Thalassemia is an autosomal recessive genetic disorder that affects the beta or alpha subunits of the hemoglobin structure. Thalassemia is classified as a hypochromic microcytic anemia and a definitive diagnosis of thalassemia is made by genetic testing of the alpha and beta genes. Thalassemia carries similar features to the other diseases that lead to microcytic hypochromic anemia, particularly iron deficiency anemia (IDA). Therefore, distinguishing between thalassemia and other causes of microcytic anemia is important to help in the treatment of the patients. Different indices and algorithms are used based on the complete blood count (CBC) parameters to diagnose thalassemia. In this article, we review how effective artificial intelligence is in aiding in the diagnosis and classification of thalassemia.

The association between the COVID vaccine and MCD is temporal and by exclusion, and it is not fully established, but it should be considered in postvvaccine MCD.

Philadelphia-negative (Ph-) myeloproliferative neoplasms (MPNs) are a group of hematopoietic malignancies identified by clonal proliferation of blood cell lineages and encompasses polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The clinical and laboratory features of Philadelphia-negative MPNs are similar, making them difficult to diagnose, especially in the preliminary stages. Because treatment goals and progression risk differ amongst MPNs, accurate classification and prognostication are critical for optimal management. Artificial intelligence (AI) and machine learning (ML) algorithms provide a plethora of possible tools to clinicians in general, and particularly in the field of malignant hematology, to better improve diagnosis, prognosis, therapy planning, and fundamental knowledge. In this review, we summarize the literature discussing the application of AI and ML algorithms in patients with diagnosed or suspected Philadelphia-negative MPNs. A literature search was conducted on PubMed/MEDLINE, Embase, Scopus, and Web of Science databases and yielded 125 studies, out of which 17 studies were included after screening. The included studies demonstrated the potential for the practical use of ML and AI in the diagnosis, prognosis, and genomic landscaping of patients with Philadelphia-negative MPNs.

Coronavirus disease 2019 (COVID-19) is commonly associated with acute respiratory distress syndrome and acute cardiac and renal injuries. However, thromboembolic events are also prevalent in COVID-19. The pathogenesis of COVID-19 hypercoagulability is not well known but may be linked to the cytokine storm induced by a viral infection or endothelial damage that triggers a cascade leading to hypercoagulability. Because vascular endothelium has angiotensin-converting enzyme 2-like lung tissue, COVID-19 targets lung tissue and vascular endothelium, leading to thrombosis. We present a rare case of a young patient with COVID-19 who presented with thrombosis of the cerebral venous system managed with anticoagulation. This case highlights the need for heightened awareness of this atypical but potentially treatable complication of the COVID-19 disease spectrum.

Herpes zoster (shingles) is a common viral infection that results from the reactivation of varicella-zoster virus (VZV), which remains dormant in sensory ganglia after initial infection. The usual presentation is radicular pain followed by eruption of vesicular rash. herpes zoster ophthalmicus (HZO) is defined as the involvement of ophthalmic division (V1) of the trigeminal nerve (V). Extraocular muscle paralysis is a rare complication of HZO. Here, we report a case of HZO that developed abducens nerve (VI) palsy and secondary raised intra-ocular pressure.

Anemia of chronic disease (ACD), also referred to as anemia of inflammation, is a prevalent and clinically significant complication of chronic infection, autoimmune disease, malignancy, and chronic kidney disease. It is characterized by inflammation‐driven iron sequestration, impaired erythropoietin (EPO) production and signaling, and suppression of effective erythropoiesis. Current therapies (iron supplementation and erythropoiesis‐stimulating agents) often address downstream consequences and may be limited by hepcidin‐driven functional iron deficiency, cytokine‐mediated EPO resistance, and safety concerns in vulnerable populations. This review re‐examines ACD through an integrated framework of hepcidin dysregulation, iron sequestration, and inflammatory inhibition of the EPO axis. We then synthesize emerging evidence that sodium–glucose cotransporter 2 (SGLT2) inhibitors produce sustained increases in hemoglobin/hematocrit beyond transient hemoconcentration across cardiovascular and kidney disease trials, including in non‐diabetic populations. Mechanistic studies suggest a coordinated biologic response that may include reduced hepcidin, improved iron mobilization, physiologic augmentation of endogenous EPO, and attenuation of systemic inflammation—pathways directly relevant to ACD. We critically re‐appraise current ACD paradigms by contrasting downstream “replacement” strategies (iron and ESAs) with pathway‐level approaches (HIF‐PHIs and SGLT2 inhibition), and we outline biomarker‐guided study designs to test whether SGLT2 inhibition may act as an adjunctive physiologic modulator of iron–erythropoietic crosstalk in well‐phenotyped inflammatory anemia cohorts, while emphasizing that current evidence remains hypothesis‐generating rather than practice‐changing.