Cases reported "Anemia, Sickle Cell"

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1/112. candida dubliniensis candidemia in patients with chemotherapy-induced neutropenia and bone marrow transplantation.

    The recently described species candida dubliniensis has been recovered primarily from superficial oral candidiasis in hiv-infected patients. No clinically documented invasive infections were reported until now in this patient group or in other immunocompromised patients. We report three cases of candidemia due to this newly emerging candida species in hiv-negative patients with chemotherapy-induced immunosuppression and bone marrow transplantation.
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2/112. Sickle cell-like crisis and bone marrow necrosis associated with parvovirus B19 infection and heterozygosity for haemoglobins S and E.

    In the literature, heterozygosity for haemoglobins S and E is known as a clinically benign condition. Nevertheless, we present a case of double heterozygosity manifesting as an infarctive sickle cell-like crisis with acute chest syndrome and reversible bone marrow necrosis. Importantly, these complications were associated with serologically documented parvovirus B19 infection. Reviewing the literature, this case emphasizes a specific role of parvovirus B19 as a precipitating cause. Furthermore, it demonstrates how important the consideration of haemoglobin disorders can be even outside of the historically known areas.
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3/112. Malignant haemangioendothelioma of bone in a HbSC disease patient--a case report.

    We report here a 35-year-old man with sickle cell disease (SCD), who presented in 1989 with pain in the (R) hip of 7 years duration and swelling of the (R) calf of 3 months duration. Clinical examination revealed a hard tender mass in the (R) calf. histology of the (R) calf mass revealed haemangioendothelioma (HE), similar to the histology of the (R) iliac bone mass obtained in another institution previously. He was treated with external radiotherapy with the 1.25 megavoltage beam to antero-posterior fields of the (R) hemipelvis and (R) calf, with good response. Chemotherapy was subsequently administered using 6 cycles of VAC regime. The patient remained in remission for 12 months. In 1991 he had lymphoedema of (R) lower limb and received further radiotherapy and chemotherapy after an isotope bone scan had revealed disease activity in the (R) hemipelvis, (R) femur and (L) upper tibia. He responded again with complete regression of the lymphoedema and remained well until April 1993 when the lymphoedema recurred. He died while being evaluated for further treatment. Although there is no evidence to suggest that SCD confers any protection from development of neoplasms, the co-existence of SCD with a neoplasm is not common. We consider the occurrence of HE of bone, a rare malignancy, in a HbSC patient worthy of reporting.
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4/112. A 'made in one piece' skeleton in a 22-year-old man suffering from sickle cell anaemia.

    A 22-year-old African male with known sickle cell anaemia was referred by a Congolese medical centre with a request to improve his poor physical condition. He was unable to walk, stand or sit because his large joints and his spine were either ankylosed or very rigid. Radiographs showed joint fusion from the third to the fifth cervical vertebrae, of both hips, of the left knee, and a bilateral osteonecrosis of the humeral head. There was no scintigraphic evidence for an active osteomyelitis (99mTc-MDP (methyldiphosphonate) bone scan, Tc monoclonal antigranulocyte scan and 99mTc sulphur colloid scan). To improve his mobility the right femoral head was resected in June 1997; 14 days later the left femoral head was resected. Four months after the resection of the right hip, a right uncemented total hip prosthesis was implanted on this side. One month later the same type of hip arthroplasty was performed on the left side. During the postoperative rehabilitation period the patient regained autonomy. We have found no previous reports of such severe and multiple joint complications in a single patient suffering from sickle cell anaemia.
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5/112. Bone marrow necrosis in sickle cell disease: a description of three cases and a review of the literature.

    Bone marrow necrosis (BMN) ranges from a localized to a widespread generalized process. Most often seen in patients with leukemia and other malignant conditions, generalized BMN has also been observed in patients with sickle cell disease (SCD), where it is almost certainly a consequence of blood vessel occlusion. Activation of the clotting system seems to play a role in this clinical setting. Systemic fat embolism and acute multi-organ failure syndrome can also complicate BMN in patients with SCD. We describe here 3 cases of BMN associated with SCD. Each patient exhibited an unusually severe vaso-occlusive crisis accompanied by persistent fever, a high level of serum lactate dehydrogenase, leukoerythroblastosis, and large numbers of nucleated red cells. Despite such suggestive clinical features, diagnosis of BMN still requires a bone marrow biopsy. Particularly in patients with SCD, the early institution of transfusion therapy can be life-saving. The ominous prognosis ascribed to generalized BMN seems to reflect the poor outcome of such underlying conditions as leukemia; however, the prognosis of generalized BMN is not so poor in association with SCD and other nonmalignant states.
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6/112. Treatment of superior vena cava syndrome with recombinant tissue plasminogen activator in a sickle cell patient undergoing bone marrow transplantation.

    Superior vena cava (SVC) syndrome is a well-recognized clinical entity seen with mediastinal malignancies and intraluminal venous thrombosis. The role of recombinant tissue plasminogen activator (rt-PA) in the resolution of SVC syndrome caused by thrombosis in the bone marrow transplant settings has not been described. The authors report a case of SVC syndrome with good clinical response in a 16-year-old female with sickle cell disease undergoing an allogeneic bone marrow transplant (BMT) from her HLA identical sibling. Shortly after her transplant, she was found to have significant facial edema and swelling above the neck. Concomitantly, her renal function deteriorated with progressive elevation of serum urea nitrogen and creatinine levels, requiring the use of continuous veno-venous hemofiltration. An upper extremity venogram showed complete SVC obstruction (type III) with apparent inferior reflux into the azygos system. rt-PA was started at a dose of (0.5 mg/kg/day) for 2 days. There was a dramatic resolution of her symptoms, including significant improvement in renal function with increase in urine output. A repeat venogram showed free flow from the distal tip of the central line consistent with a patent superior vena cava. There was no evidence of any bleeding manifestations with rt-PA. This report highlights the usefulness of rt-PA as a treatment modality for SVC syndrome in the BMT settings.
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7/112. Hyperhemolytic transfusion reaction in sickle cell disease.

    BACKGROUND: An atypical form of life-threatening hemolytic transfusion reaction (HTR) in patients with sickle cell disease (SCD) has been well described in the literature. Continuation of blood transfusion may be lethal, as it can further exacerbate hemolysis. The pathophysiologic mechanism of HTR is not well understood. case reports: Two cases of severe HTR in SCD after the transfusion of compatible RBC units are reported. hemolysis of both autologous and transfused cells was documented in Case 1 by urine Hb high-performance liquid chromotography. Multispecific HLA antibodies were identified in Case 1. Reticulocytopenia was noted in both cases during the acute hemolytic process. This was followed by a rise in reticulocyte count during receipt of IVIG and steroid therapy. bone marrow examination during reticulocytopenia in Case 2 showed erythroid hyperplasia. CONCLUSION: In SCD, both mature sickle cells and sickle reticulocytes adhere more readily to macrophages. In view of the bone marrow aspiration results, it appears that the recipients' HbS cells are destroyed by hyperactive macrophages and that the reticulocytopenia observed during HTR is likely to be due to peripheral consumption (i.e., destruction by macrophages), rather than suppression of erythropoiesis. Cessation of hemolysis during IVIG and steroid treatment may be due to IVIG's blocking of the adhesion of sickle cells and reticulocytes to macrophages, together with steroid suppression of macrophage activity.
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keywords = macrophage, bone
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8/112. Sickle cell disease with orbital infarction and epidural hematoma.

    Although bone infarction is a common feature in sickle cell disease, the involvement of the orbit is an unusual complication. Intracranial bleeding is another uncommon and serious complication. Few cases of orbital infarction alone have been reported. We report imaging findings (CT, bone scan, MRI) in a 16-year-old boy with sickle cell disease with orbital infarction and epidural hematoma. The precise cause of epidural hematoma is not well known, but it is probably related to vaso-occlusive episodes and the tearing of small vessels.
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9/112. 111In chloride bone marrow scintigraphy and ferrokinetic studies in a case of sickle cell anemia with transient erythroid aplasia.

    A patient with sickle cell anemia was hospitalized because of an acute erythropoietic aplastic crisis. 111In chloride bone marrow scintigraphy performed during the aplastic crisis showed markedly impaired uptake of the radionuclide and simultaneous 59Fe clearance T 1/2 studies were prolonged (420.9 min). Following recovery from the aplastic crisis 111In scintigraphy revealed an expanded marrow and the radioiron clearance T 1/2 was accelerated (20.9 min). The clinical course, hemograms and bone marrow aspirations correlated with marrow scintigraphy. 111In appears to be a valuable marrow scanning agent for assessing the presence of intramedullary erythropoietic activity.
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10/112. Co-existent sickle cell disease and juvenile rheumatoid arthritis. Two cases with delayed diagnosis and severe destructive arthropathy.

    We describe 2 pediatric patients with sickle cell disease (SCD) who developed seropositive juvenile rheumatoid arthritis (JRA). Both patients have severe joint damage, the compound effect of both disease processes. The bone and cartilage destruction, which poses serious therapeutic challenges, highlights the difficulty of making a diagnosis of chronic inflammatory disease in the setting of SCD. There may be a correlation between increased levels of tumor necrosis factor-alpha in the synovial tissue of joints damaged by arthritis and local sickling. The resultant ischemia and corresponding inflammatory infiltrates could in turn worsen existing synovial proliferation and cartilage destruction as well as trigger further sickling.
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