Background: Anti-leucine-rich glioma inactivated 1 limbic encephalitis (anti-LGI1 LE) is one of the most frequent autoimmune encephalitis, commonly coexisting with other autoimmune diseases. Rheumatoid arthritis (RA) and monoclonal gammopathy of unknown significance (MGUS) are commonly associated with autoimmune phenomena. However, neither RA nor MGUS have been described in the literature to date as coexisting with anti-LGI1 LE. Case description: We present the case of anti-LGI1 LE in a male patient with rheumatoid arthritis, who was also found to have an MGUS. The patient was initially treated with corticosteroids and IV immunoglobulin. After a mild relapse, his treatment was complemented with rituximab, resulting in complete regression of the disease symptoms. Conclusions: Our report provides evidence for the coexistence of anti-LGI1 LE with RA and/or MGUS, thus extending the differential diagnosis of patients suffering with these disease entities that present with neuropsychiatric symptoms suggestive of encephalitis. Moreover, this case raises challenges on the management of the coexistence of these diseases, given the lack of therapeutic guidelines and their potential interaction on a pathophysiological and a clinical level.

Background/Objectives: Acutely ill patients in hospital are at high risk for thrombosis, even post-discharge. However, the safest and most effective strategy for thromboprophylaxis in such patients is still under debate. Our aim was to compare the subcutaneous use of low-dose prophylactic enoxaparin versus intermediate-dose tinzaparin. Methods: Patients in an internal medicine clinic of a tertiary hospital in Athens, Greece, with increased risk for thrombosis (PADUA score ≥ 4) received either intermediate-dose tinzaparin (8000 anti-Xa units) or 40 mg enoxaparin as thromboprophylaxis. Efficacy and adverse effects were evaluated and compared up to 14 days post-discharge. Results: A total of 251 patients who received tinzaparin were compared with 95 patients under enoxaparin thromboprophylaxis. No statistically significant difference was found in the number of bleeding and/or clinically evident thrombotic events between the two groups [6 versus 14 bleeding (p = 0.2603) events and 0 versus 1 venous thrombotic event (p = 0.999) in the enoxaparin and tinzaparin groups, respectively]. Moreover, no difference was found in length of stay [enoxaparin: 10 days (95%CI: 9–12 days); tinzaparin: 8 days (95%CI: 8–10 days, HR = 1.18, 95%CI: 0.91–1.54, p = 0.2] or mortality [11 deaths with enoxaparin (11.58%, 95%CI: 6.59–19.55%) and 50 deaths with tinzaparin (19.92%, 95%CI: 15.45–25.30%, OR: 1.9, 95%CI: 0.94–3.83, p = 0.069)]. The use of thromboprophylaxis for two weeks post-discharge did not result in any bleeding or clinically evident thrombotic events in either group. Conclusions: In our cohort, the use of intermediate-dose tinzaparin was similar to the use of low-dose enoxaparin for patients with a high PADUA score in terms of thrombotic and/or bleeding events.