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Showing papers by "Katsumi Tanaka published in 2022"


Journal ArticleDOI
TL;DR: It is provided that a regimen that contained irinotecan and steroid could cause hypotension and the mechanism is partially explained by inhibiting choline esterase and adrenal insufficiency.
Abstract: Most hypotension during chemotherapy is caused by an allergic mechanism. Conversely, non‐allergic hypotension due to chemotherapy is rare. In this case report, we present a patient who suffered severe hypotension followed by the administration of irinotecan‐based chemotherapy and some supportive care such as steroids for preventing emesis. A 71‐year‐old man with hypertension was diagnosed with stage IV small cell lung cancer (sT1cN3M0). Severe hypotension occurred in the patient after every administration of chemotherapy. Finally, he was able to receive all four courses of chemotherapy as planned along with the medical staff’s support care. This case provides that a regimen that contained irinotecan and steroid could cause hypotension and the mechanism is partially explained by inhibiting choline esterase and adrenal insufficiency. We should be careful about non‐allergic hypotension when we administer irinotecan‐based chemotherapy.

3 citations


Journal ArticleDOI
TL;DR: A possible mechanism by which lansoprazole may lead to cardiovascular events is inhibiting the generation of epoxyeicosatrienoic acids from arachidonic acids, an intrinsic cardioprotective activator via CYP2C19 inhibition.
Abstract: This study aimed to identify the components of proton pump inhibitors (PPIs) or potassium-competitive acid blocker (PCAB) that lead to cardiovascular events in individuals of working age. We analyzed large claims data of individuals who were administered PPIs or PCAB. We enrolled working-age individuals administered PPI or PCAB without cardiovascular history with a 12-month screening and 12-month observation period and determined the proportion of cardiovascular events and the predictive factors of cardiovascular events in this population. Among the eligible individuals, 0.5% (456/91098) had cardiovascular events during the 12-month observation period. Predictive factors for cardiovascular events were age for +1 year (p < 0.0001), male sex (p < 0.0001), hypertension (p = 0.0056), and diabetes mellitus (p < 0.0001). The cardiovascular disease risk was higher in working-age individuals administered lansoprazole than in those administered other drugs (vs. rabeprazole; p = 0.0002, vs. omeprazole; p = 0.0046, vs. vonoprazan; p < 0.0001, and vs. esomeprazole; p < 0.0001). We identified the risk for cardiovascular events in individuals being treated with lansoprazole. Lansoprazole is known for its higher CYP2C19 inhibition activity compared with other PPIs or PCAB. A possible mechanism by which lansoprazole may lead to cardiovascular events is inhibiting the generation of epoxyeicosatrienoic acids from arachidonic acids, an intrinsic cardioprotective activator via CYP2C19 inhibition. Thus, we recommend avoiding administering lansoprazole to working-age individuals require PPIs or PCAB.

2 citations


Journal ArticleDOI
TL;DR: The developed method is applicable to the confirmation of appropriate use for UTIs treatment as a therapeutic drug monitoring of cefazolin and may contribute to the appropriate use of antibiotics to prevent antimicrobial resistance (AMR) in pediatric patients with UTIs.
Abstract: Recently, global health concerns regarding increasing multidrug resistance have arisen. This study aimed to develop a simple, inexpensive, and rapid high-performance liquid chromatography-ultraviolet (HPLC-UV) method for determining urinary concentrations of a 1st generation cephem antibiotic in pediatric patients with urinary tract infections (UTIs). HPLC-UV was used to analyze urinary cefazolin concentrations at a detection wavelength of 254 nm. The assay used contained 10-fold diluted urine with an internal standard (cephapirin). The standard calibration curve for cefazolin was linear in the concentration range of 31.25-500 μg/mL (r2 >0.999). The retention times of cefazolin and the internal standard were 4.2 and 4.9 min, respectively. The within-day and between-day coefficients of variation were at these concentrations ranged 1.2-15.2 and 5.5-19.2 %, respectively. The urinary cefazolin concentration of a pediatric patient with a UTI was 1,476.6 μg/mL, which was over 700-fold higher than the minimum inhibitory concentration (MIC) of cefazolin (≤ 2 μg/mL). The developed method is applicable to the confirmation of appropriate use for UTIs treatment as a therapeutic drug monitoring of cefazolin. Therefore, the findings of this study may contribute to the appropriate use of antibiotics to prevent antimicrobial resistance (AMR) in pediatric patients with UTIs.

1 citations


Journal ArticleDOI
TL;DR: Aicardi-Goutières syndrome (AGS) is a rare genetic disorder characterized by progressive encephalopathy, involving microcephaly, intracranial calcification, and cerebrospinal fluid lymphocytosis with increased interferon-α concentrations as mentioned in this paper .
Abstract: Aicardi–Goutières syndrome (AGS) is a rare genetic disorder characterised by progressive encephalopathy, involving microcephaly, intracranial calcification, and cerebrospinal fluid lymphocytosis with increased interferon-α concentrations. The clinical features of AGS overlap with fetal cerebral anomalies caused by congenital infections, such as TORCH (toxoplasmosis, other, rubella, cytomegalovirus, and herpes), or with those of other genetic disorders showing neonatal microcephaly, including Cockayne syndrome (CS) with transcription-coupled DNA repair deficiency, and Seckel syndrome (SS) showing aberrant cell-cycle checkpoint signaling. Therefore, a differential diagnosis to confirm the genetic cause or a proof of infection should be considered. In this report, we describe an individual who showed primordial dwarfism and encephalopathy, and whose initial diagnosis was CS. First, we conducted conventional DNA repair proficiency tests for the patient derived fibroblast cells. Transcription-coupled nucleotide excision repair (TC-NER) activity, which is mostly compromised in CS cases, was slightly reduced in the patient's cells. However, unscheduled DNA synthesis (UDS) was significantly diminished. These cellular traits were inconsistent with the diagnosis of CS. We further performed whole exome sequencing for the case and identified a compound heterozygous loss-of-function variants in the SAMHD1 gene, mutations in which are known to cause AGS. As SAMHD1 encodes deoxyribonucleoside triphosphate triphosphohydrolase, we reasoned that the deoxyribonucleoside triphosphate (dNTP) pool size in the patient's cells was elevated, and the labeling efficiency of UDS-test was hindered due to the reduced concentration of phosphorylated ethynyl deoxyuridine (EdU), a nucleoside analogue used for the assay. In conclusion, UDS assay may be a useful diagnostic tool to distinguish between AGS with SAMHD1 mutations and other related diseases.

1 citations