Acral Necrosis in a COVID-19-Infected Man Treated with Botulinum Toxin Type A

COVID-19 has been associated with acral ischemia and digital necrosis. Standard treatment of acral ischemia and digital or acral necrosis includes ongoing therapy with vasodilators and anticoagulants. However, these treatments are not always efficient to avoid the progression of necroses, which in the worst case can lead to amputation. Here, we report a case in which interdigital Botox^® (botulinum toxin type A) nerve cord injection stopped the progression of acral necroses arising from an underlying vasculopathy due to COVID-19. Moreover, Botox^® injection eliminated inflammation in the affected acral area within 2 weeks. This is the first case report to suggest Botox^® injection as a new and improving treatment for acral necroses due to COVID-19.

Severe Acral Necrosis Complicating Thrombotic Microangiopathy in Two Toddlers

Acral ischemia/necrosis is one of the rarest but most dreadful complications of thrombotic microangiopathy in pediatric patients. It is more reported with thrombotic thrombocytopenic purpura than with hemolytic and uremic syndrome. Even with anticoagulant therapy, it is often irreversible, leading to amputation.

Expression of a constitutively active humanSTINGmutant in hematopoietic cells produces anIfnar1-dependent vasculopathy in mice

STING-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disorder characterized by blood vessel occlusions, acral necrosis, myositis, rashes, and pulmonary inflammation that are the result of activating mutations in the STimulator of Interferon Genes (STING). We generated a transgenic line that recapitulates many of the phenotypic aspects of SAVI by targeting the expression of the human STING-N154S–mutant protein to the murine hematopoietic compartment.hSTING-N154Smice demonstrated failure to gain weight, lymphopenia, progressive paw swelling accompanied by inflammatory infiltrates, severe myositis, and ear and tail necrosis. However, no significant lung inflammation was observed. X-ray microscopy imaging revealed vasculopathy characterized by arteriole occlusions and venous thromboses. Type I interferons and proinflammatory mediators were elevated inhSTING-N154Ssera. Importantly, the phenotype was prevented inhSTING-N154Smice lacking the type I interferon receptor gene (Ifnar1). This model, based on a mutant human STING protein, may shed light on the pathophysiological mechanisms operative in SAVI.

Acral necrosis and upper brachial plexus palsy after prenatal fetal thrombosis

Intrauterine fetal thrombosis is an extremely rare event with a devastating outcome. The etiology of the condition often remains unclear. A 29-year-old 2