Contributions
Abstract: P1208
Type: Poster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Background: The alemtuzumab is a multiple sclerosis (MS) treatment causing rapid depletion of B and T lymphocytes with nadir one month after last infusion. Cytomegalovirus (CMV) infections in MS patients treated with alemtuzumab are recently described.1 The CMV may be the causative agent for hepatic involvement in immunocompromised hosts.2
Case report: A 45-year-old woman affected by MS, with a 10-year history of inefficacy and intolerance to different therapies, began alemtuzumab (12 mg/day i.v. for 5 days). On the first day of infusion, she started oral prophylaxis with acyclovir 200 mg/twice/day. After three weeks of last alemtuzumab infusion, she was hospitalised for fever (38°C). The laboratory tests showed: alanine transaminase (ALT) 46 UI/l, aspartate transaminase (AST) 41 UI/l, gamma-glutamil transpetidase (GGT) 63 UI/l and C-reactive Protein 75,5 mg/l. The CMV viral DNA polymerase chain reaction (PCR) was positive for 17.318 copies/ml, anti-CMV IgG antibodies were positive (48 U/ml) and IgM antibodies were negative indicating a CMV reactivation. The liver ultrasonography, demonstrated multiple small hypoechoic lesions (maximum sizes 1 cm) diffusely scattered in the hepatic lobes suggesting hepatic microabscesses, not detected in previous hepatic ultrasonography. Oral valganciclovir was administered at dose of 450 mg twice daily for
4 weeks. The CMV viral load became undetectable 13 days after the beginning of valganciclovir. Fever, inflammation indexes and hypertransaminasemia resolved in two weeks. At the follow-up liver ultrasonography (two months) the microabscesses regression was demonstrated.
Discussion: Hepatic microabscesses during CMV reactivation have been described in immunosuppressed patients, especially in liver transplant recipients.2 Because of the acyclovir prophylaxis could be ineffective against the CMV reactivations, all patients that develop fever and increase of transaminases after alemtuzumab treatment should undergo CMV PCR essay3 and also the liver ultrasonography to demonstrated hepatic involvement how in this case. This surveillance would allow a promptly switch from acyclovir to antiviral specific treatment (ganciclovir or valganciclovir) in case of CMV reactivation.
Conclusions: This report highlight further the risk of CMV reactivation in the first month following alemtuzumab infusion and suggest that an appropriate surveillance is needed in this period to manage this potential and treatable opportunistic infection.
Disclosure:
Stefania Barone: nothing to disclose;
Sara Scannapieco: nothing to disclose;
Carlo Torti: nothing to disclose;
Enrica Filippelli: nothing to disclose;
Vincenzo Pisani: nothing to disclose;
Alfredo Granata: nothing to disclose;
Domenico Console: nothing to disclose;
Giulio Demonte: nothing to disclose;
Tiziana Tallarico: nothing to disclose;
Serena Polidoro: nothing to disclose;
Aldo Quattrone: nothing to disclose;
Paola Valentino: nothing to disclose.
Abstract: P1208
Type: Poster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Background: The alemtuzumab is a multiple sclerosis (MS) treatment causing rapid depletion of B and T lymphocytes with nadir one month after last infusion. Cytomegalovirus (CMV) infections in MS patients treated with alemtuzumab are recently described.1 The CMV may be the causative agent for hepatic involvement in immunocompromised hosts.2
Case report: A 45-year-old woman affected by MS, with a 10-year history of inefficacy and intolerance to different therapies, began alemtuzumab (12 mg/day i.v. for 5 days). On the first day of infusion, she started oral prophylaxis with acyclovir 200 mg/twice/day. After three weeks of last alemtuzumab infusion, she was hospitalised for fever (38°C). The laboratory tests showed: alanine transaminase (ALT) 46 UI/l, aspartate transaminase (AST) 41 UI/l, gamma-glutamil transpetidase (GGT) 63 UI/l and C-reactive Protein 75,5 mg/l. The CMV viral DNA polymerase chain reaction (PCR) was positive for 17.318 copies/ml, anti-CMV IgG antibodies were positive (48 U/ml) and IgM antibodies were negative indicating a CMV reactivation. The liver ultrasonography, demonstrated multiple small hypoechoic lesions (maximum sizes 1 cm) diffusely scattered in the hepatic lobes suggesting hepatic microabscesses, not detected in previous hepatic ultrasonography. Oral valganciclovir was administered at dose of 450 mg twice daily for
4 weeks. The CMV viral load became undetectable 13 days after the beginning of valganciclovir. Fever, inflammation indexes and hypertransaminasemia resolved in two weeks. At the follow-up liver ultrasonography (two months) the microabscesses regression was demonstrated.
Discussion: Hepatic microabscesses during CMV reactivation have been described in immunosuppressed patients, especially in liver transplant recipients.2 Because of the acyclovir prophylaxis could be ineffective against the CMV reactivations, all patients that develop fever and increase of transaminases after alemtuzumab treatment should undergo CMV PCR essay3 and also the liver ultrasonography to demonstrated hepatic involvement how in this case. This surveillance would allow a promptly switch from acyclovir to antiviral specific treatment (ganciclovir or valganciclovir) in case of CMV reactivation.
Conclusions: This report highlight further the risk of CMV reactivation in the first month following alemtuzumab infusion and suggest that an appropriate surveillance is needed in this period to manage this potential and treatable opportunistic infection.
Disclosure:
Stefania Barone: nothing to disclose;
Sara Scannapieco: nothing to disclose;
Carlo Torti: nothing to disclose;
Enrica Filippelli: nothing to disclose;
Vincenzo Pisani: nothing to disclose;
Alfredo Granata: nothing to disclose;
Domenico Console: nothing to disclose;
Giulio Demonte: nothing to disclose;
Tiziana Tallarico: nothing to disclose;
Serena Polidoro: nothing to disclose;
Aldo Quattrone: nothing to disclose;
Paola Valentino: nothing to disclose.