Hyperhaemolysis caused by anti-HI antibodies in a patient with myelodysplastic syndrome following a first ever red cell transfusion.

BACKGROUND: Hyperhaemolysis is a rare and life-threatening delayed haemolytic transfusion reaction characterised by complement-mediated destruction of both host and transfused red cells. It is well recognised as a complication of transfusion in patients with haemoglobinopathies and has occasionally been described in haematological malignancy and anaemia of chronic disease. Anti-HI antibodies are usually clinically insignificant but have rarely been associated with haemolytic transfusion reactions, including cases of hyperhaemolysis in sickle cell disease. METHODS AND MATERIALS: Here, we describe a novel case of a patient with myelodysplastic syndrome developing hyperhaemolysis as a result of an anti-HI alloantibody following their first-ever transfusion. The patient required multiple lines of treatment, including erythropoietin, haematinic supplementation, corticosteroids, intravenous immunoglobulin and rituximab. RESULTS: Following treatment, steady-state haemoglobin was achieved with quiescent haemolysis, and complement inhibition with eculizumab was considered but ultimately not required. CONCLUSION: This is the first known report of hyperhaemolysis with an anti-HI antibody in a non-haemoglobinopathy patient. The treatment of hyperhaemolysis is evolving, and future commissioning needs to consider the role of complement inhibition in non-haemoglobinopathy patients.

Use of methylnaltrexone for the treatment of opioid-induced constipation in critical care patients.

Gastrointestinal dysmotility and constipation are common problems in critical care patients. The majority of critical care patients are treated with opioids, which inhibit gastrointestinal (GI) motility and lead to adverse outcomes. We reasoned that methylnaltrexone (MNTX), a peripheral opioid antagonist approved for the treatment of opioid-induced constipation in patients with advanced illness receiving palliative care when response to laxative therapy has not been sufficient, could improve GI function in critically ill patients. The present study included all patients in our intensive care unit who required rescue medication for GI stasis during the 10-week period from September 1 to November 15, 2009. We compared conventional rescue therapy with subcutaneous MNTX. We performed a retrospective chart review of the 88 nonsurgical critical care patients receiving fentanyl infusions, 15 (17%) of whom met the criteria of absence of laxation within 72 hours of intensive care unit admission despite treatment with senna and sodium docusate. Eight of these 15 patients subsequently received conventional rescue therapy (combination of sodium picosulfate [5 mg] and 2 glycerin suppositories [4-g mold]), and 7 patients received MNTX (subcutaneous injection, 0.15 mg/kg). Laxation occurred within 24 hours in 6 of the 7 MNTX patients (86%) but in none of the 8 patients receiving conventional rescue therapy (P=.001). The median difference in time to laxation between the 2 groups was 3.5 days (P<.001). Although not statistically significant, all 7 patients treated with MNTX, but only 4 of 8 (50%) who received conventional rescue therapy, progressed to full target enteral feeding (P=.08). Intensive care unit mortality was 2 of 7 MNTX patients (29%) vs 4 of 8 (50%) in the standard therapy group (P=.61). We hypothesize that MNTX may play an important role in restoration of bowel function in critically ill patients.

Humoral and cellular immunity to primary H1N1 infection in patients with hematologic malignancies following stem cell transplantation.

Limited data are available on immunologic responses to primary H1N1 infection in patients with hematologic malignancies. We present a prospective, case-surveillance study of such patients with real-time polymerase chain reaction (RT-PCR) confirmed H1N1-influenza who presented to our institution between September 2009 and January 2010. Ninety-two patients presented with influenza-like symptoms, and 13 had H1N1 infection confirmed by RT-PCR, including 4 allogeneic stem cell transplant recipients (1 with acute myelogenous leukemia, 1 with chronic lymphoblastic leukemia [CLL], 1 with non-Hodgkin lymphoma, and 1 with chronic myelogenous leukemia), 5 patients with multiple myeloma following autologous stem cell transplantation, 1 patient with multiple myeloma perimobilization, 2 patients with NHL post chemotherapy, and 1 patient with CLL. All 13 patients required hospitalization. Six (43%) were admitted to the intensive care unit (ICU), of whom 4 (67%) died. We evaluated B cell and T cell responses to H1N1 infection prospectively in these patients compared with those in 4 otherwise healthy controls. Within 12 weeks of diagnosis, only 6 of 11 patients developed seropositive antibody titers as measured by hemagglutination-inhibition or microneutralization assays, compared with 4 of 4 controls. H1N1-specific T cells were detected in only 2 of 8 evaluable patients compared with 4 of 4 controls. H1N1-specific T cells were functional, capable of producing interferon γ, tumor necrosis factor α, and CD107a mobilization. Furthermore, CD154 was up-regulated on CD4(+) T cells in 3 of 4 controls and 2 of 2 patients who had both B cell and T cell responses to H1N1. Post-H1N1 infection, 5 of 8 patients developed seasonal influenza-specific T cells, suggesting cross-reactivity induced by H1N1 infection. These data offer novel insights into humoral and cell-mediated immunologic responses to primary H1N1 infection.