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Although most of the evidence regarding the type antifungal nail paint discount sporanox online master card, frequency, and etiology of these complications has been studied in adults,260 there are increasing reports in children. After liver transplant, 36% of children will have a hematologic problem, and of these, 54% are anemic events, 19% anemia and neutropenia, 12% thrombocytopenia, 8% neutropenia, and 2% pancytopenia. In the next section, discussion of the hematologic complications of solid organ transplantation is divided into cell type and by organ type when feasible. Much of the data are derived from adult studies, but information from pediatric studies is emphasized. When transfusing platelets or freshfrozen plasma, the product should be compatible with both the recipient and donor. Red Blood Cells Anemia is a common problem after transplantation, occurring in 66% of kidney transplant recipients at the time of transplant263 and 60% to 84% after transplant. Hemolytic Uremic Syndrome/Microangiopathic Hemolytic Anemia Early Posttransplant Anemia Early posttransplant anemia is defined as anemia that occurs within 6 months from the time of transplant. After renal transplantation, additional causes are iron deficiency or prior uremia or bone disease Passenger Lymphocyte Syndrome Passenger lymphocyte syndrome is a graft-versus-host reaction. This direct antiglobulinpositive immune hemolytic anemia occurs within 3 to 24 days after transplant. The median time of onset is 30 days after transplant, ranging from 8 days to 9 months,270 and 80% of cases are within 90 days and 96% within 1 year. However, other genetic abnormalities of the complement system are not associated with this high rate of recurrence. Genetic screening is recommended before transplantation not only to determine risk but to develop posttransplant management plans273 (see later). Sirolimus alone and especially in combination with cyclosporin has been associated with development of thrombotic microangiopathy. Treatment consists of discontinuing or decreasing the dose or switching the calcineurin inhibitor. Late Posttransplant Anemia Anemia occurring greater than 6 months after transplant is termed late posttransplant anemia. Causes of late anemia that are common to all solid organ transplants include:261-263,265,267 1. This may be because of the large donor kidney with higher erythropoietin levels and creatinine clearance relative to the size of the patient. The authors postulate an auto- or alloimmune mechanism to explain this phenomenon. One possible mechanism of the development of autoimmune antibodies posttransplant is the chronic T-cell suppression resulting from the use of these agents followed by release of B-cell control. This variation may be a result of the lack of a specific test for drug-associated anemia and the lack of prospective studies. In a study of children and young adults after cardiothoracic transplantation, approximately 25% of the cases of anemia were attributed to tacrolimus, primarily because no other cause was found. Only one patient had a direct antiglobulin study performed, and the results were negative. Four of five patients with simultaneous anemia and neutropenia recovered counts within 5 weeks of switching to CsA. In another study of 50 pediatric renal transplant patients, the prevalence of anemia was 60%, with 30% having hemoglobin levels below 10 g/dL. Of interest, in a study of adults after liver transplantation, erythropoietin production was found to be reduced in patients receiving cyclosporin but not tacrolimus. In a retrospective study of 81 patients (median age, 39 years; range, 12-66 years) after lung transplantation, 20% developed hemolytic anemia in the first year after transplant. Review of the literature in 2006 revealed 91 cases of parvovirus B19 infection posttransplant reported in adults. A total of 99% were anemic, with one-third also having leukopenia and 18% thrombocytopenia. The three deaths were only seen in patients after liver transplant who developed myocarditis and cardiogenic shock. Of interest, in a prospective study of 47 solid organ transplant recipients, none were found to have molecular evidence of parvovirus B19 in the first year posttransplant. There were no associated symptoms in seven of 14, but other reported symptoms include cytopenias, rash, myocarditis, and pneumonia. Platelets Problems with platelets including thrombocytopenia and thrombocytopathy have been reported after transplant primarily in adults. After liver transplantation, almost all patients develop a transient thrombocytopenia. Immediate Thrombocytopenia After Liver Transplantation More than 90% of adults have been reported to have thrombocytopenia within the first week after liver transplantation. An increase in thrombopoietin is seen on days 4 to 6, and increased reticulated platelets are noted on days 7 and 8. Lack of resolution is associated with a poor prognosis for graft and overall survival. One theory is that it is a nonimmune consumptive process reflected by increased markers of thrombin generation. A second theory is that it is unlikely to be a consumptive process because of the lack of platelet activation after day 1. The thrombocytopenia is more likely a result of low levels of thrombopoietin seen pretransplant. With new production and rising levels of thrombopoietin from the new liver, there is a subsequent increase in platelet production, resulting in normalization of the platelet count soon after transplantation.
Primary immune disorders fungi budding definition generic sporanox 100 mg with amex, at time of initial diagnosis, may be asymptomatic or patients can have recurrent infections or lymphoproliferations. Mortality rates for agespecific neoplasms in patients with primary immune disorders is 10200 times more than for the general population [5]. IgA immunodeficiency is usually subclinical and its incidence in Caucasians is estimated at 1 in 600 [7]. However, no increased association with lymphoproliferative disorders or lymphomas has been shown [8]. Higher rates are noted in populations with high consanguinity rates or among genetically isolated populations. Congenital defects of phagocyte number, function, or both (a) X-linked chronic granulomatous disease 6. Chronic antigenic stimulation in a host with impaired immune response is considered a significant mechanism of tumor development [9]. The sites of presentation are variable, and may involve lymph nodes, spleen, and mainly extranodal sites, of which the most commonly affected sites are the gastrointestinal tract, lung, and central nervous system. The clinical presentation is variable, and in general patients present with recurrent infections. Patients present with erythroderma, eosinophilia, lymphadenopathy, and hepatosplenomegaly. Patients with X-linked lymphoproliferative syndrome may present with lymphadenopathy and/or hepatosplenomegaly or fatal infectious mononucleosis. Laboratory findings are variable and specific diagnosis may require highly specialized immunologic and molecular testing [16]. Specialized testing includes functional evaluation of T-cells (delayed hypersensitivity skin tests, proliferative response to mitogens and cytokine production), B-cells (natural or acquired antibodies, response to protein or carbohydrate antigens) and phagocytic function (chemotaxis, bactericidal activity, reduction of nitroblue tetrazolium) [16]. In the following discussion, lesions are separated as non-neoplastic and neoplastic. It is common to find lymphocyte depletion and atrophic follicles with progressive depletion of germinal centers. Secondary changes include follicular and interfollicular lymphoid hyperplasia and granulomatous inflammation that can be associated with infections. Histologically, lymphoid follicles lack germinal centers and there is an accumulation of IgM+ plasma cells in nodal and extranodal sites, the latter including the gastrointestinal tract, spleen, liver, and gallbladder. These lesions may not become clonal, but may cause massive organ enlargement and occasionally are fatal. Molecular studies may reveal transient clonal populations of B cells with V-J rearrangements. Findings include a systemic polymorphous proliferation of B-lymphocytes, plasmacytoid, and immunoblastic cells. Hemophagocytic syndrome is common in cases of fulminant infectious mononucleosis and is better seen in bone marrow aspirates. The most common histologic types are nonHodgkin lymphoma (50 %) diffuse large B-cell lymphoma, followed by Burkitt lymphoma, Hodgkin lymphoma (9 %) and peripheral T-cell lymphoma. More rarely, T-and B- lymphoblastic leukemia/lymphoma and T-cell prolymphocytic leukemia have been reported. Various patterns of viral latency may be observed, depending on the degree of immune competence of the host. Monotypic cytoplasmic immunoglobulin may be detected in cases with plasmacytic differentiation. Studies of clonality used for lymphoproliferative disorders in reactive and neoplastic processes apply for lymphoproliferative disorders associated with primary immune disorders. Therefore, the presence of clonal populations by molecular testing of antigen receptor genes of T- or B-cell lineage support the presence of a neoplastic clone, and this information requires integration with clinical and pathologic findings. These include breakpoints at 14q1112, 7q32-35, 7p15, inv(7)(p13q35), t(7;7)(p13q35), t(7;14) (p13;q11), t(14;14)(q11;q32), as well as the immunoglobulin genes. However, lymphoid proliferations in other primary immune disorders may be aggressive. In general, a conservative approach is recommended for self-limited or indolent cases. Prophylactic antibiotics and/or intravenous immunoglobulin reduce rates of infections and increase survival of patients with common variable immunodeficiency [17]. Hodgkin and non-Hodgkin lymphomas are treated with standard therapy used in immunocompetent patients with similar neoplasms. These features are morphologically suspicious of a lymphoma, thus extensive workup was performed in this lymph node, but no evidence of clonality by immunophenotypic or molecular studies were found. The presence of hyperplastic, although distorted, germinal centers hints that the molecular damage does not affect the formation of germinal center cells. Overview of lymphoproliferative disorders associated with primary immune deficiency disorders. Cancer risk among patients with IgA deficiency or common variable immunodeficiency and their relatives: a combined Danish and Swedish study. Patient-centred screening for primary immunodeficiency: a multi-stage diagnostic protocol designed for nonimmunologists. The disease becomes clinically evident in childhood as patients present with lymphadenopathy, hepatosplenomegaly, and multilineage cytopenias [2]. Apoptosis is a program of cell death, triggered by cell surface mechanisms (the extrinsic pathway) or by activation of mitochondrial proteins (the intrinsic pathway) and results in activation of caspases and their downstream targets.
In the postoperative period fungus gnats mint order cheapest sporanox, platelet count changes reflect several processes, including initial hemodilution (immediate platelet count decrease) and increased platelet consumption (first 2 to 4 days), at which point the platelet count begins to rise due to increased platelet production; when the platelet count reaches its postoperative peak- usually about 14 days after surgery-platelet production decreases somewhat, and the platelet count returns to baseline. As part of the physical examination, evidence of hemostatic impairment should be sought, as well as secondary causes of thrombocytopenia. The signs of platelet-related bleeding include petechiae and purpura (see Chapter 130). Petechiae typically occur in the dependent regions of the body or on traumatized areas. Spontaneous mucous membrane bleeding (wet purpura), epistaxis, and gastrointestinal bleeding indicate a more serious hemostatic defect. Although petechiae are common in patients whose platelet counts are less than 10 to 20 × 109/L, most patients with platelet counts over 50 × 109/L have no signs of hemostatic impairment. Timing of Onset and Severity of Thrombocytopenia Many thrombocytopenic disorders-particularly those involving an immune pathogenesis-exhibit characteristic temporal features that can aid in the diagnosis. Occasionally, thrombocytopenia worsens in the first few days after surgery; this can occur in multiorgan system failure. In contrast, thrombocytopenia of insidious onset that progresses over several years suggests chronic liver disease, with evolution to progressive portal hypertension and associated splenomegaly. Because the platelet aggregates are not counted by the electronic particle counter, the automated platelet count appears falsely low. The correct platelet count usually can be determined by collecting the blood into sodium citrate or heparin or by performing the count on nonanticoagulated finger prick samples; maintaining the blood sample at 37°C often attenuates platelet clumping. A much less common (one in 10,000 blood samples) antibody-mediated pseudothrombocytopenic disorder is platelet satellitism, in which rosette-like clusters of platelets surround neutrophils. Bone marrow examination can be helpful for assessment of platelet production, particularly if megakaryocytes are reduced in number or abnormal in appearance. When the mechanism of chronic thrombocytopenia is unclear, an autologous platelet survival study using 111In-labeled platelets may be informative. Three patterns can be seen: (1) normal platelet survival and recovery (underproduction), (2) marked reduction in the platelet life span (increased destruction), and (3) reduced recovery but a normal or near-normal life span (sequestration). Therapy the risk of bleeding in patients with thrombocytopenia can be reduced by avoiding drugs that impair hemostasis. If drug-induced thrombocytopenia is suspected, as many medications as possible should be stopped. Lifethreatening bleeding episodes should be treated with platelet transfusion regardless of the mechanism of the thrombocytopenia. The underlying cause and anticipated natural history of the thrombocytopenic disorder influence the decision about prophylactic platelet transfusion. As a general rule, patients with chronic thrombocytopenic disorders characterized by increased platelet destruction. The blood film is examined to exclude pseudothrombocytopenia, which is characterized by in vitro platelet clumping. Initial platelet count declines result from hemodilution and increased platelet consumption, with the platelet count nadir occurring between days 1 to 4 (median, day 2). Consequently, prophylactic platelet transfusions are seldom indicated for such patients except when they are at risk of bleeding because of trauma or major surgery. When platelets are given, the platelet count should be maintained above 50 × 109/L. Invasive procedures such as thoracentesis, paracentesis, and liver biopsy are not usually associated with excess bleeding if the platelet count is greater than 50 × 109/L. However, bleeding in the setting of severe thrombocytopenia may justify platelet transfusion even in these disorders. In adults, the spleen weighs between 150 to 200 g and measures approximately 11 cm in length. The anatomy of the spleen is uniquely suited for its function; progressive branching of the splenic artery into trabecular and central arteries helps separate the plasma from the cellular elements (see Chapter 162). The central arteries arise perpendicularly from the trabecular arteries and skim the plasma layer from the cells. Soluble antigens in the plasma are delivered to the white pulp, where phagocytic cells process them and antibody production is initiated. Some of this blood flows directly to the splenic veins (the closed system), but most moves into the splenic cords (the open system). Here, the cellular elements percolate through a meshwork of reticulum fibers, reticuloendothelial cells, and supporting cells to reach the splenic sinuses. The cells enter the sinuses by passing through narrow fenestrations in the basement membrane of the endothelial cells lining the sinuses. Because the veins in the portal system lack valves, any increase in portal pressure is transmitted to the splenic microcirculation. It is the largest lymphoid organ in the body and contributes to host defense by clearing microorganisms and antibody-coated cells. The spleen also is important for antibody synthesis, especially antibodies directed against soluble antigens. The usual postoperative platelet count nadir is seen between postoperative days 1 to 3 (inclusive). The spleen also acts as a reservoir of platelets (accommodating about one-third of the platelet mass in normal individuals).