Elevated troponin identifies a subset of patients with sepsis at higher risk of death. Further studies are needed to define the precise role of troponins and their optimal cut-offs.

The pathogenesis of livedoid vasculopathy (LV) is still unclear. However, with increasing knowledge of disorders of coagulation over the past few years, the cause of some cases of LV has been elucidated. LV has now been described in association with hyperhomocysteinaemia, activated protein C resistance, and prothombin gene mutations in the absence of significant underlying inflammatory disease. When LV is seen in association with systemic lupus erythematosus or polyarteritis nodosa, it is probably due to the pro-coagulable state induced by these diseases rather than being true vasculitis. We review recent insights into LV provided by published clinical cases and discuss its pathogenesis.

Although oral manifestations of sarcoidosis are unusual, physicians should be aware that this specific localization is frequently the first manifestation of the disease. Treatment modalities range from observation in asymptomatic patients to immunosuppressants for severe involvement.

Livedoid vasculitis (LV) may be an isolated condition or associated with an underlying systemic disease, including coagulation disorders, periarteritis nodosa and systemic autoimmune diseases. The classic histological features of LV (fibrin deposition on dermal vessels and the absence of important perivascular infiltrate or leucocytoclasia) argue against a primary vasculitis and is more in keeping with a thrombotic process. Factor V Leiden mutations have rarely been reported in association with LV. We report a patient with LV, who had doubly inherited thrombophilia, with heterozygous mutations in the Factor V Leiden (G1691A) and prothrombin (G20210A) genes.

Axitinib is an oral second-generation selective inhibitor of vascular endothelial growth factor receptors recently approved for the treatment of advanced renal cell carcinoma. Numerous cases of acute pancreatitis have been reported after treatment with nonselective tyrosine kinase inhibitors such as sorafenib and sunitinib. We present the first report of a patient under axitinib treatment presenting with acute pancreatitis for which no other etiology has been found. The patient was a 29-year-old woman treated for renal cell carcinoma. The patient had no history of chronic illness, gallstone-related disease, or alcohol consumption. She had been previously treated with sunitinib and everolimus. Four months after the onset of axitinib treatment she was hospitalized for acute pancreatitis. Symptoms and blood lipase levels normalized within a few days after axitinib was withheld. We believe that acute pancreatitis should be recognized as a potential axitinib-related adverse event.

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Primary biliary cirrhosis (PBC) is an autoimmune liver disease characterised by chronic cholestasis usually associated with antimitochondrial antibodies. Moreover, several types of antinuclear antibodies have been associated with primary biliary cirrhosis. We describe an 83-year-old man, in whom the exploration of a chronic cholestasis led to the diagnosis of primary biliary cirrhosis despite negative antimitochondrial antibodies, regarding the presence of anti-gp210 antibodies. Found in 25% of patients, these antinuclear antibodies must be sought before a strong suspicion of primary biliary cirrhosis with antimitochondrial antibodies negative, as they are highly specific of the disease. They are generally associated with a more aggressive form of PBC.