weeks earlier. An ultrasound of the kidneys was normal and an auto-antibody screen was negative. The use of the Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 5) between the patient’s development of acute renal failure and eltrombopag therapy. Literature review identified only one other case of nephrotic syndrome and acute kidney injury associated with eltrombopag therapy in which a kidney biopsy revealed focal segmental glomerulosclerosis. Due to the challenges faced during the prevailing SARS-CoV-2 pandemic and persistent low platelet counts a renal biopsy was not undertaken. On stopping eltrombopag, the patients renal function stabilised and he successfully went into remission following treatment with high dose corticosteroids and diuretics. This report of a serious case of reversible renal failure and nephrotic syndrome after treatment with eltrombopag may serve to inform clinicians about the possible severe renal adverse effects of eltrombopag before its commencement for future use.

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