Iron-deficiency anemia is frequently accompanied by reactive thrombocytosis, yet the mechanisms underlying this association remain incompletely understood. Beyond impaired erythropoiesis, iron availability has emerged as an active regulator of hematopoietic lineage decisions. This review synthesizes current evidence on how iron deficiency influences megakaryocytic-erythroid balance, with emphasis on progenitor-level regulation, iron sensing pathways and downstream megakaryocyte maturation. We discuss experimental and clinical studies supporting compensatory hematopoietic responses under iron-deficient conditions and propose an integrated framework linking systemic iron status to altered platelet and erythroid output.

Anemia is a frequent complication in cats with chronic kidney disease (CKD), mainly due to decreased erythropoietin (EPO) production resulting from a loss of renal erythropoietin-producing (REP) cells. Anemia affects both survival and quality of life by inducing clinical signs such as lethargy and anorexia. Early detection of anemia by monitoring hematocrit/packed cell volume (Htc/PCV) trends is essential to initiate treatment before progressive renal damage limits therapeutic effectiveness. Molidustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI), is a novel oral drug stimulating endogenous erythropoietin synthesis. However, treatment has to be started when REP cells are still functional, with PCV target ranges between 30-40%. Regular monitoring following the International Renal Interest Society (IRIS) guidelines is essential to keep PCV within the target range and to determine when treatment should be started, stopped, or restarted. Moreover, monitoring the iron status is important since both functional and absolute iron deficiency might be seen in cats with CKD and can impair response to treatment.

The prevalence of anemia is high in people with chronic kidney disease (CKD) and increases as the disease advances. The Kidney Disease Outcomes Quality Initiative (KDOQI) convened a work group to review the Kidney Disease: Improving Global Outcomes (KDIGO) 2026 clinical practice guideline for the management of anemia in CKD. The previous KDIGO anemia guideline was published in 2012; in 2019 and 2021 KDIGO convened conferences addressing controversies in iron management and hypoxia-inducible factor-prolyl hydroxylase inhibitor (HIF-PHI) use, respectively. The KDOQI work group provides perspective for implementation of the KDIGO 2026 anemia guideline within the context of clinical practice in the United States. The KDOQI work group agrees with most of the KDIGO recommendations, particularly the proactive use of intravenous (IV) iron in hemodialysis patients and the preference for erythropoiesis stimulating agents (ESAs) over HIF-PHIs for first-line anemia therapy, due to greater familiarity with safety of the former. Specific issues regarding recommendations and practice points for providers in the United States include higher serum ferritin targets and mean levels among people receiving hemodialysis than in the rest of the world; the availability of a single HIF-PHI product with approval only for patients receiving dialysis for ≥3 months; and payment barriers that may drive the choice of therapeutic agents. Additional commentary is provided on topics including IV iron therapy in people receiving hemodialysis and an iron-based phosphate binder, the incidence and significance of hypophosphatemia among people with CKD not on dialysis but receiving IV iron therapy, the physiologic importance of iron repletion in people with CKD and iron deficiency without anemia, possible therapeutic benefits of HIF-PHIs compared with ESAs, and assessing risk versus harm of red blood cell transfusions.

Collagenous gastritis is a rare pediatric disease characterized by chronic gastritis with superficial, irregular mucosal involvement, focal atrophy of the gastric glands, an inflammatory infiltrate predominantly composed of lymphocytes and plasma cells, and areas of epithelial erosion. Focal collagen deposition in the subepithelial region of the lamina propria is a hallmark feature. Gastric epithelial erosions can cause hematemesis and, more generally, occult gastrointestinal bleeding, leading to chronic iron-deficiency anemia. Currently, there are no established management guidelines, and data on long-term follow-up are lacking. We report a clinical case of collagenous gastritis, emphasizing its features and therapeutic approach.

Hereditary hemorrhagic telangiectasia (HHT) is a genetic disorder of the vasculature associated with mucocutaneous telangiectasia and visceral arteriovenous malformations (AVMs). These manifestations can frequently lead to chronic blood loss and iron deficiency anemia. In some cases, anemia can be severe and transfusion-dependent, reflecting an advanced disease phenotype with persistent vascular involvement and cumulative blood loss. This report presents a case of a 58-year-old female with a known diagnosis of HHT who presented with fatigue, dizziness, and chronic melena, and was found to have a hemoglobin level of 4.7 g/dL. Imaging revealed persistent pulmonary AVM disease, which may increase cardiopulmonary demand, particularly in the setting of severe anemia, and may contribute to complications if left untreated. The patient required transfusion of five units of packed red blood cells and underwent endoscopic ablation of multiple telangiectasias in the stomach and duodenum. This case underscores the persistent nature of HHT-related gastrointestinal bleeding and the cardiopulmonary consequences of multi-system AVM burden. It emphasizes the necessity for multidisciplinary care and ongoing surveillance in patients with HHT to prevent symptom progression.

Collagenous gastritis (CG) is an extremely rare chronic inflammatory gastropathy with non-specific symptoms and high misdiagnosis rate. We report a 21-year-old female with 6-month postprandial epigastric discomfort, anorexia, dizziness, fatigue, and severe iron deficiency anemia. Endoscopy showed diffuse erythema, erosions, and typical nodular elevation-depression lesions in the gastric corpus. Histopathology and Masson's trichrome staining verified subepithelial collagen band thickening (>10 μm), confirming CG. After 8-week oral iron and proton pump inhibitor treatment, clinical symptoms resolved and hematological parameters improved markedly, but histological changes persisted. This case indicates that CG should be considered in young adults with unexplained iron deficiency anemia and atypical endoscopic features, and nodule-depression pattern serves as a key diagnostic clue.

ObjectiveThe diagnostic utility of serum iron in identifying iron deficiency anemia among patients with inflammatory bowel disease remains underreported. This study aimed to evaluate the true diagnostic value of serum iron.MethodsA total of 160 patients with iron deficiency anemia from a grade-A general hospital in Sichuan Province between January 2022 and January 2025 were enrolled. Eighty patients with inflammatory bowel disease and iron deficiency anemia were included in the test group, while 80 patients with iron deficiency anemia without inflammation were included in the control group. Iron metabolism parameters, including serum iron and serum ferritin, complete blood count indices, and biochemical markers, were collected and compared. Differences in diagnosing iron deficiency anemia using serum iron and serum ferritin among patients with inflammatory bowel disease were compared using the chi-square test. Spearman correlation analysis was performed among serum iron, serum ferritin, and other indicators. Meanwhile, potential factors affecting serum iron levels were investigated using linear regression, and the significance of serum iron in diagnosing inflammatory bowel disease with iron deficiency was evaluated using the receiver operating characteristic curve.ResultsAmong patients with inflammatory bowel disease, ulcerative colitis and Crohn's disease showed no significant differences in serum iron and serum ferritin levels. The real clinical results showed that when using 1-6.6 times the lower limit of normal of serum ferritin as a threshold to diagnose patients with inflammatory bowel disease and iron deficiency anemia, a statistically significant difference was observed compared with the serum iron lower limit of 1 time (p < 0.01). The positivity rate of iron deficiency anemia was 88.75% (71/80) for serum iron and 61.25% (49/80) for 3.3-time serum ferritin. Correlation analysis revealed that serum iron was positively correlated with serum ferritin (r = 0.263, p = 0.018) and negatively correlated with most inflammatory parameters (p < 0.05). Multiple linear regression analysis showed that when serum iron was used as the dependent variable, the optimal regression model with the independent variables serum ferritin, hemoglobin, platelet count, and monocyte-to-lymphocyte ratio had regression coefficients (β) of 0.246, 0.231, -0.405, and -0.187, respectively, all of which were significantly different (p < 0.05). Moreover, according to the European Crohn's and Colitis Organization diagnostic criteria for iron deficiency, patients with inflammatory bowel disease were divided into an iron deficiency group involving 41 patients and a non-iron deficiency group involving 39 patients. By comparing the parameters of the two groups and constructing the receiver operating characteristic curve, serum iron alone yielded the highest Youden index and the largest area under the curve for diagnosing iron deficiency (area under the curve = 0.764, p < 0.001). However, when the false-positive rate was controlled at 20%, the sensitivity of serum iron for diagnosing iron deficiency was 62.00%.ConclusionsIn patients with inflammatory bowel disease, serum iron is inversely associated with inflammation and appears to be more sensitive than serum ferritin in detecting iron deficiency anemia. These findings suggest that combined measurement of serum iron and serum ferritin may enhance the diagnosis of iron deficiency anemia in clinical practice.

Iron deficiency is the most common cause of anemia worldwide, yet desiderosmia remains rarely described as one of its manifestations. The term "desiderosmia" was first proposed in a case series by Hansen et al. to describe compulsive olfactory cravings for specific scents observed in three symptomatic patients with iron deficiency, derived from the Latin word "desiderare" for desire and the Greek word "osme" for smell. Desiderosmia appears to be closely related to pica, a common manifestation of iron deficiency, though the key difference is that patients report olfactory cravings without the desire to consume the scent-producing substance. As far as the authors of this report are aware, the number of published cases of desiderosmia is extremely scarce, and the term itself has yet to become recognized in medical literature, owing to its novelty. We report the case of a 32-year-old woman with menorrhagia and iron deficiency anemia (IDA) refractory to oral ferrous sulfate despite adherence. Despite her hemoglobin improving from 9.1 to 9.9 g/dL (reference range: 12-15.5 g/dL), her ferritin remained critically low at 1 ng/mL (reference range: 30-400 ng/mL). At that time, she developed an intense urge to smell pine-scented cleaning products, alongside migraines and restless leg syndrome, hypothesized to be neuropsychological symptoms linked to altered CNS iron homeostasis. We speculate that desiderosmia may share a similar neurological mechanism, correlating more closely with the severity of iron store depletion rather than with anemia severity. Recognition of this symptom prompted identification of IDA not improving with oral iron and escalation of therapy to IV ferrous carboxymaltose. Following treatment with intravenous iron repletion, her ferritin increased to 52 ng/mL, and she no longer experienced desiderosmia or any other iron deficiency symptoms. This case highlights the need for validating studies of desiderosmia's potential as a diagnostic marker in cases of severe iron deficiency and the symptom's pathophysiology.

Guidelines clearly recommend endoscopic investigation for iron deficiency anemia but are ambiguous for iron deficiency without anemia. We aimed to compare gastrointestinal malignancy rates between patients with iron deficiency without anemia and iron deficiency anemia, and to identify factors associated with malignancy. We performed a retrospective cohort study of adult patients who underwent bidirectional endoscopic examination for iron deficiency (ferritin levels < 45 µg/l) at two major Jordanian hospitals over 1.5 years. The total cohort consisted of 480 patients and was divided into two groups: iron deficiency anemia (274 patients) and iron deficiency without anemia (206 patients). Patients with iron deficiency anemia were significantly older (mean age 56.0 vs. 52.2 years, p = 0.007) and included a higher proportion of females (68.2% vs. 57.8%, p = 0.018). There was no significant difference in the rate of gastrointestinal malignancy between patients with anemia (1.8%) and those without anemia (2.4%), with an overall prevalence of malignancy of 2.1%. Colorectal adenocarcinoma was the most common malignancy (7 out of 10 cases). Notably, all gastric malignancies (3 cases) occurred in patients without anemia. Increasing age emerged as the only significant predictor of malignancy. These preliminary findings suggest that endoscopic evaluation may be considered for all patients with iron deficiency, regardless of anemia status, particularly for older patients. Larger prospective studies are needed to clarify the true risk.