The Committee for Treatment Guidelines of Mood Disorders, Japanese Society of Mood Disorders, published a Japanese guideline for the treatment of late‐life depression in 2020. Based on that guideline, the present guideline was developed and revised to incorporate the suggestions of global experts and the latest published evidence. In the diagnosis of late‐life depression, it is important to carefully differentiate it from bipolar disorders, depressive states caused by physical and organic brain disease, drug effects, and dementia, and to determine the comorbidity between late‐life depression and dementia. It is necessary to fully understand the clinical characteristics and psychosocial background of late‐life depression, evaluate the patient's condition, and provide basic interventions based on these factors. Problem‐solving therapy, reminiscence therapy/life review therapy, and behavioral activation therapy, and other forms of psychotherapy can reduce depressive symptoms. In terms of pharmacotherapy, newer antidepressants or non‐tricyclic antidepressants are recommended for late‐life depression, and it is recommended that the efficacy of least the minimal effective dosage should first be determined. Switching antidepressants and aripiprazole augmentation can be used to treatment‐resistant therapy. Electroconvulsive therapy and repetitive transcranial magnetic stimulation have demonstrated usefulness for late‐life depression. Exercise therapy, high‐intensity light therapy, and diet therapy also show some effectiveness and are useful for late‐life depression. Continuation therapy should be maintained for at least 1 year after remission.

Using CE-EUS to measure MN height provides a highly accurate method for differentiating benign from malignant BD-IPMN.

IgG4-related disease (IgG4-RD) is a recently designated disease entity and its full picture has not yet been elucidated. Here, we report an unusual case of a patient with gastric wall thickening secondary to IgG4-RD. A 68-year-old male visited our hospital with itchy skin lesions and an episode of organizing pneumonia. On the suspicion of malignancy-associated skin lesions, computed tomography (CT) was performed. The CT revealed prominent thickening of the gastric wall. Due to the possibility of malignancy, the patient underwent distal gastrectomy. Histopathological examination showed fibrosis of the submucosa and prominent thickening of the muscularis propria. Most of infiltrating cells were IgG4-positive plasma cells. Post-operative blood test revealed significantly high serum levels of total IgG and IgG4. Based on these histological features, the patient was given a definitive diagnosis of IgG4-RD. Further accumulation of cases like the present case that develop IgG4-RD with rare manifestations would lead to the elucidation of pathogenesis.

ObjectiveTo determine the prevalence, background factors, and progression of and recovery from clozapine‐induced agranulocytosis in Japan.MethodsData on treatment‐resistant schizophrenia patients registered with the Clozaril Patient Monitoring Service (CPMS) between July 29, 2009 and January 20, 2016 were extracted. Patients with a neutrophil count <500/mm3 were defined as having agranulocytosis, and those with a leukocyte count <3,000/mm3 or a neutrophil count <1,500/mm3 but not meeting the criteria for agranulocytosis were defined as having leukopenia/neutropenia.ResultsOf 3,746 patients, agranulocytosis and leukopenia/neutropenia were observed in 38 (1.0%) and 182 (4.9%) patients, respectively. Age was significantly higher in the agranulocytosis group (p < .001). Decreased leukocyte counts 1 week prior to discontinuation were observed only in the agranulocytosis group. The median number of days to recovery from agranulocytosis and leukopenia/neutropenia was 10 and 4, respectively, with more variation in the latter.ConclusionsAlthough some patients with leukopenia/neutropenia might carry less pathologic significance, the results of this study reconfirmed the importance of regular blood monitoring for preventing agranulocytosis.

BackgroundUpadacitinib (UPA) is an oral, JAK1-selective inhibitor found to be effective in Phase 2 and 3 studies in rheumatoid arthritis (RA) patients with inadequate response or intolerance to csDMARDs and bDMARDs.1–4 ObjectivesTo evaluate the efficacy and safety of UPA in Japanese active RA patients with inadequate response to csDMARDs (csDMARD-IR).MethodsDuring the 12 week double-blind period, patients on stable csDMARDs were randomised to receive UPA 7.5,15 or 30 mg once daily or PBO (1:1:1:1). The primary endpoint was proportion of patients achieving ACR20 at Wk 12 (NRI).ResultsOf 197 patients treated, 187 completed the double-blind period. At Week 12, more patients receiving UPA 7.5, 15 and 30 mg vs PBO met ACR20 (75.5%, 83.7%,80% vs 42.9%, p<0.001). A significant difference in ACR20 was observed as early as Week 1 (table 1). The more stringent responses, such as ACR50/70, DAS28-CRP≤3.2, were achieved by significantly higher proportions of patients on UPA vs PBO with more patients on UPA 15 mg and 30 mg achieving these responses vs UPA 7.5 mg (Table). At Week 12, patients receiving UPA vs PBO had greater improvements from baseline (p<0.001) in DAS28-CRP (−2.08,–2.39, −2.41 vs −0.79) and HAQ-DI (−0.41,–0.45, −0.49 vs −0.10).Overall adverse events (AE), serious AEs, infections (including serious infections, opportunistic infections and herpes zoster) were numerically higher in UPA 30 mg. There were no events of pulmonary embolism, deep vein thrombosis, tuberculosis or malignancy and there were no deaths. Mean haemoglobin levels improved with UPA 7.5 (+0.35 g/dL) and remained stable with UPA 15 (-0.03 g/dL) vs UPA 30 (-0.54 g/dL) and PBO (−0.17 g/dL). CPK elevations and lymphopenia occurred more frequently in UPA 30 mg.ConclusionsIn this Japanese RA csDMARD-IR population, the efficacy of UPA was demonstrated, with better responses for more stringent endpoints on UPA 15 mg and 30 mg vs 7.5 mg. The frequency of overall AEs was numerically higher in UPA 30 mg. Overall, safety and tolerability were consistent with Phase 2 and 3 studies to date.References[1] Burmester, et al. Arth Rheum2017;69:S10.[2] Genovese, et al. Arth Rheum2017;69:S10.[3] Kremer, et al. Arth Rheum2016;68(12).[4] Genovese, et al. Arth Rheum2016;68(12).AcknowledgementsAbbVie, Inc was the study sponsor, contributed to study design, data collection, analysis and interpretation, and to writing, reviewing, and approval of final version. Statistical support: Masuyuki Yokoyama, Medical writing support:Naina Barretto, both employees of AbbVie.Disclosure of InterestY. Tanaka Grant/research support from: Mitsubishi-Tanabe Pharma Corporation, Takeda Pharmaceutical Company Ltd, Bristol-Myers Squibb Company, Chugai Pharmaceutical Co Ltd, Astellas Pharma Inc, AbbVie GK, MSD K.K., Daiichi Sankyo Company Ltd, Pfizer Japan Inc., Kyowa Hakko Kirin Co., Ltd, Eisai Co., Ltd, Ono Pharmaceutical Co., Ltd, Speakers bureau: Daiichi Sankyo Company Ltd, Astellas Pharma Inc, Pfizer Japan Inc., Mitsubishi-Tanabe Pharma Corporation, Bristol-Myers Squibb Company, Chugai Phar...