Iron deficiency anemia (IDA) remains a prevalent health issue, especially among Japanese women, and may be influenced by dietary patterns and lipid metabolism. This study aimed to investigate the association between circulating bile acid (BA) concentrations and iron-related biomarkers in young Japanese women. Blood biochemical and anthropometric data were collected from 33 healthy young women aged 20. The participants can be divided into two groups based on the levels of total-iron binding capacity (TIBC), although their hemoglobin and ferritin levels were in the normal ranges. When participants were divided based on TIBC, the low TIBC group showed significantly higher levels of 12-hydroxylated, non-12-hydroxylated, and total BAs, as well as significantly lower blood glucose levels compared to the normal group (p<0.05). Positive correlations were observed between TIBC and specific BA species, such as glycolithocholic acid (ρ = 0.3993, p<0.0288), cholic acid (ρ = 0.4767, p<0.0077), and taurocholic acid (ρ = 0.4423, p<0.0144). Additionally, transferrin levels were positively correlated with glycolithocholic acid (ρ = 0.3649, p<0.0474). These findings suggest that TIBC may serve as an early indicator of hypoglycemia, reflecting preclinical metabolic disturbance, in addition to being a latent IDA marker.

Proinsulin-secreting neuroendocrine tumors (NETs) are a rare cause of severe hypoglycemia, characterized by normal or low insulin levels and disproportionate elevations of proinsulin. Clinical features and optimal management of unresectable cases remain poorly defined, in part due to such few cases described in the literature. We describe a 47-year-old female with metastatic large-cell neuroendocrine carcinoma who presented with obstructive jaundice and was incidentally found to have profound, asymptomatic fasting hypoglycemia. Initial insulin and C-peptide levels were within reference ranges, but proinsulin concentrations were markedly elevated. The patient developed recurrent, refractory hypoglycemia requiring high-dose corticosteroids, glucagon, diazoxide, octreotide, and ultimately central-line infusion of 70% concentrated dextrose via total parenteral nutrition. Glycemic control could not be achieved despite maximal medical therapy, and the patient experienced rapid clinical deterioration leading to comfort-focused hospice management. This case highlights the diagnostic challenges of proinsulin-driven hypoglycemia and underscores the need for earlier recognition and improved treatment pathways for patients with proinsulin-secreting NETs.

Despite the increasing number of patients diagnosed with postprandial reactive hypoglycemia (PRH), standardized diagnostic criteria and evaluation methods have not been established. Since PRH is generally defined as "hypoglycemia occurring due to elevated endogenous insulin levels following a high-carbohydrate meal in people without diabetes mellitus", prediabetes is considered one of the obvious pathologies of PRH. However, it has recently been reported that early diabetes can enter a state of "remission"; therefore, it is difficult to distinguish between prediabetes and early diabetes. We present a case of PRH in an obese woman with prediabetes, identified through oral glucose tolerance testing and continuous glucose monitoring. She experienced severe hypoglycemia, which sometimes resulted in loss of consciousness. However, her PRH symptoms were effectively treated with an α-glucosidase inhibitor. We believe it would be beneficial for clinicians to study this case, as it clearly demonstrates a pathology of PRH in a patient with prediabetes and/or early diabetes.

Carbohydrate counting is central to dietary self-management in patients with type 1 diabetes mellitus (T1DM). However, objective assessments of carbohydrate counting knowledge and its relationship with psychosocial outcomes are scarce in Gulf populations. This study assessed carbohydrate counting knowledge, diabetes distress, and hypoglycaemia awareness in patients with T1DM attending a tertiary diabetes centre in the United Arab Emirates.

The cohesin complex, composed of SMC1, SMC3, RAD21, and STAG1/STAG2, is essential for chromosome cohesion, DNA repair, and transcriptional regulation. Pathogenic variants in cohesin components cause cohesinopathies. The classical characteristics of cohesinopathies include developmental delay (DD), intellectual disability (ID), feeding difficulties, hypotonia, short stature, hearing loss, and dysmorphic features. Here, we present a 5-year-old boy with classical cohesinopathy features, including DD/ID and feeding difficulties, along with non-classical features such as hypoglycemia, recurrent fever, and immunodeficiency. Trio exome sequencing identified a novel de novo missense variant of uncertain significance (NM_005862.3:c.643G>A(p.Val215Ile)) in the STAG1 gene. The variant localizes to the RAD21 interaction interface, and molecular dynamics (MD) simulations revealed conformational changes comparable to other STAG1 variants reported as likely pathogenic in patients, supporting a deleterious effect which may disrupt the STAG1-RAD21 interaction interface. This case expands the phenotypic and molecular spectrum of STAG1-related cohesinopathy and advances our understanding of the disease mechanism.

Insulinoma is the most common functional pancreatic neuroendocrine tumor, typically benign, solitary, and sporadic, with an estimated incidence of 1-4 cases per million per year worldwide. It causes recurrent hypoglycemia through inappropriate insulin secretion, classically presenting as Whipple's triad and confirmed by a prolonged supervised fasting test. Surgical enucleation remains the preferred treatment for small, well-localized benign insulinomas, allowing maximal preservation of pancreatic parenchyma. We report two cases of sporadic pancreatic insulinoma managed by open enucleation at a tertiary referral center in Senegal, West Africa, where advanced diagnostic modalities such as endoscopic ultrasound (EUS), somatostatin receptor scintigraphy, and selective arterial secretagogue injection (SASI) testing were unavailable. The first case was a 30-year-old woman presenting with a severe hypoglycemic coma complicated by status epilepticus on postpartum day 10. Abdominal CT scan identified a pancreatic head lesion. Biochemical workup confirmed insulinoma with a fasting blood glucose of 0.30 g/L (30 mg/dL; 1.7 mmol/L), elevated fasting insulin at 32.7 µU/mL, and C-peptide at 2.92 ng/mL. Open enucleation was performed; the postoperative course was complicated by a transient infectious syndrome managed with broad-spectrum antibiotics. Histopathology confirmed a well-differentiated Grade 1 neuroendocrine tumor. Complete resolution of hypoglycemic episodes was achieved with no recurrence at 1 year. The second case involved a 55-year-old man with a 12-year history of recurrent neuroglycopenic episodes. CT scan revealed an isthmic pancreatic lesion. Enucleation was performed; the postoperative course was complicated by a high-output pancreatic fistula (Grade B, ISGPS 2016 classification), managed conservatively with fasting, parenteral nutrition, and close radiological monitoring, without surgical reintervention. Histopathology confirmed a low-grade neuroendocrine tumor. No recurrence of hypoglycemia was observed at 5 months. These cases demonstrate that open enucleation is a feasible, effective, and parenchyma-sparing option for benign sporadic insulinomas, even in resource-limited settings where advanced localization and intraoperative techniques remain unavailable.

Insulinomas are rare functional pancreatic neuroendocrine tumors. Metastasis is found in up to 15% of patients and is difficult to predict at diagnosis.

Background and Aims Dumping syndrome (DS) and postbariatric hypoglycemia (PBH) represent common complications after Roux-en-Y gastric bypass (RYGB). Transoral outlet reduction (TORe) addresses the rapid passage of food through the gastrojejunal anastomosis which is central in pathophysiology. In this prospective multicenter study, technical feasibility and short-term clinical efficacy of a new clip-based endoscopic system (BARS) were evaluated. Methods Twenty-three consecutive patients at three centers in Germany were included. The primary endpoint was feasibility measured as reduction of anastomotic diameter and surface. Secondary endpoints included changes of the Dumping symptom score and glycaemia in modified oral glucose tolerance tests (mod. oGTT), anastomotic diameter, quality of life after 12 weeks and adverse events. Results The procedure was technically feasable in all cases. Median anastomotic diameter was reduced from 40 mm (IQR: 30-50) to 9 mm (IQR: 7-10); -77%) at baseline (p < 0.001). At week 12, median Sigstad-Score decreased from 17,5 (IQR: 12.8-21.0) to 5 (IQR: 0-11; p < 0.001). Median anastomotic diameter was still reduced to 20 mm (IQR: 12-30; p = 0.004; -47%). Modified oGTT demonstrated abolished DS in 3 of 23 patients (13%) while no effect was seen in PBH at 12 weeks. Median BMI decreased from 30.6 kg/m [2] (IQR: 28-35.6) to 29.25 kg/m [2] (IQR: 26.7-33.4; p = 0.001). Quality of life (QoL) improved significantly in five of eight subcategories of the SF-36. Conclusion Clip-based anastomotic reduction for DS and PBH seems feasible, safe and showed significant improvements in Sigstad scores and QoL in short-term analysis.

Hypoglycemic encephalopathy (HE) is a rare yet critical consequence of extended low blood sugar, often resulting in altered mental status, seizures, and coma. Because its presentation mirrors various other neurological disorders, prompt recognition is difficult, and treatment delays risk permanent brain damage. This report describes a 56-year-old Black man with Type 1 diabetes mellitus (DM) on Neutral Protamine Hagedorn (NPH) insulin who discovered nonresponsiveness roughly eight hours post insulin injection. Upon admission, he was presented with a blood glucose of 43 mg/dL and a Glasgow Coma Scale (GCS) score of 7/15, with brain magnetic resonance imaging (MRI) findings consistent with HE. Despite immediate treatment with intravenous (IV) 40% dextrose (50 mL), a continuous dextrose-saline infusion, and antiepileptic medication to control seizures, his neurological function stabilized without further improvement, leaving his GCS score between 8 and 10. Following a four-month period of stabilization during home care the patient developed pneumonia and septicemia in the fifth month. This complication triggered progressive neurological deterioration, ultimately resulting in death at five months postevent. This case underscores the importance of timely detection and treatment of hypoglycemia in diabetic patients, particularly those receiving insulin. Regular glucose monitoring, patient education, and careful insulin adjustment are essential to prevent HE and its devastating outcomes.

Hypoxia upregulated 1 (HYOU1) is a stress-inducible ER chaperone. We investigated 2 unrelated patients carrying biallelic HYOU1 variants and presenting with primary immunodeficiency. Patient 1, homozygous for p.Pro444His, displayed failure to thrive, hypoglycemia, B cell lymphopenia, and neutropenia. Patient 2, compound heterozygous for p.Arg262Gln and p.Pro757_Glu758insAla, exhibited recurrent infections, enteropathy, and hypogammaglobulinemia. In Patient 1, while HYOU1 transcription was preserved, the protein was severely reduced. Tunicamycin treatment of dermal fibroblasts showed a blunted unfolded protein response and defective induction of ER stress-responsive genes. Immunophenotyping showed near-absence of circulating B cells, and single-cell RNA sequencing of bone marrow identified an arrest at the pro-B cell stage. Neutrophils displayed hypogranulation and dysregulated IFN- and apoptosis-associated transcriptional signatures, unresponsive to G-CSF. HYOU1 deficiency hence results in ER stress-induced proteostasis failure that simultaneously impairs adaptive immunity through B cell developmental arrest and innate immunity through neutrophil dysfunction and IFN pathway imbalance. This work expands the spectrum of HYOU1 deficiency and further identifies ER proteostasis as a central determinant of immune homeostasis.