An Unusual Cause of Secondary ITP in a 34-Year-Old Hispanic Male

Secondary immune thrombocytopenic purpura (ITP) associated with Helicobacter pylori (H. pylori) infection has been described in the literature. It appears to have a geographic distribution; mostly encountered in countries with a higher prevalence for H. pylori such as Italy or Japan. H. pylori eradication has been recommended in the management of ITP with studies showing improvement in the platelet count in some patients. Substantial platelet count increases in patients with severe thrombocytopenia (platelet counts <30 × 103 microliter), however, are uncommon with H. pylori treatment alone. Here, we present a 34-year-old Hispanic male with worsening chronic thrombocytopenia that resolved following eradication of his H. pylori infection. Herein, we highlight a rare and reversible cause of secondary ITP. With this case report, we hope to encourage physicians to include H. pylori testing in the evaluation of thrombocytopenia.

A rare case of Acute Motor and Sensory Axonal Neuropathy (AMSAN) and Immune Thrombocytopenic Purpura (ITP) related to Hemophilus influenzae

We describe a rare case presenting with both signs of acute motor and sensory axonal neuropathy (AMSAN) and immune thrombocytopenic purpura (ITP) possibly triggered by Hemophilus influenzae. Guillain-Barre is an autoimmune disorder purported to be due to molecular mimicry, often with a preceding infection, leading to myelin sheath or even axonal damage, AMSAN, in the peripheral nervous system (PNS). Rarely, there have been case reports of concurrent acute autoimmune disorders leading to a more complex presentation and additional comorbidities. A 42-year-old man presented with 2 days of progressive lower and upper extremity paresthesia’s, ataxia preceded by an upper respiratory infection. Examination showed areflexia and purpura, recent oral mucosal hemorrhage. Lab results showed severe thrombocytopenia suspicious for ITP. Over the ensuing weeks while inpatient, his condition quickly deteriorated to requiring an intubation for respiratory failure and not immediately responsive to IVIG. Recovery, both for AMSAN confirmed by EMG and ITP, was eventually achieved with time and five treatments of plasmapheresis and eventually was discharged to a rehabilitation facility. A thorough infectious workup revealed a possible trigger being Haemophilus influenzae. There have been rare occasions of concurrent GBS and ITP, but even more rare is the presence of both AMSAN and ITP which requires quick recognition and evaluation. This case highlights the need for a thorough initial history taking and a general physical exam, in addition to unique management decisions and strategies in patients with suspected GBS as there may be signs of other associated disorders that require immediate attention.

Catastrophic anti-phospholipid syndrome with Libman-Sacks endocarditis following eltrombopag therapy for immune thrombocytopenic purpura: A case report

Background Immune thrombocytopenic purpura (ITP) is an autoimmune disease, with accelerated destruction of platelets, estimated to affect 1.6–3.9 in 100,000 adults every year in the European Union. Glucocorticoids and intravenous immunoglobulins are common drug therapies. In refractory cases, drugs that enhance thrombopoiesis may be used. Eltrombopag is a thrombopoietin receptor agonist, known to increase platelet count in patients with refractory ITP. Thrombotic adverse events have been described in association with Eltrombopag administration. Case report A young female patient of Ethiopian ancestry with systemic lupus erythematosus, triple Antiphospholipid (APLA) positive serology and refractory ITP who received Eltrombopag and 2 weeks later developed catastrophic APLA syndrome with severe Libman-Sacks endocarditis of the mitral and aortic valves, multiple intracerebral infracts and arterial thrombosis of the left upper limb. Conclusion Eltrombopag is a salvage drug, used in refractory ITP. Thrombotic adverse events, some of which may be life-threatening, are a possible complication, especially in high-risk patients.

Oral Manifestations of Immune Thrombocytopenic Purpura

Introduction: Hemorrhagic lesions of the oral mucosa are the most common clinical manifestations of Immune thrombocytopenic purpura (ITP). Case Report: A 41-year-old female patient consulted the oral surgery department of the dental consultation and treatment center in Rabat for spontaneous gingivorrhagia. Clinical examination and further examination showed severe thrombocytopenia associated with an anemic syndrome. The diagnosis of ITP was made. Treatment was based on oral corticosteroids and immunoglobulin in the hospital. Conclusion: These manifestations sometimes lead the patient to consult his dental surgeon in the first intention, hence the need to make the diagnosis based on a thorough global examination and to refer the patient to an adapted structure.

A rare presentation of immune thrombocytopenic purpura

Immune thrombocytopenic purpura (ITP) is defined as a hematologic disorder, characterized by isolated thrombocytopenia without any apparent cause. Some patients may be diagnosed during routine blood investigations or may present with bleeding diathesis. Treatment required for moderate to severe thrombocytopenia or those with bleeding manifestations. We present a case of 43 year old male, sputum positive pulmonary tuberculosis on isoniazid (H), rifampin (R), pyrazinamide (Z), and ethambutol (E) (HRZE) with persistent thrombocytopenia. He developed hepatitis hence isoniazid (INH) and rifampicin were stopped. He had fever, rash, purpura, hematuria and blood tinged sputum with platelet count of 10,000. 4 random donor platelets (RDPs) given. He suffered from mild COVID-19 infection and recovered in 2 weeks but platelets remained low. Bone marrow examination was suggestive of ITP. Inspite of steroid therapy no improvement was seen. Later was treated with injection romiplostim, and started on systemic lupus erythematosus (SLE) regimen for tuberculosis and discharged with regular follow up. Last platelet count being 1,20000/dl, liver function tests normal and now restarted on HRZE.

HUWE1 Causes an Immune Imbalance in Immune Thrombocytopenic Purpura by Reducing the Number and Function of Treg Cells Through the Ubiquitination Degradation of Ets-1

Background: Immune thrombocytopenic purpura (ITP) is an autoimmune bleeding disorder and the decreased number and immunosuppressive dysfunction of Treg cells are key promoters of ITP. However, their mechanisms in ITP development have not been fully clarified.Methods: HUWE1 mRNA and protein levels in CD4+ T cells in peripheral blood from ITP patients were assessed by quantitative real-time PCR and Western blot. HUWE1 function in ITP was estimated using flow cytometry, enzyme-linked immunosorbent assay and immunosuppression assay. Besides, the HUWE1 mechanism in reducing the number and function of Treg cells in ITP was investigated by immunoprecipitation, cycloheximide-chase assay, ubiquitin experiment and immunofluorescence assay.Results: HUWE1 expression was elevated in CD4+ T cells in peripheral blood from ITP patients and HUWE1 mRNA level was negatively correlated with platelet counts and Treg cell percentage. Moreover, the interference with HUWE1 increased the number of Treg cells and enhanced its immunosuppressive function, and the HUWE1 overexpression produced the opposite results. For the exploration of mechanism, HUWE1 interacted with E26 transformation-specific-1 (Ets-1) and this binding was dependent on the negative regulation of the phosphorylation level of Ets-1 (Thr38) and HUWE1 facilitated the ubiquitin degradation of Ets-1 protein to restrain Treg cell differentiation and weaken their immunosuppressive functions. The in vivo assay confirmed that the HUWE1 inhibitor alleviated ITP in mice.Conclusion: HUWE1 induced the immune imbalance in ITP by decreasing the number and weakening the function of Treg cells through the ubiquitination degradation of Ets-1.