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Introduction. Haptoglobin binds the globin portion of free hemoglobin. Serum haptoglobin measurement is used as a laboratory marker for the diagnosis of hemolytic anemia. Since stored blood contains free hemoglobin, transfusion may affect haptoglobin levels. Study Objectives. The aim of the study was to evaluate whether serum haptoglobin could be measured to assess hemolysis in recently transfused patients. Patients and Methods. Twenty-one patients, receiving more than one unit of packed red blood cells (PRBCs) for presumed nonhemolytic indications, were enrolled. Serum haptoglobin levels were recorded before, immediately after, and 24 and 48 hours after transfusion. Observations and Results. Analysis of variance with a repeated measures was used to examine the serum haptoglobin levels at different time periods and no significant difference was found (P = .28). Conclusion. The results suggest that serum haptoglobin can be used in the diagnosis of hemolysis in patients receiving multiple units of PRBC.

IntroductionMixed warm and cold autoimmune hemolytic anemia runs a chronic course with severe intermittent exacerbations. Therapeutic options for the treatment of hemolysis associated with autoimmune hemolytic anemia are limited. There have been only two reported cases of the effective use of rituximab in the treatment of patients with mixed autoimmune hemolytic anemia. We report a case of severe mixed autoimmune hemolytic anemia that did not respond to steroids and responded to four weekly doses of rituximab (one cycle).Case presentationA 62-year-old Caucasian man presented with dyspnea, jaundice and splenomegaly. His blood work revealed severe anemia (hemoglobin, 4.9 g/dL) with biochemical evidence of hemolysis. Exposure to cold led to worsening of the patient's hemolysis and hemoglobinuria. A direct antiglobulin test was positive for immunoglobulin G and complement C3d, and cold agglutinins of immunoglobulin M type were detected. A bone marrow biopsy revealed erythroid hyperplasia. A positron emission tomographic scan showed no sites of pathologic uptake. There was no other evidence of a lymphoid or myeloid disorder. Initial therapy consisted of avoidance of cold, intravenous methylprednisolone and a trial of plasmapheresis. However, there was no clinically significant response, and the patient continued to be transfusion-dependent. He was then started on 375 mg/m2/week intravenous rituximab therapy. After two treatments, his hemoglobin stabilized and the transfusion requirement diminished. Rituximab was continued for a total of four weeks and led to the complete resolution of his hemolytic anemia and associated symptoms. At the patient's last visit, about two years after the initial rituximab treatment, he continued to be in complete remission.ConclusionTo the best of our knowledge, this is the first reported case of mixed-type autoimmune hemolytic anemia that did not respond to steroid therapy but responded completely to only one cycle of rituximab. The previous two reports of rituximab use in mixed autoimmune hemolytic anemia described an initial brief response to steroids and the use of rituximab at the time of relapse. In both of these case reports, the response to one cycle of rituximab was short-lived and a second cycle of rituximab was required. Our case report demonstrates that severe hemolysis associated with mixed autoimmune hemolytic anemia can be unresponsive to steroid therapy and that a single cycle of rituximab may lead to prompt and durable complete remission.

Background:Multiple gliomas represent approximately 2 to 5% of all high-grade gliomas which are categorized as multifocal or multicentric depending on the timing, location and pattern of spread. We present a patient with bi-hemispheric, noncontiguous, low- and high-grade gliomas proven by biopsy. She underwent surgical excision and radiotherapy, but unfortunately succumbed to her disease shortly thereafter.Case Description:A 64-year-old female presented to the hospital with confusion, disorientation and retrograde amnesia after an unwitnessed fall. There were no symptoms of headaches or visual disturbances before presentation. Magnetic resonance imaging (MRI) with and without gadolinium revealed a nonenhancing left temporal lobe mass without surrounding edema, an enhancing left frontal lobe mass with surrounding edema, and an enhancing right parietal lobe mass with surrounding edema. The patient underwent a left frontal craniotomy with gross total resection of the left frontal mass and a left temporal craniotomy, anterior temporal lobectomy and sub-total resection of the temporal lobe mass. Intraoperative Brainlab® image-guided navigation was used. Postoperative treatment consisted of radiotherapy.Conclusion:This is the first reported case of multiple separate glial tumors, each with differing grades in which an MRI can be correlated with the tissue diagnoses. This case also highlights the possible mechanisms of transformation of glial tumors in the continuum from benign to malignant forms, lending insight to the possibility of using advanced genetic analysis in the treatment and diagnosis of these entities.

Desmoplastic small round-cell tumor is an uncommon, highly aggressive tumor with a predilection for pediatric age groups and young adults. It is very unusual in the elderly population. Although Agent Orange has been associated with soft-tissue sarcoma, an association with desmoplastic small round-cell tumor has not been reported. A 52-year-old male presented with abdominal distention, dyspnea, and a 9 kg weight loss. Prior history was significant for hepatitis C and diabetes. He was a Vietnam veteran and he admitted being exposed to Agent Orange. On physical examination, the abdomen was distended and tense. Computed tomography scan of the chest, abdomen and pelvis demonstrated extensive mediastinal and retroperitoneal adenopathy, diffuse omental masses and extensive pleural, intra-abdominal and pelvic ascites. Omental core needle biopsy was consistent with desmoplastic small round-cell tumor based on morphology and immunohistochemistry. He responded poorly to chemotherapy with high-dose cyclophosphamide, doxorubicin and vincristine and died 5 months after presentation secondary to neutropenic sepsis despite G-CSF support and antibiotics.