Management of Acute Ulcerative Colitis with Iron Deficiency Anemia and Thrombocytosis (Platelet Count 800)
Initiate thromboprophylaxis with low-molecular-weight heparin immediately, treat the underlying ulcerative colitis aggressively, and use intravenous iron rather than oral iron for the iron deficiency anemia.
Immediate Thromboprophylaxis
All patients with acute severe ulcerative colitis require subcutaneous prophylactic low-molecular-weight heparin to reduce the risk of thromboembolism, which is markedly increased during disease flares and is independent of other thromboembolic risk factors. 1
- The thrombocytosis (platelet count 800 × 10⁹/L) is reactive, secondary to the inflammatory state of active ulcerative colitis 2
- Platelets amplify inflammatory and immune responses in chronic inflammation, potentially worsening disease activity 2
- The combination of active inflammation, thrombocytosis, and iron deficiency anemia creates a particularly high thrombotic risk 2
- Do not delay thromboprophylaxis while awaiting other investigations or treatments 1
Treatment of Underlying Ulcerative Colitis
Treating the underlying inflammatory bowel disease is the essential first step, as chronic inflammation is the key driver of both the anemia and thrombocytosis. 1
- Intravenous corticosteroids (methylprednisolone 60 mg every 24 hours or hydrocortisone 100 mg four times daily) remain the mainstay of conventional therapy for acute severe ulcerative colitis 1
- Ensure adequate IV fluid and electrolyte replacement, with potassium supplementation of at least 60 mmol/day 1
- Consider second-line medical therapy with infliximab, ciclosporin, or tacrolimus early (on or around Day 3 of steroid therapy) if response is inadequate 1
- The thrombocytosis will typically resolve as the inflammatory activity is controlled 2
Iron Deficiency Anemia Management
Use intravenous iron as first-line therapy rather than oral iron, given the active inflammatory state and severity of anemia. 1
Why Intravenous Iron is Preferred
- Intravenous iron is advisable for patients with pronounced disease activity and severe anemia (hemoglobin level <10 g/dL) 1
- Inflammation-induced hepcidin elevation severely impairs intestinal iron absorption, making oral iron ineffective during active disease 3
- IV iron is more effective (odds ratio 1.57 for achieving 2.0 g/dL hemoglobin increase) and better tolerated than oral iron in inflammatory bowel disease patients 3
- Oral iron may potentially exacerbate inflammatory bowel disease through generation of reactive oxygen species 1
Specific IV Iron Protocol
- Choose IV iron preparations that can replace iron deficits with 1-2 infusions rather than multiple infusions 4
- Ferric carboxymaltose (500-1000 mg single doses, delivered within 15 minutes) is a preferred formulation 3
- Iron isomaltoside is another single-dose option that can deliver up to 1000 mg 3
- Avoid iron dextran preparations due to higher risk of anaphylaxis requiring test doses 3
Expected Response
- Hemoglobin should rise by approximately 2 g/dL after 3-4 weeks of treatment 1, 4
- Continue monitoring hemoglobin every 3 months for the first year after successful treatment 1
Erythropoiesis-Stimulating Agents Consideration
If anemia does not improve despite intravenous iron therapy and control of inflammation, consider erythropoietic therapy combined with continued IV iron supplementation. 1
- However, use erythropoiesis-stimulating agents (ESA) with extreme caution given the thrombocytosis, as ESA is a risk factor for thrombosis, which is already a common complication in ulcerative colitis 1
- The therapeutic goal with ESA should be hemoglobin of 11-13 g/dL, not higher, to minimize thrombotic risk 1
- ESA therapy should always be combined with intravenous iron administration to prevent functional iron deficiency 1
- Optimal iron supply requires transferrin saturation of 30-40% and serum ferritin concentration of 200-500 mcg/L 1
Monitoring for Thrombotic Complications
Screen for venous thromboembolism risk and maintain prophylactic anticoagulation throughout the acute phase. 2
- The combination of active ulcerative colitis, thrombocytosis, and potential ESA use creates compounded thrombotic risk 2
- Continue low-molecular-weight heparin throughout hospitalization and acute disease phase 1
- Monitor for signs of deep vein thrombosis or pulmonary embolism clinically 2
Critical Pitfalls to Avoid
- Do not use oral iron in patients with active inflammatory bowel disease and hemoglobin <10 g/dL—this is ineffective and potentially harmful 1
- Do not withhold thromboprophylaxis despite the anemia—the thrombotic risk far outweighs bleeding risk in this setting 1
- Do not assume the thrombocytosis requires specific treatment—it is reactive and will resolve with control of the underlying inflammation 2
- Do not delay second-line rescue therapy if steroids are ineffective by Day 3—prolonged ineffective steroid therapy increases morbidity 1
- If using ESA, do not target hemoglobin >13 g/dL given the already elevated thrombotic risk from thrombocytosis 1
Nutritional Support
- Provide enteral nutrition if the patient is malnourished, as it is associated with fewer complications than parenteral nutrition (9% vs 35%) 1
- Check vitamin B12 and folate levels at least annually, or if macrocytosis is present 1
- Bowel rest through IV nutrition does not alter outcomes and is not necessary 1