Utilizing questionnaires for medication counselling of patients taking antipsychotics during the COVID-19 pandemic: a single site, community pharmacy-based survey study.

BACKGROUND: During the coronavirus disease (COVID-19) pandemic, general strategies for preventing infectious diseases, such as social distancing and the use of protective equipment have resulted in communication barriers between pharmacists and patients in community pharmacies. METHODS: To resolve these communication challenges to medication counselling during the COVID-19 pandemic, during their waiting time at our community pharmacy, we administered two questionnaires to patients receiving at least one antipsychotic drug. The first questionnaire, Questionnaire (A), included questions about any problems with wearing a mask and face shield, forgetting to take medication and adverse effects of their medication. The second questionnaire, Questionnaire (B), included questions regarding the evaluation of medication counselling and the ease of using the first questionnaire. RESULTS: Questionnaire (A) showed that 26.8% of participants had communication problems due to the mask and face shield and 33.8% sometimes forgot to take their medication. The most common adverse effects of the medications were weight gain (43.7%), dry mouth (39.4%) and sexual dysfunction (31%). In the case of Questionnaire (B), more than 80% responded that it was either very easy or easy to fill out Questionnaire (A). Additionally, 93% participants responded that they felt either very good or good about the pharmacist's medication counselling using Questionnaire (A). CONCLUSIONS: These results strongly suggest that the utilization of questionnaires in medication counselling may be a useful strategy for preventing communication problems between pharmacists and patients receiving antipsychotics in community pharmacies during and after the COVID-19 pandemic.

A community pharmacist's intervention in antipsychotic drug-induced sexual dysfunction in a patient with schizophrenia.

The community pharmacist interviewed a patient with sexual dysfunction (SD) and suggested a change in prescription. Early intervention by the community pharmacist ameliorated antipsychotic drug-induced SD timeously.

[SIGNIFICANCE OF IgG4 IN IDIOPATHIC RETROPERITONEAL FIBROSIS].

(Objective)Retroperitoneal fibrosis is largely divided into the idiopathic and secondary types. Some idiopathic cases include IgG4-related diseases, which are often similar to malignant diseases, such as lymphoma and sarcoma. The diagnostic criteria for IgG4-related disease are used and pathologic examination is necessary for a definitive diagnosis of IgG4-related retroperitoneal fibrosis. The first choice of treatment for IgG4-related retroperitoneal fibrosis is steroid administration, but no consensus has been established regarding its dose and tapering schedule. We investigated the significance of IgG4 in diagnosis and treatment of idiopathic retroperitoneal fibrosis. (Patients and methods)We examined 14 cases diagnosed as idiopathic retroperitoneal fibrosis between April 2013 and March 2019. Serum IgG4 was measured at the time of diagnosis in 13 cases, and changes over time in serum IgG4 before and after the induction of steroid therapy were measured in 6 cases. Computed tomography-guided biopsy was performed on 4 cases. (Results)Of all cases, 1 patient was diagnosed as IgG4-related retroperitoneal fibrosis and 5 patients were classified as possible group. Ten patients were administered steroid therapy. Percutaneous nephrostomy tube was placed in 3 patients and was removed in 2 of these patients after steroid therapy. The serum high levels of IgG4 were confirmed in all 4 patients who were classified into the possible group and who were treated with steroids. (Conclusion)Although histologic examination is necessary for the diagnosis of retroperitoneal fibrosis, tissue collection by open or laparoscopic surgery is highly invasive. CT-guided biopsy may be useful in high-risk cases, such as elderly patients on anticoagulation. After excluding other diseases in high-risk cases, response to empiric steroid therapy may be diagnostic. In the possible group, changes in serum IgG4 levels may reflect the disease condition and might be useful in determining the maintenance dose of steroids.

Repeated spontaneous migration of ureteral stent in hemiplegia patient during ureteral stone treatment.

A 48-year-old man with a history of cerebral infarction presented with gross hematuria. The patient's limping accompanies twisting trunk on his walking. The diagnosis was right upper ureteral stone. Prior to Extracorporeal shockwave lithotripsy (ESWL) ureteral stent was inserted. After the second ESWL ureteral stent was displaced upwardly without patient's unknown. Retrograde intrarenal surgery (RIRS) was performed for both removal of ureteral stent and fragmentation of residual stone. Spontaneously, post RIRS ureteral stent was migrated upwardly to the same position. Ureteral stent migration is uncommon. Twisting walk may cause the position of ureteral stent upwardly.

[A Case of Consciousness Disturbance Due to Hyperammonemia Associated with Urinary Tract Infections].

We describe the case of a patient with hyperammonemia owing to urinary tract infections. The patient, a 66-year-old-woman, was previously diagnosed with bilateral hydronephrosis. She was admitted to the emergency room with macrohematuria and bilateral lumbar pain, which persisted for 2 days. She was hospitalized with the diagnosis of pyelonephritis. Despite antibiotic treatment, she developed sudden disturbance in consciousness on the 2nd day of illness. To improve the hyperammonemia and metabolic acidosis, we initiated continuous hemodiafiltration (CHDF) and urinary drainage by bilateral nephrostomy, after which her consciousness improved, and she was discharged on day 19. For patients with urinary tract infections and who are unaware of disturbance in consciousness, it is important to consider that obstructive urinary tract infections can cause hyperammonemia.

Reduction in peripheral lymphocytes and thymus atrophy induced by organotin compounds in vivo.

To clarify the involvement of apoptosis in the immunotoxicity of organotin compounds, we examined the induction of apoptosis in the peripheral lymphocytes and thymus of mice treated with triphenyltin (TPT), tributyltin (TBT) or dexamethasone (Dex). Application of TPT or TBT and Dex resulted in a transient reduction in peripheral lymphocytes at 3 to 6 hr, and thymus atrophy was observed at 6 and 24 hr after administration. Lymphocyte subpopulation analysis showed that TPT and TBT induced a greater reduction in B cells than in T cells. The maximum levels of organotin in the blood were about 450 ng TPT/ml in the TPT-treated mice, and 170 ng TBT/ml in the TBT-treated mice. When the isolated peripheral lymphocytes were incubated with the organotins at 500 ng/ml, TPT and TBT induced necrosis in over 70% of cells, while both organotins caused lower percentages of apoptosis as well as necrosis after 3 hr at 100 ng/ml. In the thymus, although in vivo treatment of mice with Dex caused apoptosis, neither apoptotic nor necrotic thymocytes were observed in the TPT- and TBT-treated mice, indicating that the thymus atrophy might be caused by the antiproliferative effects of these organotin compounds. Thus, our results did not support the idea that apoptosis played a decisive part in the immunotoxicity of the organotin compounds in vivo.

Estimation of hydroxyl radical generation by salicylate hydroxylation method in kidney of mice exposed to ferric nitrilotriacetate and potassium bromate.

Hydroxyl radical (*OH) generation in the kidney of mice treated with ferric nitrilotriacetate (Fe-NTA) or potassium bromate (KBrO3) in vivo was estimated by the salicylate hydroxylation method, using the optimal experimental conditions we recently reported. Induction of DNA lesions and lipid peroxidation in the kidney by these nephrotoxic compounds was also examined. The salicylate hydroxylation method revealed significant increases in the *OH generation after injection of Fe-NTA or KBrO3 in the kidneys. A significant increase in 8-hydroxy-2'-deoxyguanosine in nuclei of the kidney was detected only in the KBrO3 treated mice, while the comet assay showed that the Fe-NTA and KBrO3 treatments both resulted in significant increases in DNA breakage in the kidney. With respect to lipid peroxidation, the Fe-NTA treatment enhanced lipid peroxidation and ESR signals of the alkylperoxy radical adduct. These DNA breaks and lipid peroxidation mediated by *OH were diminished by pre-treatment with salicylate in vivo. These results clearly demonstrated the usefulness of the salicylate hydroxylation method as well as the comet assay in estimating the involvement of *OH generation in cellular injury induced by chemicals in vivo.

Assessment of DNA damage in multiple organs of mice after whole body X-irradiation using the comet assay.

The comet assay was performed to elucidate the linearity of calibration curves and detection limits for DNA damage in multiple organs of whole body X-irradiated mice, and rates of reduction in DNA damage by DNA repair during the irradiation period were estimated in the respective organs by comparing the rates of increase in DNA damage at different absorbed dose rates of X-rays. Of the assay parameters, tail length and the percentage DNA in the tail showed a higher sensitivity to DNA damage in most organs than Olive tail moment. Data at the higher absorbed dose rates (2.22 or 1.44 Gy/min) showed good correlations between absorbed doses and these two parameters, with correlation coefficients of more than 0.7 in many organs. However, this assay had difficulty detecting DNA damage at the lower absorption dose rate (0.72 Gy/min). The estimated rates of increase in DNA damage and those of DNA repair during the irradiation period in the respective organs suggested differences in the radiosensitivity of nuclear DNA and DNA repair capacity among organs. Our results indicated that absorbed dose rates of 1.0-1.3 Gy/min or greater were needed to induce detectable DNA damages by the comet assay in many organs.

Estimation of hydroxyl radical generation by salicylate hydroxylation method in multiple organs of mice exposed to whole-body X-ray irradiation.

Appropriate experimental conditions for the estimation of hydroxyl radical generation by salicylate hydroxylation were determined for multiple organs of X-irradiated mice in vivo. The in vitro experiments showed that there were significant correlations between the salicylic acid (SA) concentration, the amount of 2,3-dihydroxy benzoic acid (2,3-DHBA) and the X-ray exposure dose, and we obtained two linear-regression equations to calculate the amounts of hydroxyl radicals generated by the X-irradiation. The optimum dosage of SA and the appropriate sampling time for in vivo experiments was determined, and significant increases in the ratio of 2,3-DHBA to SA were detected in several organs of mice after X-irradiation. The hydroxyl radical equivalents of the 2,3-DHBA increases were also calculated. Our results clearly demonstrated the usefulness of the salicylate hydroxylation method in estimating hydroxyl radical generation in multiple organs in vivo.

Effects of butyltin compounds on mitochondrial respiration and its relation to hepatotoxicity in mice and Guinea pigs.

Because the mechanisms responsible for the difference in toxicity between different experimental animal species remain unclear, the effects of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) on mitochondrial respiration were compared among the livers of mice and guinea pigs in vitro and in vivo. Further, the levels of these butyltin compounds and their derivatives in the mitochondrial fractions of the hepatocytes were investigated in these animal species. Administration of TBTC and DBTC to mice resulted in the obvious elevation of serum enzymatic activities, as well as the inhibition of succinate-linked State 3 respiration in hepatic mitochondria at 24 h after administration. On the other hand, these metal compounds failed to induce such hepatotoxicity or to inhibit mitochondrial respiration in guinea pigs. There was no significant difference between mice and guinea pigs in the IC50 (metal concentration observed in 50% inhibition of mitochondrial respiration) of TBTC and DBTC against the succinate-linked State 3 respiration of hepatic mitochondria in vitro, although the mitochondrial respiration of succinate-linked State 3 was inhibited in the liver of mice treated with the metals in vivo. The levels of total butyltin compounds in the mitochondrial fractions of hepatocytes were higher in the mice than in the guinea pigs, and the main butyltin compound in the mitochondrial fractions was DBTC in both species at 24 h after TBTC or DBTC administration. The amount of sulfhydryl groups, which were capable of binding with DBTC, in mice hepatic mitochondria was twice as large as that in guinea pigs, and the affinity of DBTC for the isolated hepatic mitochondria was higher in mice than in guinea pigs in vitro. These results suggested that the induction of hepatotoxicity by TBTC and DBTC in vivo was closely associated with the depression of mitochondrial respiration and that the difference in susceptibility to the metal-induced mitochondrial damages between mice and guinea pigs might result from the high affinity of butyltin compounds, in particular DBTC, for hepatic mitochondria in mice containing higher levels of sulfhydryl groups, compared with guinea pigs.

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice, rats and guinea pigs.

The hepatotoxicity of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) was compared among mice, rats and guinea pigs in vivo. Further, the metabolism of these butyltin compounds in the liver was also investigated in these species. The oral administration of TBTC and DBTC to mice induced obvious liver injury, as demonstrated by both serodiagnosis and histopathological diagnosis. The concentrations of TBTC and DBTC that induced hepatotoxicity in mice at 24 h after oral administration were 180 and 60 micro mol/kg, respectively. In the case of rats, the liver injury induced by TBTC and DBTC was detected at 24 h by the serodiagnosis, but not by histopathological diagnosis. On the other hand, in guinea pigs, TBTC and DBTC administration did not produce any clear liver injury at 24 h, as evaluated by these two diagnostic methods. Thus, the following ranking was obtained with regard to increasing order of sensitivity to liver injury caused by TBTC and DBTC: mice, rats and guinea pigs. The total butyltin contents in the liver of mice were equivalent at 3 h and 24 h after the administration of TBTC or DBTC; however, the contents in the liver of rats and guinea pigs were relatively lower at 3 h and higher at 24 h than those of mice, although there were no differences between rats and guinea pigs in the total liver butyltin content. Concerning the liver metabolism of these butyltin compounds, the main form of butyltin compounds in these animals treated with TBTC was DBTC within 3 h after oral administration, while the main metabolites at 24 h were different in each species, indicating that the liver metabolism of TBTC might vary by animal type. When the animals were treated with DBTC orally, DBTC was hardly metabolized in the livers of these animals even at 24 h, and the liver levels of DBTC were two times greater in mice and guinea pigs than in rats at 3 h and were lower in mice at 24 h than in rats and guinea pigs. The analysis of cellular distributions of DBTC in the liver at 3 h after the administration showed that the levels of DBTC in the nuclear, microsomal and mitochondrial fractions of mice hepatocytes were relatively higher than in those of rats, which were greater than in those of guinea pigs. These results suggest differences in the sensitivity of mice, rats and guinea pigs to hepatotoxicity caused by butyltin compounds and demonstrate that the difference in the sensitivity of these animals to the hepatotoxicity induced by TBTC and DBTC may be partly due to differences in hepatic metabolism of TBTC and in the distribution of DBTC within cell organelles, respectively.