Endometrial cancer commonly metastasizes to the pelvic and para-aortic lymph nodes, vagina, peritoneum, and lungs. Unusual sites of metastasis include the bone, brain, abdominal wall, muscles, and intra-abdominal organs. To our knowledge, there have been no documented cases of synchronous or metachronous metastasis of endometrial cancer to the renal pelvis or colon. Metastatic tumors in the renal pelvis and colon indicate nonspecific radiological findings, making them difficult to distinguish from primary tumors. We describe a case of a 55-year-old female previously treated for endometrial cancer, who was subsequently found to have metastatic masses in the renal pelvis and colon. The two masses were initially misidentified as primary urothelial carcinoma and colon adenocarcinoma.

Endometrial cancer commonly metastasizes to the pelvic and para-aortic lymph nodes, vagina, peritoneum, and lungs. Unusual sites of metastasis include the bone, brain, abdominal wall, muscles, and intra-abdominal organs. To our knowledge, there have been no documented cases of synchronous or metachronous metastasis of endometrial cancer to the renal pelvis or colon. Metastatic tumors in the renal pelvis and colon indicate nonspecific radiological findings, making them difficult to distinguish from primary tumors. We describe a case of a 55-year-old female previously treated for endometrial cancer, who was subsequently found to have metastatic masses in the renal pelvis and colon. The two masses were initially misidentified as primary urothelial carcinoma and colon adenocarcinoma.

Endometrial cancer commonly metastasizes to the pelvic and para-aortic lymph nodes, vagina, peritoneum, and lungs. Unusual sites of metastasis include the bone, brain, abdominal wall, muscles, and intra-abdominal organs. To our knowledge, there have been no documented cases of synchronous or metachronous metastasis of endometrial cancer to the renal pelvis or colon. Metastatic tumors in the renal pelvis and colon indicate nonspecific radiological findings, making them difficult to distinguish from primary tumors. We describe a case of a 55-year-old female previously treated for endometrial cancer, who was subsequently found to have metastatic masses in the renal pelvis and colon. The two masses were initially misidentified as primary urothelial carcinoma and colon adenocarcinoma.

Objective: We intended to investigate the relationships between visual sensory impairment (VSI) or auditory sensory impairment (ASI) and brain pathological changes associated with cognitive decline in older adults. Methods: We primarily tried to examine whether each sensory impairment is related to Alzheimer’s disease (AD) pathology, specifically beta-amyloid (Aβ) deposition, through both cross-sectional and longitudinal approaches in cognitively unimpaired older adults. Self-report questionnaires on vision and hearing status were administered at the baseline.Neuroimaging scans including brain [ 11 C] Pittsburgh Compound B PET and MRI, as well as clinical assessments, were performed at baseline and 2-year follow-up. Results: Cross-sectional analyses showed that the VSI-positive group had significantly higher Aβ deposition than the VSI-negative group, whereas there was no significant association between ASI positivity and Aβ deposition. Longitudinal analyses revealed that VSI positivity at baseline was significantly associated with increased Aβ deposition over 2 years (β = 0.153, p = 0.025), although ASI positivity was not (β = 0.045, p = 0.518). VSI positivity at baseline was also significantly associated with greater atrophic changes in AD-related brain regions over the 2-year follow-up period (β = −0.207, p = 0.005), whereas ASI positivity was not (β = 0.024, p = 0.753). Neither VSI nor ASI positivity was related to cerebrovascular injury, as measured based on the white matter hyperintensity volume. Conclusion The findings suggest that VSI is probably related to AD-specific pathological changes, which possibly mediate the reported relationship between VSI and cognitive decline. In contrast, ASI appears not associated with AD pathologies but may contribute to cognitive decline via other mechanisms.

Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.

This study investigated the association between serum phosphate level and mortality in acute kidney injury (AKI) patients undergoing continuous kidney replacement therapy (CKRT) and evaluated whether this association differed according to disease severity. Methods: Data from eight tertiary hospitals in Korea were retrospectively analyzed. The patients were classified into four groups (low, normal, high, and very high) based on their serum phosphate level at baseline. The association between serum phosphate level and mortality was then analyzed, with further subgroup analysis being conducted according to disease severity. Results: Among the 3,290 patients identified, 166, 955, 1,307, and 862 were in the low, normal, high, and very high phosphate groups, respectively. The 90-day mortality rate was 63.9% and was highest in the very high group (76.3%). Both the high and very high groups showed a significantly higher 90-day mortality rate than did the normal phosphate group (high: hazard ratio [HR], 1.35, 95% confidence interval [CI], 1.21–1.51, p < 0.001; very high: HR, 2.01, 95% CI, 1.78–2.27, p < 0.001). The low group also exhibited a higher 90-day mortality rate than did the normal group among those with high disease severity (HR, 1.47; 95% CI, 1.09–1.99; p = 0.01) but not among those with low disease severity. Conclusion: High serum phosphate level predicted increased mortality in AKI patients undergoing CKRT, and low phosphate level was associated with increased mortality in patients with high disease severity. Therefore, serum phosphate levels should be carefully considered in critically ill patients with AKI.

Retroperitoneal ectopic pregnancy is a rare form of ectopic pregnancy. Owing to its rarity and nonspecific symptoms, diagnosing retroperitoneal ectopic pregnancy at the initial presentation poses a significant challenge. Typically, the diagnosis relies on non-radiation imaging modalities, such as ultrasonography and MRI, whereas CT is infrequently used. Herein, we report a rare case of a retroperitoneal ectopic pregnancy, which was diagnosed using CT.

Rectal syphilis is a rare form of syphilis presentation and its symptoms, endoscopic and radiologic findings are nonspecific. Rectal syphilis typically presents with features such as concentric rectal wall thickening, mucosal hyperemia, perirectal fat stranding, and lymphadenopathy. Rectal cancer exhibits asymmetric wall thickening and lymph node necrosis, aiding in the differentiation between these two diseases. However, due to the considerable overlap in their respective manifestations, distinguishing between rectal syphilis and rectal cancer is extremely challenging without considering the patient’s medical history. Rectal syphilis often leads to unnecessary tests or delayed treatment, as it can be mistaken for other benign diseases such as inflammatory bowel diseases in addition to rectal cancer. In this case report, we aim to provide a detailed report on the endoscopic, imaging, and pathological findings based on our experience with a case of suspected rectal malignancy that turned out to be rectal syphilis.

Objective: We intended to investigate the relationships between visual sensory impairment (VSI) or auditory sensory impairment (ASI) and brain pathological changes associated with cognitive decline in older adults. Methods: We primarily tried to examine whether each sensory impairment is related to Alzheimer’s disease (AD) pathology, specifically beta-amyloid (Aβ) deposition, through both cross-sectional and longitudinal approaches in cognitively unimpaired older adults. Self-report questionnaires on vision and hearing status were administered at the baseline.Neuroimaging scans including brain [ 11 C] Pittsburgh Compound B PET and MRI, as well as clinical assessments, were performed at baseline and 2-year follow-up. Results: Cross-sectional analyses showed that the VSI-positive group had significantly higher Aβ deposition than the VSI-negative group, whereas there was no significant association between ASI positivity and Aβ deposition. Longitudinal analyses revealed that VSI positivity at baseline was significantly associated with increased Aβ deposition over 2 years (β = 0.153, p = 0.025), although ASI positivity was not (β = 0.045, p = 0.518). VSI positivity at baseline was also significantly associated with greater atrophic changes in AD-related brain regions over the 2-year follow-up period (β = −0.207, p = 0.005), whereas ASI positivity was not (β = 0.024, p = 0.753). Neither VSI nor ASI positivity was related to cerebrovascular injury, as measured based on the white matter hyperintensity volume. Conclusion The findings suggest that VSI is probably related to AD-specific pathological changes, which possibly mediate the reported relationship between VSI and cognitive decline. In contrast, ASI appears not associated with AD pathologies but may contribute to cognitive decline via other mechanisms.

Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.