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Query: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rheologic properties of red blood cells and hemostasis were studied in patients with acquired autoimmune hemolytic anemia who received antilymphocytic globulin (ALG). Hypocoagulation changes attended by elevation of red blood cell aggregation activity were detected in the patients already at their admission to the hospital. After administration of ALG, growth of these shifts, characteristic of disseminated intravascular blood coagulation (DIC) syndrome, was noted. It was shown that erythrocytic thromboplastin and antiheparin factor action on blood coagulation, mainly at the expense of the young cell fraction, was responsible for disorders in hemostasis. Nevertheless, despite the presence of DIC syndrome, in the group of patients, who received ALG, no clinical signs of this state were recorded, that could be explained by the protective effect of red blood cell intensified capacity for aggregation leading to the improvement of blood coagulation parameters.
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PMID:[Rheological properties of erythrocytes and hemostasis in patients with acquired autoimmune hemolytic anemia treated with anti- lymphocyte globulin]. 221 Mar 16

The development of immune-mediated hemolytic anemia is a well-recognized complication after allogeneic bone marrow transplantation (BMT). The majority of reported cases, however, have been alloimmune in origin due to ABO or minor red blood cell antigen incompatibilities between the donor and recipient. In this study, we report seven adult patients who developed autoimmune hemolytic anemia (AIHA) between June 1985 and January 1993. These patients were identified from a total of 236 adult patients who received T cell-depleted (TCD) grafts as graft-versus-host disease (GVHD) prophylaxis. The onset of AIHA was at a median of 10 months (range 7-25 months) post-transplant and occurred in 5% of all patients transplanted with TCD grafts who survived at least 6 months. Six patients had a warm reacting autoantibody, while one patient had a cold-reacting antibody with a thermal amplitude up to 30 degrees C. All were receiving immunosuppressive treatment for GVHD at the time of diagnosis. Initial treatment in all patients consisted of steroids. Three of the seven had a partial response while the four remaining patients failed to respond to corticosteroids. Splenectomy was performed in three patients with two partial responses. Four patients were treated with additional therapeutic interventions, including plasmapheresis, immunoglobulin infusions, staphylococcus protein A column, or other immunosuppressive agents. In five cases, erythropoietin was administered as adjunctive treatment to maintain adequate hematocrit levels. Two patients are presently in complete remission after prolonged courses of steroids, while a third patient has compensated hemolysis requiring low-dose steroids. Four patients died due to either infectious complications or disseminated intravascular coagulation secondary to cold agglutinin disease. These data indicate that AIHA is a clinically significant and not infrequent complication in allogeneic marrow transplant recipients. The response to conventional treatment is generally unsatisfactory as even patients who ultimately remit require prolonged courses of immunosuppressive therapy.
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PMID:Autoimmune hemolytic anemia following T cell-depleted allogeneic bone marrow transplantation. 880 20

Autoimmune hemolytic anemia is rare in children. It is generally diagnosed in relation to a viral or bacterial infection but has also been described in association with drugs, autoimmune disease, malignancy, and immunodeficiency. The authors describe a 5-month-old infant who presented with severe autoimmune hemolytic anemia and disseminated intravascular coagulation as his initial manifestation of HIV infection.
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PMID:HIV infection presenting as severe autoimmune hemolytic anemia with disseminated intravascular coagulation in an infant. 1470 3

Disseminated intravascular coagulation (DIC) due to red cell hemolysis has been previously attributed to transfusion-related hemolytic reactions, but not to autoimmune hemolytic anemia. We report a case of DIC in a child with complement-fixing IgM-mediated cold-agglutinin autoimmune hemolysis, which resulted in arterial thrombosis and gangrene of the upper and lower extremities.
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PMID:Disseminated intravascular coagulation due to IgM-mediated autoimmune hemolytic anemia. 2167 68

Splenic infarction is most commonly caused by cardiovascular thromboembolism; however, splenic infarction can also occur in hematologic diseases, including sickle cell disease, hereditary spherocytosis, chronic myeloproliferative disease, leukemia, and lymphoma. Although 10% of splenic infarction is caused by hematologic diseases, it seldom accompanies autoimmune hemolytic anemia (AIHA). We report a case of a 47-year-old woman with iron deficiency anemia who presented with pain in the left upper abdominal quadrant, and was diagnosed with AIHA and splenic infarction. Protein C activity and antigen decreased to 44.0% (60-140%) and 42.0% (65-140%), respectively. Laboratory testing confirmed no clinical cause for protein C deficiency, such as disseminated intravascular coagulation, sepsis, hepatic dysfunction, or acute respiratory distress syndrome. Protein C deficiency with splenic infarction has been reported in patients with viral infection, hereditary spherocytosis, and leukemia. This is a rare case of splenic infarction and transient protein C deficiency in a patient with AIHA.
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PMID:Splenic infarction in a patient with autoimmune hemolytic anemia and protein C deficiency. 2225 34

Oxaliplatin in combination with a fluoropyrimide is a treatment option for colorectal cancer patients in the adjuvant and metastatic settings. Very few hematological emergencies have been reported associated with Oxaliplatin. These include autoimmune hemolytic anemia, thrombocytopenia and pancytopenia. We present a case report of a patient who developed hematuria and disseminated intravascular coagulation while receiving the second cycle of FOLFOX and bevacizumab for metastatic colon cancer.
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PMID:Oxaliplatin induced disseminated intravascular coagulation: A case report and review of literature. 2284 49

Evan syndrome (ES) is a rare hematological disorder that involves 2 or more immune cytopenias. It usually includes autoimmune hemolytic anemia and autoimmune thrombocytopenia. Although occasionally associated with immune neutropenia, its association with disseminated intravascular coagulation (DIC) is rare. And, early diagnosis with appropriate intervention is important because mortality from ES is known to be greater than that of isolated immune hemolytic anemia and probably worse in the presence of DIC. Considering that the presence of DIC can make the diagnosis of ES challenging, a strong clinical suspicion is important as early initiation of therapy is critical to reducing the morbidity and mortality associated with this syndrome. We report a case of ES complicated by DIC.
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PMID:Primary Evan Syndrome With Disseminated Intravascular Coagulation Suggests Progressive Immune Dysregulation and Early Immunosuppressive Intervention is Key to Improving Outcomes. 2541 43

Infectious complications are a major cause of morbidity and mortality in patients with chronic lymphocytic leukemia (CLL) due to impaired immunity secondary to the disease itself and to the immunosuppressive therapies administered to these patients. We report a 78-year-old woman with CLL who was treated with steroids for autoimmune hemolytic anemia (AIHA). A few weeks later, she was admitted for severe acute hepatitis with disseminated intravascular coagulation (DIC). Despite the symptomatic treatment of DIC, standard reanimation and probabilistic antibiotics, the patient died within 24h with severe hepatic failure. Autopsy was in favor of a disseminated viral infection with esophageal, hepatic and pulmonary cytopathologic lesions with acidophilic intranuclear inclusions suggestive of herpes virus, even though HSV 1 and 2, CMV and HHV6 PCRs were negative. This case of severe viral hepatitis with esophagitis occurring three weeks after the introduction of high-dose steroid treatment for AIHA in a CLL patient calls for anti-herpetic prophylaxis in such patients, immunodepressed by their diseases and the treatment they receive.
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PMID:Severe viral hepatitis in a patient with chronic lymphocytic leukemia (CLL) complicated with autoimmune hemolytic anemia (AIHA), treated with steroids. 2554 74

An 80-year-old man with autoimmune hemolytic anemia (AIHA) received immunosuppressive therapy with prednisolone (1 mg/kg). One month later, his hemoglobin level had normalized, and the prednisolone dose was tapered. The next day, he complained of acute and progressive back pain. He was admitted to our hospital for further examination approximately 24 h after the pain had started. Computed tomography revealed only localized pneumonia. However, he showed signs of severe disseminated intravascular coagulation (DIC), liver dysfunction, and respiratory failure. Empiric broad-spectrum antibacterial therapy was started with a presumptive diagnosis of severe bacterial infection. However, his condition rapidly deteriorated, and he died 17 h after admission. Varicella-zoster virus (VZV) was detected by quantitative PCR in the peripheral blood sample and by immunohistochemistry in all organs except for the brain at autopsy. Visceral VZV infection is a severe disease with a high mortality rate. Although appropriate diagnosis and treatment is crucial, in cases without the characteristic skin rash the diagnosis is difficult. The possibility of visceral VZV infection should be taken into consideration when administering prednisolone to patients with AIHA.
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PMID:[Fulminant visceral disseminated varicella-zoster virus infection without skin involvement in a patient with autoimmune hemolytic anemia on prednisolone therapy]. 2716 52

Intravascular hemolysis is relatively rare but can lead to acute kidney injury (AKI), from increased destruction of erythrocytes and release of free hemoglobin. Since hemolysis and hemoglobinuria are known causes of acute kidney injury we sought to define clinicopathologic findings and outcomes of patients with hemolysis-associated hemoglobin cast nephropathy through a retrospective analysis of 27 cases. The mean patient age was 47 years (range 19-79) and the female-to-male ratio was 1.3:1. All patients presented with AKI with a mean serum creatinine of 8.0 (range 2.9-17.0) mg/dL. Etiologies included autoimmune hemolytic anemia (30%), medication (26%), paroxysmal nocturnal hemoglobinuria (7%), procedural/mechanical causes (7%), transfusion of incompatible blood (4%), toxin ingestion (4%), disseminated intravascular coagulation (4%), and hemoglobinopathy (4%). All biopsies showed acute tubular injury and pigmented, proteinaceous casts characterized by positive hemoglobin immunohistochemistry. After a mean follow-up of nine months (range 0.5-26), the mean serum creatinine was 1.3 (range 0.6-3.3) mg/dL, with 78% of patients returning to normal kidney function. Thus, based on our clinicopathologic case series, hemolysis-associated hemoglobin cast nephropathy is an important entity for clinicians and pathologists to recognize as treatment hinges upon elimination of the pathogenic driver of intravascular hemolysis.
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PMID:Hemolysis-associated hemoglobin cast nephropathy results from a range of clinicopathologic disorders. 3166 30


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