Background: The incidence of early-onset colorectal cancer (EOCRC), defined as CRC diagnosed in individuals under age 50, is rising globally. This systematic review and meta-analysis synthesizes global epidemiological trends, risk factors, clinical characteristics, and outcomes of EOCRC. Methods: Following PRISMA 2020 guidelines, we systematically searched PubMed, Scopus, and Web of Science from January 2000 to August 2025. Studies reporting incidence, prevalence, risk factors, or outcomes in EOCRC populations were included. Quality assessment employed the Cochrane Risk of Bias Tool for randomized studies and ROBINS-I for observational studies. Meta-analyses were performed using random-effects models where sufficient homogeneity existed. Results: From 3,847 screened records, 115 studies met inclusion criteria. EOCRC incidence is rising in 27 of 50 countries, with average annual percentage changes ranging from 1.3% to 4.0%. Pooled analysis showed EOCRC accounts for 10-12% of all CRC diagnoses globally. Risk factors include obesity (RR 1.54, 95% CI 1.31-1.81), hereditary syndromes (25% of cases), and Western dietary patterns. EOCRC presents with distinct clinicopathologic features including higher rates of left-sided tumors and signet ring histology. Conclusions: EOCRC represents a growing global health burden with unique epidemiological and clinical characteristics requiring tailored prevention, screening, and management strategies. Bangladesh J Medicine 2026; 37(3): 183-191
Background: Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal hematopoietic disorder that may coexist with myelodysplastic syndrome (MDS), leading to diagnostic complexity. Case: A 45-year-old male presented with generalized weakness and dark-colored urine, with a 10-year history of transfusion-dependent anemia. Examination revealed mild anemia and jaundice. Urine analysis showed hemoglobinuria without red blood cells. Bone marrow study demonstrated hypercellularity with dysplastic changes suggestive of MDS. Flow cytometry confirmed a PNH clone with CD55 and CD59 deficiency. Diagnosis: PNH with MDS and urinary tract infection. Management: The patient received supportive care, antibiotics, folic acid, and azacitidine. Eculizumab was indicated but not administered due to financial constraints. Conclusion: PNH should be suspected in chronic unexplained hemolytic anemia. Coexistence with MDS necessitates detailed hematological evaluation. Limited access to definitive therapy remains a major challenMDS Bangladesh J Medicine 2026; Vol. 37, No. 2(1): pp. 241-242
Disseminated intravascular coagulation (DIC) is a severe thrombo-inflammatory syndrome characterized by systemic activation of coagulation, excessive fibrinolysis, neutrophil extracellular trap (NET) formation, and endothelial injury. It progresses from an early hypercoagulable phase—marked by widespread microvascular thrombosis—to an advanced consumptive phase with hemorrhage and multiorgan failure. Thrombosis and bleeding often coexist, with fibrinolysis typically secondary to underlying triggers rather than primary. Unlike a distinct disease, DIC resembles acute respiratory distress syndrome (ARDS) as a dysregulated host response. Sepsis remains the most common risk factor, prompting the International Society on Thrombosis and Haemostasis (ISTH) to endorse sepsis-induced coagulopathy (SIC) for early identification in septic patients. SIC scoring integrates platelet count, prothrombin time, and fibrinogen levels to enable rapid bedside diagnosis, addressing the absence of a gold-standard biomarker. Key pathophysiological mediators include thrombin-antithrombin (TAT) complexes, which reflect thrombin burst, and plasminogen activator inhibitor-1 (PAI-1), which imbalances fibrinolysis by inhibiting tissue plasminogen activator. Elevated TAT and PAI-1 levels show promise for early DIC detection, though validation in prospective trials is needed. Management prioritizes treating the underlying cause. Supportive measures are phase-specific: low-molecular-weight heparin in non-hemorrhagic early DIC to mitigate thrombosis; antifibrinolytics for hyperfibrinolysis; and blood products including fresh frozen plasma, cryoprecipitate, fibrinogen concentrates, and platelets for bleeding phases. Anticoagulant trials (e.g., antithrombin, recombinant thrombomodulin) yield mixed results, underscoring the need for personalized, biomarker-guided strategies to improve outcomes in this high-mortality condition. Bangladesh J Medicine 2026; Vol. 37, No. 2(1): pp. 197
Hemophagocytic Lymphohistiocytosis (HLH) is a rare but life-threatening hyperinflammatory syndrome caused by uncontrolled immune activation and excessive cytokine release. Secondary HLH may occur in association with infections, malignancies, or autoimmune disorders. Because its clinical manifestations overlap with severe infections and hepatobiliary diseases, HLH often presents as a diagnostic dilemma, particularly in tuberculosis-endemic regions. A 27-year-old male presented to Shaheed Suhrawardy Medical College Hospital with intermittent high-grade fever for seven months, progressive jaundice for three months, and significant weight loss. On examination he was febrile, deeply icteric, moderately anemic, and had hepatomegaly with ascites and pedal edema. Laboratory investigations revealed anemia, markedly elevated inflammatory markers, hyperbilirubinemia (total bilirubin 19.2 mg/dL), elevated liver transaminases, severe hypoalbuminemia, and markedly raised serum ferritin levels. Imaging studies including ultrasonography and contrast-enhanced CT scan demonstrated hepatomegaly, intra-abdominal lymphadenopathy, and ascites, while MRCP showed no evidence of biliary obstruction. Viral markers and autoimmune screening were negative. Bone marrow examination revealed areas of marrow necrosis with preserved hematopoiesis. The constellation of prolonged fever, hyperferritinemia, cytopenia, liver dysfunction, hepatomegaly, and bone marrow abnormalities fulfilled several HLH-2004 diagnostic criteria, raising strong suspicion of secondary HLH. Further evaluation suggested an underlying infectious trigger, possibly disseminated tuberculosis. The patient was managed with supportive therapy and evaluation for potential triggers. Recognition of the hyperinflammatory syndrome enabled timely consideration of HLH-directed management along with treatment of the underlying cause. Secondary HLH should be suspected in patients presenting with prolonged fever, hyperferritinemia, cytopenias, hepatomegaly, and liver dysfunction when routine investigations fail to reveal a clear diagnosis. Early recognition using established diagnostic criteria is crucial because delayed diagnosis significantly increases mortality. Bangladesh J Medicine 2026; Vol. 37, No. 2(1): pp. 244-245
Hypocalcemia is a frequently encountered biochemical abnormality with broad and often complex differentials encompassing endocrine, renal, and genetic disorders. We present a case series illustrating the varied etiologies and diagnostic challenges associated with hypocalcemia in a tertiary care setting. The series includes patients with Hypoparathyroidism, Pseudohypoparathyroidism, Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis (FHHNC) Type 1 and 2. We describe four young patients who presented with diverse manifestations, each ultimately diagnosed with a different underlying cause. A 21-year-old man developed recurrent carpal spasms a few days after dengue fever; evaluation revealed hypocalcemia, hyperphosphatemia, low parathyroid hormone, and widespread intracranial calcifications, leading to a diagnosis of hypoparathyroidism. The second patient, a boy with recurrent renal stones since early childhood, had low calcium and magnesium, raised creatinine, elevated parathyroid hormone, hypercalciuria, hypermagnesuria, bilateral nephrolithiasis and nephrocalcinosis; genetic testing revealed a homozygous missense mutation, confirming FHHNC type 1. The third patient, a young girl with medullary nephrocalcinosis since age 5, also exhibited myopia, horizontal nystagmus, and bilateral macular atrophy; biochemical testing showed hypomagnesemia, hypocalcemia, secondary hyperparathyroidism, renal dysfunction, urinary calcium and magnesium wasting; whole-exome sequencing identified a novel mutation, establishing FHHNC type 2. The fourth patient, a 16-year-old boy with recurrent convulsions, round facies, short stature, brachydactyly, and subcutaneous ossifications, demonstrated hypocalcemia, hyperphosphatemia, elevated parathyroid hormone, and basal ganglia calcifications, consistent with pseudohypoparathyroidism. This case series underscores that hypocalcemia is not a singular entity but a manifestation of heterogenous disorders, and careful clinical and biochemical correlation is critical for accurate diagnosis and tailored care. Bangladesh J Medicine 2026; Vol. 37, No. 2(1): pp. 245.
