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The present findings suggest that higher serum lithium levels may be protective against suicide attempts in lithium therapy-naive individuals.

A case of severe fever with thrombocytopenia syndrome (SFTS) in which a skin biopsy from the tick‐bite region was analyzed is reported. The patient was a 72‐year‐old woman who developed fever and thrombocytopenia after a tick bite. SFTS was diagnosed from polymerase chain reaction (PCR) analysis of a blood sample. Histopathological analysis of a skin biopsy specimen from the tick‐bite region showed CD20‐positive perivascular and interstitial immunoblastic cells, which were positive to anti‐SFTS virus (SFTSV) nucleoprotein antibody. In addition, SFTSV RNA was detected by real‐time PCR from this biopsy specimen. Moreover, hemophagocytosis was also found in the tick‐bite region. To the best of our knowledge, this is the first report to analyze the details of the tick‐bite region of skin in SFTS, and the first to detect virus‐infected cells in the skin. The present findings may help elucidate the mechanisms of entry of SFTSV.

Background: Baloxavir marboxil (BM) is a novel drug with a cap-dependent endonuclease inhibitory action for influenza A or B; it is highly safe and requires just a single oral dose. Patients with severe heart failure use implantable ventricular assist device (iVAD) until transplantation, but they have an increased risk of thrombosis development. Their warfarin is administered based on point-of-care testing (POCT) with a strict control of prothrombin time-international normalized ratio (PT-INR). Case report: Here, we report a case of a patient with iVAD whose PT-INR was significantly increased from the target range after BM administration. The patient was a 45-year-old man and transplanted with iVAD; warfarin treatment was started when his PT-INR target range was 3.0–3.5. At home, he frequently self-measured PT-INR by POCT and precisely controlled the warfarin dose. He had a fever, was diagnosed with influenza A and was administered BM 40 mg. Thereafter, his PT-INR continued to increase, reaching 4.8 on day 12 of BM administration, exceeding his target range; warfarin was skipped for 1 day. In this case, based on the history of BM administration and clinical course, the increase in PT-INR could be due to BM. Considering the interaction between warfarin and BM, we suspected a possibility of competition for protein-binding sites. Increased PT-INR in the patient was detected early by POCT and thus severe bleeding was avoided. Conclusion: Strict monitoring of PT-INR when using BM in patients taking warfarin is of clinical importance.

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