Contributions
Abstract: EP1763
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
A 43 year old Caucasian female developed a subacute hepatitic illness 12 months after completion of her second course of Alemtuzumab for Multiple Sclerosis. This is the first reported incidence of this unexpected outcome.
Multiple Sclerosis was diagnosed in December 2014 following episodes of sensory disturbance and gait ataxia in July and September 2014. Paraclinical findings were typical. Past history included depression and Vitamin D deficiency; a broad autoimmune screen was initially negative.
The patient underwent her first 5 day infusion of Alemtuzumab (12mg/d with 1gram Methylprednisolone on d1-3) in March 2015 without significant difficulty and had her second 3 day infusion in April 2016. Her neurological status only improved with therapy, with no further relapse and increased occupational capacity.
Post-administration the patient manifested a normal time course of lympho-depletion and restitution with mild persisting lymphopenia (0.47-0.94 x109/l). In January 2017 she travelled to Southern India and Thailand, followed the recommended vaccination schedule and experienced no serious illness.
Post-infusion monitoring detected an isolated gradual rise in ALT (163U/l) from March onwards, reaching a peak of 2018U/l by early May 2017 from which time bilirubin and ALP also began gradually rising to peaks of 347umol/l and 269U/l respectively some three weeks later. Clinical features of progressive malaise, steatorrhea, anorexia, right hypochondrial tenderness and jaundice developed contemporaneously with the hyperbilirubinaemia. No coagulopathy or gross encephalopathy arose. The neutrophil count also dropped from normal to 0.38x109/l in March, reaching a nadir of 0.19 x109/l in May 2017.
Broad viral screens were negative. Autoimmune serology returned positive for Anti-LKM. Liver Biopsy demonstrated chronic lymphocytic and plasmacytic infiltrate of portal tracts with interface hepatitis and perivenular necrosis without bilary lesions, fibrosis or cirrhosis.
A diagnosis of Autoimmune Hepatitis was made, oral prednisolone 40mg initiated and sustained clinical and haematobiochemical improvement observed. Follow up is ongoing.
Disclosure: Canham L.J.W.: Nothing to disclose in respect of this case; has received educational support from Biogen Idec, TEVA, Novartis, Roche and Sanofi-Genzyme
Mozayani B. Nothing to disclose.
Chelvaratnam U.Nothing to disclose.
Przemioslo R.Nothing to disclose.
Fry C. Nothing to disclose.
Batty T.Nothing to disclose.
Stevens J. Nothing to disclose.
Inglis K.E.A.:Nothing to disclose in respect of this case; has received educational support from Biogen Idec, TEVA, Novartis, Roche and Sanofi-Genzyme
Cottrell D.A. :Nothing to disclose in respect of this case; has received educational support from Biogen Idec, TEVA, Novartis, Roche and Sanofi-Genzyme
Abstract: EP1763
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
A 43 year old Caucasian female developed a subacute hepatitic illness 12 months after completion of her second course of Alemtuzumab for Multiple Sclerosis. This is the first reported incidence of this unexpected outcome.
Multiple Sclerosis was diagnosed in December 2014 following episodes of sensory disturbance and gait ataxia in July and September 2014. Paraclinical findings were typical. Past history included depression and Vitamin D deficiency; a broad autoimmune screen was initially negative.
The patient underwent her first 5 day infusion of Alemtuzumab (12mg/d with 1gram Methylprednisolone on d1-3) in March 2015 without significant difficulty and had her second 3 day infusion in April 2016. Her neurological status only improved with therapy, with no further relapse and increased occupational capacity.
Post-administration the patient manifested a normal time course of lympho-depletion and restitution with mild persisting lymphopenia (0.47-0.94 x109/l). In January 2017 she travelled to Southern India and Thailand, followed the recommended vaccination schedule and experienced no serious illness.
Post-infusion monitoring detected an isolated gradual rise in ALT (163U/l) from March onwards, reaching a peak of 2018U/l by early May 2017 from which time bilirubin and ALP also began gradually rising to peaks of 347umol/l and 269U/l respectively some three weeks later. Clinical features of progressive malaise, steatorrhea, anorexia, right hypochondrial tenderness and jaundice developed contemporaneously with the hyperbilirubinaemia. No coagulopathy or gross encephalopathy arose. The neutrophil count also dropped from normal to 0.38x109/l in March, reaching a nadir of 0.19 x109/l in May 2017.
Broad viral screens were negative. Autoimmune serology returned positive for Anti-LKM. Liver Biopsy demonstrated chronic lymphocytic and plasmacytic infiltrate of portal tracts with interface hepatitis and perivenular necrosis without bilary lesions, fibrosis or cirrhosis.
A diagnosis of Autoimmune Hepatitis was made, oral prednisolone 40mg initiated and sustained clinical and haematobiochemical improvement observed. Follow up is ongoing.
Disclosure: Canham L.J.W.: Nothing to disclose in respect of this case; has received educational support from Biogen Idec, TEVA, Novartis, Roche and Sanofi-Genzyme
Mozayani B. Nothing to disclose.
Chelvaratnam U.Nothing to disclose.
Przemioslo R.Nothing to disclose.
Fry C. Nothing to disclose.
Batty T.Nothing to disclose.
Stevens J. Nothing to disclose.
Inglis K.E.A.:Nothing to disclose in respect of this case; has received educational support from Biogen Idec, TEVA, Novartis, Roche and Sanofi-Genzyme
Cottrell D.A. :Nothing to disclose in respect of this case; has received educational support from Biogen Idec, TEVA, Novartis, Roche and Sanofi-Genzyme