acyclovir and Amyloidosis

Bortezomib is proteasome inhibitor used in multiple myeloma treatment. The reactivation of herpes simplex virus (HSV) and varicella-zoster virus (VZV) during bortezomib-based therapy is a well-known adverse event. Antiviral prophylaxis is mandatory. Nevertheless, reports of herpesviral encephalitis are scarce.. A 57-year-old multiple myeloma patient who during CyBorD protocol (Bortezomib, cyclophosphamide, and dexamethasone), after a transient suspension of antiviral prophylaxis presented progressive headaches unresponsive to conventional analgesics, asthenia, fever, episodic visual hallucinations, and vesicular lesions in the right supraorbital and frontal region. Herpetic encephalitis was diagnosed after detecting herpes zoster in cerebrospinal fluid.. The patient was treated with acyclovir 500mg every 6 hours for 21 days, and subsequent valacyclovir prophylaxis achieving an excellent clinical evolution. Anti-myeloma treatment was changed to lenalidomide and dexamethasone achieving a durable complete response. Herpesviral encephalitis is a rare but severe complication associated with the use of Bortezomib, especially when patients did not receive acyclovir prophylaxis. However, a rapid detection based on the clinical suspicion, and the prompt start of treatment, may lead to overcome this adverse event.

Topics: Acyclovir; Amyloidosis; Antineoplastic Agents; Antiviral Agents; Boronic Acids; Bortezomib; Dexamethasone; Encephalitis, Herpes Simplex; Herpesvirus 3, Human; Humans; Middle Aged; Multiple Myeloma; Pyrazines

Topics: Acitretin; Acyclovir; Adolescent; Amyloidosis; Antiviral Agents; Clobetasol; Glucocorticoids; Humans; Keratolytic Agents; Lichenoid Eruptions; Male; Valacyclovir; Valine

Cutaneous lesions related to chronic active Epstein-Barr virus (EBV) infection have been rarely documented in immunocompetent patients. A 30-year-old woman, fulfilling the diagnostic criteria for the chronic fatigue syndrome, had a 10-year history of pruritic brownish macules and papules on her chest and back. Her EBV serology was abnormal; the EBV genome was present in the epidermis of lesions, in oral secretions, and in peripheral mononuclear cells (PMC). Her blood lymphocytes spontaneously outgrew in culture. Histology revealed deposits of amyloid in the papillary dermis. Treatment with acyclovir and interferon-alpha rapidly improved her condition, stopped the lymphocyte outgrowth in culture, and reduced the EBV DNA content in oral secretions and in PMC. These data support an endogenous reactivation of EBV infection and suggest a causal relationship with primary amyloidosis.

Topics: Acyclovir; Adult; Amyloidosis; Antiviral Agents; Female; Herpesviridae Infections; Herpesvirus 4, Human; Humans; In Situ Hybridization; Interferon-alpha; Skin Diseases, Viral; Tumor Virus Infections