Clinical Pearls & Morning Reports
Immune thrombocytopenia is an acquired thrombocytopenia caused by antiplatelet autoantibodies directed against platelet antigens. Molecular mimicry between viral antigens and host proteins has been implicated in the pathogenesis of secondary immune thrombocytopenia, which may be associated with several acute and chronic infections. Read the NEJM Case Records of the Massachusetts General Hospital here.
Q: What are some of the sexually transmitted diseases in the differential diagnosis of proctocolitis?
A: Gastrointestinal manifestations of common sexually transmitted infections are not always recognized by clinicians. Sexual history should be considered in the evaluation of any patient who presents with rectal symptoms. Infections with Neisseria gonorrhoeae, Chlamydia trachomatis, and Treponema pallidum can all cause a spectrum of rectal symptoms, including typical features of proctitis, and severe disease can occasionally mimic inflammatory bowel disease. The most invasive serotypes of C. trachomatis can cause lymphogranuloma venereum, with a hemorrhagic proctocolitis that is typically associated with severe anorectal pain. Lymphogranuloma venereum often leads to painful lymphadenopathy and is rarely reported in the United States outside of an outbreak.
Q: Is proctocolitis due to herpes simplex virus associated with immune thrombocytopenia?
A: Herpes simplex virus can cause painful proctitis, often with associated perianal lesions. Invasive disease may involve the colon proximal to the rectum, particularly in immunocompromised patients. In the presence of immunocompromise, reactivation of latent virus is more likely than primary infection. Although proctocolitis due to herpes simplex virus has been associated with extraintestinal manifestations, including sacral anesthesia, urinary retention, and impotence, it is not frequently associated with immune thrombocytopenia or other hematologic abnormalities.
A: Transmission of CMV can occur through multiple routes, including sexual intercourse, close contacts, and occupational exposures, such as child care. Tissue-invasive CMV infection frequently involves the gastrointestinal tract, and proctocolitis has been well described with both primary infection and reactivation of latent disease. CMV infection is also associated with a range of hematologic manifestations, including anemia, the development of cold agglutinins, disseminated intravascular coagulation, and immune thrombocytopenia. CMV is a notable cause of post-transplantation complications and death. CMV-associated immune thrombocytopenia has been described in recipients of solid-organ transplants and is more likely to be associated with primary infection than with reactivation of latent disease.
A: The initial management of CMV disease in solid-organ transplant recipients includes the institution of antiviral therapy in conjunction with weekly monitoring by means of CMV nucleic acid tests performed on the same sample type (whole blood or plasma) at the same laboratory. First-line antiviral options include oral valganciclovir and intravenous ganciclovir. In patients with renal failure, dosing of these agents requires adjustment for the calculated creatinine clearance to reduce the incidence of side effects, as well as avoidance of inappropriately low doses, which may increase the risk of CMV that is refractory or resistant to treatment. Guidelines recommend the administration of antiviral therapy at therapeutic dosage for a minimum of 2 weeks, until the patient has clinically recovered and two consecutive measurements of the CMV DNA viral load separated by 1 week indicate CMV DNA eradication.