A 28‐year‐old previously healthy Hispanic man presented for evaluation of bleeding gums and rash. Four days prior he noted mild fatigue, cough, headache, and subjective fever consistent with an upper respiratory tract infection. On presentation, vital signs were stable, and physical exam revealed petechial hemorrhages on the soft palate with bleeding gums (wet purpura), with clots visible in the oral cavity, and petechiae on his extremities, abdomen, and chest. Initial labs revealed a platelet count < 1000/μL, with other cell lines preserved and a normal chemistry panel. Peripheral blood smear was without identifiable platelets, but normal red and white blood cells. Electrocardiogram, chest radiography, and abdominal ultrasound were unremarkable. A presumptive diagnosis of immune thrombocytopenia purpura (ITP) was made, and he was started on intravenous immunoglobulin (IVIG) and prednisone. After 5 days of treatment without signs of improvement, IVIG was discontinued. Serologic testing for common ITP precipitants, including human immunodeficiency virus (HIV) and hepatitis C virus (HCV) were negative. Helicobacter pylori ultimately returned positive by IgA, IgG, and stool antigen. Triple therapy with pantoprazole, amoxicillin, and biaxin was initiated, after which the patient had a brisk platelet response, and was discharged two days later, with a platelet count of 21,000/μL. On outpatient follow‐up, after completing triple therapy, his platelet count had normalized; his repeat stool H. pylori antigen was negative.
ITP is defined as a platelet count of less than 100,000/μL with no evidence of leukopenia or anemia, recently lowered from a previous threshold of less than 150,000/μL to minimize the inclusion of otherwise healthy individuals with transient and self‐limited thrombocytopenia. ITP can be divided into primary (most common) and secondary, which is related to infection resulting in molecular mimicry (often HIV, HCV, or H. pylori). These viruses contain amino acid sequences that have structural similarity to regions within platelet glycoproteins, which may allow antibodies intended for foreign pathogens to cross‐react with these endogenous proteins, causing thrombocytopenia. Rates of clinical responsiveness to treatment of H. pylori vary from study to study and by clinical region, but are generally highest in Japan and Italy, and are more heterogeneous in the United States. Furthermore, the majority of patients who received triple therapy were also treated with immunosuppression, potentially confounding results, and longer follow‐up is needed to assess if early responsiveness persists.
Given that H. pylori detection is noninvasive and relatively low cost, and eradication has minimal toxicity compared with standard ITP therapy, it should be included in the standard evaluation of individuals presenting with ITP. Eradication therapy may prove beneficial in some cases.
To cite this abstract:Sankey C, Brown C. Helicobacter Pylori As a Possible Precipitant of Immune Thrombocytopenia Purpura. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 441. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/helicobacter-pylori-as-a-possible-precipitant-of-immune-thrombocytopenia-purpura/. Accessed May 26, 2019.