Cases reported "Hemoglobinuria"

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1/57. Phenotypic variability of Filipino beta(o)-thalassemia/HbE patients in indonesia.

    Three Indonesian patients with identical genotypes, each compound heterozygotes for Filipino beta(o)-thalassemia/HbE, expressed different clinical severities. One patient has mild disease and is transfusion independent, while the other two are severely affected and transfusion dependent. The size of the Filipino beta(o)-globin gene deletion was confirmed to be 45 kb, resolving conflicting values given in the literature. Neither ameliorating genetic factors such as alpha-globin gene deletions or the XmnI restriction site polymorphism at position -158 upstream of the (G)gamma-globin gene, nor differences in beta-globin gene haplotype, explain the phenotypic variation. These observations have implications for the development of antenatal diagnosis in indonesia, as at present it is not possible to give an accurate prediction of severity of phenotype for this common genotype. ( info)

2/57. Hb Sallanches [alpha104(G11)Cys-->Tyr]: a rare alpha2-globin chain variant found in the homozygous state in three members of a Pakistani family.

    We have identified a rare alpha2-globin chain variant, Hb Sallanches [alpha104(G11) Cys-->Tyr], in a Pakistani family having three homozygous patients with transfusion-dependent Hb H disease. This variant, previously reported in a French patient and a West Indian homozygous patient with Hb H disease, is due to a mutation at codon 104 (TGC-->TAC). This is the third case of Hb Sallanches and the first case with three homozygous patients reported in pakistan. Due to the different ethnic origins of the patients, it is very likely an independent mutation. ( info)

3/57. Acute onset hemoglobinemia and/or hemoglobinuria and sequelae following Rh(o)(D) immune globulin intravenous administration in immune thrombocytopenic purpura patients.

    Rh(o)(D) immune globulin intravenous (anti-D IGIV) was licensed by the united states food and drug administration (FDA) in March 1995 to treat patients with immune thrombocytopenic purpura (ITP). Anti-D IGIV induces extravascular hemolysis, an expected adverse reaction that is consistent with the presumed mechanism of action. Between licensure and April 1999, the FDA received 15 reports of hemoglobinemia and/or hemoglobinuria following anti-D IGIV administration that met the case definition for this review. The mechanism responsible for hemoglobinemia and/or hemoglobinuria is unexplained. review of these reports was prompted by the seriousness and the unexpectedness of treatment-associated sequelae experienced by 11 patients. Of these patients, 7 developed sufficient onset or exacerbation of anemia that orders were written for packed red blood cell transfusions, although only 6 patients were transfused. Eight patients experienced the onset or exacerbation of renal insufficiency, and 2 patients underwent dialysis. One patient died due to complications of exacerbated anemia. Six patients experienced 2 to 3 sequelae. Absent validated incidence data, a 1.5% estimated incidence rate from published clinical trial data and a 0.1% estimated reporting rate from FDA and drug utilization data were calculated for reported cases of hemoglobinemia and/or hemoglobinuria. This review presents the first case series of anti-D-IGIV-associated hemoglobinemia and/or hemoglobinuria and provides pretreatment and posttreatment clinical and laboratory findings of the case series patients. The primary purpose of this review is to increase awareness of this potentially serious occurrence among physicians and health care professionals who manage ITP patients treated with anti-D IGIV, thereby enabling prompt recognition and treatment of sequelae. (blood. 2000;95:2523-2529) ( info)

4/57. Renal infarction: an uncommon mimic presenting with flank pain.

    A 39-year-old woman arrived to the emergency department complaining of a constant, progressive, left flank pain, with no beneficial effect from spasmolytic and nonsteroidal antiinflammatory drugs. Two years before, she suffered another episode of right flank pain and stranguria, but instrumental examinations (ultrasonography, urography) remained negative. Besides a mild tenderness in the left flank, physical examination was normal. blood chemistry panel showed leukocytosis (17.2 x 10(3) mL, neutrophils 82.8%) and a slight increase of serum lactate dehydrogenase (LDH) (543 U/L versus 230 to 460 U/L). Urinanalysis showed a slight hemoglobinuria (0.5 mg/dL), and sediment contained some red cells and leukocytes. Diagnostic examinations (ultrasonography, computed tomography) showed a left renal nonhomogeneous space-occupying lesion, orientative for renal malignancy. She was transferred to the urology department and operated. Both intraoperatory and histological diagnosis was ischemic infarction and, after exclusion of all possible underlying causes, final diagnosis was idiopathic renal infarction. Diagnostic procedures and literature reports are discussed. ( info)

5/57. Differential diagnosis of Hb EE and Hb E-beta(0)-thalassemia by protein and dna analyses.

    dna analysis was used to confirm the Hb EE genotype and to differentiate from the possible genotype of Hb E-beta(0)-thalassemia in two Malay patients. The first patient was a 13-year-old Malay girl, whose parents were available for family studies. The second patient was a 69-year-old Malay woman with no living family members. The presence of Hb E in both propositi was confirmed by: (1) its characteristic electrophoretic mobilities on alkaline/acid gels; (2) its chromatographic properties on anion/cation exchangers, and (3) its mildly insoluble properties. However, differential diagnosis of Hb EE and Hb E-beta(0)-thalassemia was challenging in these two cases. In the former, this was because of the possible interactions of the parents' phenotypes; i.e., the mother had a similar phenotype. In the latter, it was due to the lack of any living family members for family studies. In this communication, we present the protein and dna analyses, including data on the use of the restriction enzyme Mnl I, for the definitive diagnosis of the Hb EE genotype in the propositi of these two Malay families. ( info)

6/57. Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid.

    mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induction of tubulointerstitial damage. Excess iodine ingestion is known to produce toxicity and possible death, but acute renal failure is rare. There is evidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. iodine has not been documented to produce red cell hemolysis and hemoglobinuria. We present a unique case of acute renal failure from hemoglobinuric and acute interstitial nephritis secondary to suicidal ingestion of potassium iodide solution and also ingestion of a few mefenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfunction from alteration of renal perfusion by selective COX-1 inhibition of prostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hemodialysis and supportive therapy. ( info)

7/57. Conservative treatment of hemolytic complication following coil embolization in two adult cases of patent ductus arteriosus.

    Two adult cases of relatively large patent ductus arteriosus (PDA) were treated by coil embolization, but were complicated by hemolysis that was successfully managed by medical treatment. Case 1 was a 67-year-old woman and Case 2 was a 71-year-old woman with a PDA of minimal diameter of 5.3 mm and 5.5 mm, respectively. The approach was via the pulmonary artery and 2 coils were delivered simultaneously into the ductus, known as the 'kissing coil technique'. Although immediately after the procedure only a small residual shunt was revealed by aortogram, hemolysis occurred for several hours after the procedure in both cases. A hemolytic complication usually needs additional coil embolization or surgical treatment, but in these 2 cases it was successfully treated by haptoglobin infusion to prevent nephropathy and by antiplasmin infusion to promote thrombus formation. Hemolytic complications of coil embolization of PDA can managed by medication when the residual shunt is minimal and the degree of hemolysis is mild. ( info)

8/57. Exertional hemoglobinuria.

    A 16 years old boy had a typical exertional hemoglobinuria after walking with his new leather shoes on. The attacks of hemoglobinuria were associated with the appearance of an unstable hemoglobin in red cells. A slightly decreased fragility curve by 24 hr incubated red cells, the increase of autohemolysis and the appearance of heat labile hemoglobin were observed after exertion. These findings support that exertional hemoglobinuria may be regarded as a transitory erythropathia. ( info)

9/57. Case report. An immediate hemolytic transfusion reaction apparently caused by anti-Dia.

    The Diego blood group system has had its primary applications in population genetics and anthropology, although it can also give rise to clinical problems. Anti-Dia has ofter been reported to cause hemolytic disease of the newborn. The patient presented in the report experienced an immediate hemolytic transfusion reaction apparently due to anti-Dia. We believe it to be the only such case reported since the Diego system was first discovered in 1956. ( info)

10/57. hemoglobinuria with ribavirin treatment.

    Chronic hepatitis c virus is a major worldwide cause of hepatitis, cirrhosis, end-stage liver disease, and hepatocellular carcinomas. Combination therapy of ribavirin with short- or long-acting interferon-alpha is now the standard treatment of chronic hepatitis c. This therapy is associated with a wide range of side effects. Although hemolysis is almost an invariable result of ribavirin, black urine due to hemoglobinuria has never been previously reported. We recently encountered two cases of black urine (hemoglobinuria) in patients treated with combination therapy. Based on reports of dark urine in many of our patients, we suggest that this phenomenon may be more common than is currently appreciated. It indicates a marked degree of hemolysis, which prompts immediate measurement of hemoglobin level. ( info)
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