INTRODUCTION: Osteoporosis is currently health problem with mortality rate that can reach 12–20%. Diabetes mellitus (DM) is one of the independent risk factors for osteoporosis. An area requiring further study during osteoporosis treatment, in which various agents are selected according to the patient, is the metabolic parameters that change with treatment. The aim of this study is to comparatively evaluate the metabolic effects of bisphosphonates and denosumab, agents commonly used in osteoporosis treatment on glucose, HbA1c, and lipid profile according to the presence of diabetes.
METHODS: The data of 4552 patients who presented to our clinics between January 2011 and March 2024 and were diagnosed with osteoporosis were retrospectively reviewed. After excluding patients lost to follow-up or with missing data, 733 adult patients were included in the study. Patients were grouped according to the antiosteoporotic medication used and the presence of a diabetes diagnosis, and laboratory results before and after treatment were analyzed.
RESULTS: Post-treatment glucose levels varied by group in both treatment arms, whereas HbA1c levels showed a statistically significant increase in non-DM (p<0.001). According to subgroup analyses, bisphosphonate use did not cause significant change in HbA1c levels in non-diabetic patients, whereas denosumab use led to a significant increase in HbA1c. In contrast, the osteoporosis medications used in the diabetic patient group did not lead to a statistically significant change in metabolic parameters, although significant post-treatment decrease in triglyceride levels was recorded in the bisphosphonate group.
DISCUSSION AND CONCLUSION: The metabolic effects of anti-osteoporotic therapies, particularly HbA1c and LDL, emerged clearly in nonDM individuals, whereas these effects were not observed in diabetic patients, likely owing to their pre-existing metabolic dysregulation. In contrast to some literature suggesting that RANKL inhibitors contribute positively to glucose metabolism, the increases in HbA1c and LDL observed in this study indicate that this issue warrants investigation through larger-scale clinical studies.

INTRODUCTION: The prognostic significance of proteinuria in preeclampsia remains uncertain. This study aimed to compare maternal, laboratory, and perinatal outcomes between women with dipstick proteinuria <2+ and ≥2+ and to evaluate the association between proteinuria ≥2+ and adverse outcomes.
METHODS: This retrospective cohort included 260 women with preeclampsia, categorized according to dipstick proteinuria as <2+ (0/1+; n=126) or ≥2+ (n=134). Maternal, laboratory, and perinatal outcomes were compared between the groups. Binary logistic regression was used to evaluate the association between proteinuria ≥2+ and the composite adverse neonatal outcome, adjusting for maternal age, nulliparity, and severe hypertension.
RESULTS: Dipstick proteinuria ≥2+ was present in 134 women (51.5%). Compared with the <2+ group, women with proteinuria ≥2+ had higher blood urea nitrogen and creatinine levels and lower estimated glomerular filtration rate (all p≤0.013). Median birthweight was lower in the ≥2+ group (2315 vs 2520 g; p=0.002), whereas gestational age at delivery and Apgar scores did not differ significantly. The composite adverse neonatal outcome was more frequent with proteinuria ≥2+ (57.5% vs 44.4%; p=0.036), while severe hypertension and composite adverse maternal outcome rates were similar. Proteinuria ≥2+ was associated with the composite adverse neonatal outcome in the unadjusted analysis (OR 1.69, 95% CI 1.03–2.76; p=0.036) and in the primary adjusted model (adjusted OR 1.74, 95% CI 1.03–2.93; p=0.037). After gestational age at delivery was added in the sensitivity model, the association was attenuated (adjusted OR 1.40, 95% CI 0.72–2.71; p=0.317), while model discrimination increased from an AUC of 0.658 to 0.864.
DISCUSSION AND CONCLUSION: Dipstick proteinuria ≥2+ was associated with greater renal biochemical involvement, lower birthweight, and higher odds of a composite adverse neonatal outcome, but not with severe hypertension or the composite adverse maternal outcome. The attenuation after adjustment for gestational age at delivery suggests that the neonatal association was not independent of the timing of birth.

INTRODUCTION: In intrahepatic cholestasis of pregnancy (ICP), risk assessment rests on bile acid concentrations measured at diagnosis or at their peak. We asked whether a prespecified ≥50% decrease in total serum bile acids (TSBA) after ursodeoxycholic acid (UDCA) treatment predicts adverse perinatal outcomes.

METHODS: We retrospectively studied 200 singleton pregnancies with ICP (TSBA ≥19 µmol/L) treated with UDCA between January 2020 and January 2026. Women with a ≥50% decrease in TSBA at follow-up were classified as biochemical responders (n=135); the remainder were non-responders (n=65). The primary outcome was a composite of preterm birth, meconium-stained amniotic fluid, fetal distress, neonatal intensive care unit admission, or stillbirth. Logistic regression was adjusted for maternal age, body mass index, gestational age at diagnosis, and baseline TSBA.

RESULTS: The composite outcome occurred in 49.6% of responders and 69.2% of non-responders (adjusted odds ratio [aOR] 0.41, 95% confidence interval [CI] 0.21-0.80, p=0.009). The percentage decrease in TSBA discriminated the composite outcome better than baseline (area under the curve 0.613 versus 0.523) or peak TSBA (0.537, p<0.001). The group difference was confined to iatrogenic preterm birth (9.6% versus 29.2%, p<0.001); spontaneous preterm birth was similar, and a composite excluding iatrogenic preterm birth showed no association (aOR 0.87, p=0.659).

DISCUSSION AND CONCLUSION: The biochemical response to UDCA carries prognostic information beyond static bile acid values, but the association operates mainly through iatrogenic preterm delivery. Response assessment may support surveillance and counseling; it should not by itself trigger intervention.

Background/Aim: Primary ovarian mucinous adenocarcinoma and pulmonary mucinous adenocarcinoma are distinct entities; however, their overlapping histopathological and immunohistochemical features may create significant diagnostic challenges, particularly in distinguishing primary tumors from metastatic disease. This case report aims to highlight the diagnostic challenge of distinguishing primary pulmonary mucinous adenocarcinoma from metastatic ovarian mucinous adenocarcinoma and to emphasize the importance of integrating clinical, histopathological, and immunohistochemical findings in the differential diagnosis.
Case: A 49-year-old female patient presented with pain. Her medical history revealed that she underwent fertility-sparing surgery and debulking for a right ovarian mass in 2001, followed by chemotherapy and successful pregnancy via in vitro fertilization. Molecular analysis was negative for EGFR, ROS1, and BRAF mutations. The patient had a history of living in Kahramanmaraş for over 20 years, and environmental exposure included possible dye exposure related to her spouse’s occupation. In 2017, lesions were detected in the right upper and lower lobes of the lung. Histopathological examination revealed mucinous adenocarcinoma in both lobes. Immunohistochemically, tumor cells were CK7 and CA125 positive, focally CK20 positive, and negative for TTF-1, Napsin-A, CDX2, PAX8, ER, PR, and p16. The presence of “mucinous adenocarcinoma in situ” areas in both lesions supported the diagnosis of two separate primary lung tumors rather than metastatic disease. Additionally, anthracosis and emphysematous changes were observed in the surrounding lung parenchyma.
Conclusion: Distinguishing between primary and metastatic mucinous tumors requires a comprehensive evaluation of clinical, radiological, histopathological, and immunohistochemical findings. This case highlights the diagnostic complexity of mucinous tumors and underscores the importance of a multidisciplinary approach in accurate tumor classification and management.

May–Thurner syndrome (MTS) is a rare cause of venous thromboembolism (VTE) in children and adolescents and is often underdiagnosed. Here we present an adolescent male with extensive iliofemoral deep vein thrombosis (DVT) in whom MTS was identified as one of several contributing etiological factors. His first presentation revealed acute unilateral swelling and pain in the left lower extremity following minor trauma. Doppler ultrasonography disclosed extensive acute iliofemoral DVT, and further evaluation by computed tomography angiography demonstrated extrinsic compression of the left common iliac vein by the right common iliac artery, consistent with May–Thurner syndrome. He was also found to have homozygous Factor V Leiden mutation, probable hereditary protein C deficiency, hyperhomocysteinemia, and celiac disease, together indicating a multifactorial thrombotic process. This case highlights the importance of considering anatomical venous compression syndromes in adolescents presenting with extensive and unexplained iliofemoral DVT.