Practical Recommendations from the Gulf Region on the Therapeutic Use of Cladribine Tablets for the Management of Relapsing Multiple Sclerosis: Impact of the Latest Real-World Evidence on Clinical Practice.

Cladribine tablets (CladT), like alemtuzumab, acts as an immune reconstitution therapy. However, CladT is administered orally (alemtuzumab is given by infusion) and without the potential for serious side effects that limit the therapeutic use of alemtuzumab in multiple sclerosis (MS). Treatment with CladT, given initially as short courses of treatment 1 year apart, provides years of freedom from MS disease activity in responders to treatment. The appearance of mild or moderate MS disease activity after the initial 2 years of treatment may prompt careful follow-up or a further course of CladT, depending on the nature of the activity and individual circumstances. The appearance of severe MS disease activity requires a switch to an alternative high-efficacy disease-modifying treatment (DMT). The accumulating data from CladT-treated people with MS in real-world studies, including those with follow-up durations extending for years beyond the initial treatment, have demonstrated long-term freedom from MS disease activity in a good proportion of patients. This clinical experience has also confirmed that treatment with CladT is generally safe and well tolerated. The best time to prescribe a high-efficacy DMT is the subject of debate, with evidence that earlier versus later use of such agents may provide more effective long-term protection from disability progression. High-efficacy DMTs have traditionally been reserved for use in people with MS and high disease activity on presentation or breakthrough disease on one or more DMTs, as per the current product labels. The latest evidence from real-world studies suggests that CladT is effective and safe in DMT-naïve patients, including those with shorter disease duration.

Cerebral Venous Thrombosis and Acute Pulmonary Embolism following Varicella Infection.

Varicella infection is caused by varicella-zoster virus (VZV) and commonly presents as a self-limiting skin manifestation in children. VZV also causes cerebral arterial vasculopathy and antibody-mediated hypercoagulable states leading to thrombotic complications in children, although there are very few such reports in adults. Postulated causal factors include vasculitis, direct endothelial damage, or acquired protein S deficiency secondary to molecular mimicry. These induced autoantibodies to protein S could lead to acquired protein S deficiency and produce a hypercoagulable state causing venous sinus thrombosis. Here we report the case of a 26-year-old man who presented with cortical venous sinus thrombosis and acute pulmonary embolism following varicella infection. Both conditions responded to anticoagulation treatment. LEARNING POINTS: Varicella infection caused by varicella-zoster virus (VZV) can rarely present with thrombotic complications after a period of latency.Postulated causal factors include vasculitis, direct endothelial damage, and acquired protein S deficiency secondary to molecular mimicry.The prognosis of post-varicella thrombosis is good, but a prothrombotic screen after recovery to diagnose hereditary prothrombotic states is advisable.