Background Anti-Rh(D) has appeal for use in immune thrombocytopenia (ITP) due its rapid onset of action (24 hours) and short infusion time (10 minutes). There is reluctance by some physicians to use anti-Rh(D), however, following FDA reports in 2000 of 15 cases of acute hemoglobinemia and/or hemoglobinuria (Gaines Blood 2000) and in 2005 of 6 cases of disseminated intravascular coagulation in association with acute hemoglobinemia and/or hemoglobinuria (Gaines Blood 2005). On 03/11/10, the FDA issued a black box warning stating that patients with ITP treated with WinRho (anti-Rh(D)) should be monitored in a healthcare setting for 8 hours following infusion for symptoms of intravascular hemolysis and for hemoglobinuria. Our institution adopted this 8-hour monitoring practice. Specific Aims To determine if the FDA black box warning has impacted on anti-Rh(D) utilization at St. Luke's-Roosevelt Hospital Center, New York, NY. Methods Institutional Review Board approval was obtained. The charts of consecutive patients with ITP treated with anti-Rh(D) who were followed in a hematology-oncology practice between 01/01/06 and 06/30/13 were reviewed. The ICD-9 code 287.31 for ITP was used to identify inpatients treated with anti-Rh(D) between 01/01/06 and 06/30/13. The number of outpatient and inpatient anti-Rh(D) infusions per annum was computed. Results The annual number of outpatient and inpatient anti-Rh(D) infusions is shown in Table 1. Infusions occurred predominantly in the outpatient setting. Eight-hour monitoring has been adhered to. While there has been some fluctuation in anti-Rh(D) utilization, there has not been a significant decline. Conclusion Despite the FDA requirement for patients to spend increased time at health care centers following anti-Rh(D) infusions, anti-Rh(D) utilization at our institution has not declined. Disclosures: No relevant conflicts of interest to declare.
4646 Rationale: Anti-Rh(D) is an effective treatment for acute immune thrombocytopenia [ITP]. It has a faster onset of action (1 day) vis a vis corticoids (3 days) and intravenous immunoglobulin [IVIG] (4 days). A direct comparison of length of stay for adult inpatients receiving these therapies has hitherto not been performed. We hypothesized that the length of stay would be shortest for patients treated with anti-Rh(D). Methods: A retrospective chart review was conducted to assess length of stay in relation to treatments proffered for ITP. The defining diagnosis of ITP [coded 287.31] was rendered from the computerised record at St. Luke's-Roosevelt Hospital Center and identified 303 patients, of which 147 received treatments for active ITP within a period spanning 01SEP2005 through 29FEB2012. Treatments consisted of prednisone alone, dexamethasone alone, anti-Rh(D) alone, IVIG alone, and combinations of corticoids and the latter two. An average length of stay was tabulated for each treatment regimen. Age and gender were also recorded. Results: A total of 147 hospitalisations for ITP were noted and the analysis of variance statistical calculation applied thus. The median age was 48 years and the male:female ratio was 1.1:1. Eleven groups were delineated and the means for length of hospital stay with confidence intervals derived. The groups were as follows: Prednisone, Dexamethasone, Methylprednisolone, Anti-Rh(D), IVIG, Prednisone and Anti-Rh(D), Dexamethasone and Anti-Rh(D), Prednisone and IVIG, Dexamethasone and IVIG, Methylprednisolone and IVIG, and Anti-Rh(D) and IVIG or Dexamethasone, Anti-Rh(D), and IVIG. The overall p-value for length of stay was 0.0016 (Table 1). The shortest stays were recorded for the corticoid alone groups; however, the mean stay for anti-Rh(D) was shorter than that of IVIG, both in sole and combined modality treatments. Conclusion: Anti-Rh(D) is favourable with respect to hospital stay duration. Although corticoids result in still shorter lengths of stay, anti-Rh(D) demonstrated a shorter length of stay compared with IVIG. Combined with its single dosing and relative cost savings, anti-Rh(D) is an excellent alternative to IVIG. Disclosures: No relevant conflicts of interest to declare.
5165 Purpose of the study: To characterize the significance of Glucose-6- Phosphate Dehydrogenase (G6PD) levels measured in pregnancy. Case series and results: We saw 3 patients referred to Hematology clinic over the past 1 year. The G6PD levels were measured in pregnancy by the obstetrician while working up the anemia (Table 1). They did not have any evidence of hemolysis during the time of workup and it is unclear as to why the G6PD levels were sent. The G6PD levels were found to be low and all 3 patients had iron deficiency anemia, that improved with iron supplementation. There was no evidence of pregnancy induced hypertension, urinary tract infections, or infections during pregnancy. All the pregnancies were uneventful resulting in healthy babies and the G6PD levels normalized after the delivery in all the patients. We did a literature search to see the significance of such an association and if there were any recommendations for further testing in these individuals. Discussion: G6PD deficiency is one of the most common inherited red cell disorders transmitted in an X-linked recessive fashion affecting approximately 400 million people worldwide. In the United States, black males are most commonly affected, with a prevalence of approximately 10 percent. Acute hemolysis is caused by infection, ingestion of fava beans, or exposure to an oxidative drug. G6PD catalyzes nicotinamide adenine dinucleotide phosphate (NADP) to its reduced form, NADPH, in the pentose phosphate pathway. NADPH protects cells from oxidative damage. G6pd deficiency predisposes cells to increased oxidative damage predisposing to hemolysis. G6PD deficiency in pregnancy may manifest as increased urinary tract infections, preeclamsia, neonatal jaundice, hydrops fetalis and still birth. Vergnes et al. [Lancet 1968] reported that low erythrocyte G6PD levels were found in 25% of women in early pregnancy and in up to 65% of women in late pregnancy. In their study G6PD levels normalized after delivery. The reason for this decrease is unclear. Pregnancy is shown to cause increased oxidative stress, alteration in neutrophil G6PD trafficking [ Kindzelskii et al. J Clin Invest 2002] though it is unclear if any of these mechanisms are implicated in the decreased levels of G6PD during pregnancy. Conclusions: There are no clear guidelines for the subsequent testing and management of low levels of G6PD diagnosed in the setting of pregnancy. Evidence based guidelines would be helpful towards identifying the subset of patients with true G6PD deficiency. Disclosures: No relevant conflicts of interest to declare.
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