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Anemia: Approach to Diagnosis
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Normocytic anemia not resulting from acute blood loss is divided into one of two categories that can be separated by the reticulocyte index. The reticulocyte index rises as the result of either acute blood loss or destruction of red cells. The clinical presentation, history, and physical examination will often suggest a source of blood loss. In the absence of a clear diagnosis, then, the clinician must obtain a reticulocyte index, review serial hemoglobin and hematocrit values, and follow the patient clinically until hemorrhage is excluded.
Haematology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Findings in haemolysis:1 ↑ reticulocyte index.2 ↑ unconjugated bilirubin.3 ↑ LDH.4 ↓ or absent serum haptoglobin.5 Haemosiderinuria (in cases of moderate haemolysis).96 Haemoglobinuria (in cases of severe haemolysis).
Hemophagocytic lymphohistiocytosis associated with parvovirus B19-induced aplastic crisis in a hereditary spherocytosis patient: A case report and literature review
Published in Pediatric Hematology and Oncology, 2022
Ki Tae Kim, Kyung Taek Hong, Bo Kyung Kim, Hong Yul An, Jung Yoon Choi, Yoon Hwan Chang, Hyoung Jin Kang
A 7-year-old girl, who was previously healthy, presented with fever, vomiting, and dyspnea for three days and visited the emergency room. Her initial body temperature was 38.5 °C. Her initial systolic blood pressure was 66 mmHg; therefore, inotropes were administered. Oxygen therapy was initiated because her peripheral oxygen saturation (SpO2) decreased. Splenomegaly was observed on physical examination. Her laboratory test findings indicated severe anemia (3.9 g/dL), thrombocytopenia (41,000 cells/µL), mild leukopenia (2,840 cells/µL), mild neutropenia (1,392 cells/µL), mild elevation of aspartate aminotransferase levels (78 IU/L), and hyperbilirubinemia (2.3 mg/dL). The reticulocyte count was 1.72%, and the reticulocyte index was 0.33, which suggested hypoproliferation of red blood cells. Serum ferritin levels had markedly increased (18,525 ng/mL), while the triglyceride and fibrinogen levels were in the normal range (97 mg/dL and 216 mg/dL, respectively). Her soluble interleukin-2 receptor levels had also increased (2,483 U/mL). However, natural killer cell activity could not be assessed because the testing facility is not available at our institution. Pleural effusion was observed on chest radiography. Abdominal ultrasonography revealed hepatosplenomegaly (spleen size, 12.7 cm). A bone marrow examination was performed under the suspicion of HLH, and hemophagocytes were observed in the bone marrow aspirate (Figure 1A). Because the patient fulfilled 5 out of the 8 diagnostic criteria for HLH diagnosis (fever, splenomegaly, cytopenia, hemophagocytosis, elevated ferritin levels), chemoimmunotherapy using the HLH-2004 protocol (with a regimen including etoposide, dexamethasone, and cyclosporine A)12 was started based on the treatment experience in our institution to reduce early mortality. Moreover, spherocytes were observed in the peripheral blood smear (Figure 1B). The parvovirus B19 viral load was elevated (849,467,820 copies/mL), while a negative result was obtained for the presence of CMV antibodies (immunoglobulin G and M) and the EBV viral load was not detected. Bone marrow examination revealed a decrease in erythropoiesis and the formation of giant pronormoblasts (Figure 1C, D), while the cellularity was 81–90%. Therefore, coexistence of HS with aplastic crisis due to parvoviral infection was suspected.
Molecular genetic testing enabled the diagnosis of otherwise undiagnosable cases of pyruvate kinase deficiency
Published in Pediatric Hematology and Oncology, 2022
Physical examination of the patient upon admission to our center confirmed pallor and scleral icterus; however, no hepatomegaly or splenomegaly was observed. Complete blood testing revealed a Hb level of 7.8 g/dL, close to the value reported by the previous hospital, a red blood cell (RBC) count of 2.9 × 109/L, a mean corpuscular volume of 81.7 fL, a mean corpuscular hemoglobin level of 26.9 pg, a mean corpuscular hemoglobin concentration of 32.9 g/dL, and a red cell distribution width of 19.6%. Peripheral blood smear examination revealed marked anisocytosis, polychromasia, poikilocytosis, and basophilic stippling, as well as the presence of rare elliptocytes, ovalocytes, and spherocytes. The reticulocyte count was 11.2% (328 × 106/L) with a corrected reticulocyte index of 5.89%. Mild hyperbilirubinemia was detected, with a total bilirubin content of 3.5 mg/dL, direct bilirubin content of 0.8 mg/dL, and high levels of lactate dehydrogenase (700 U/L). The level of haptoglobin was below 10 mg/dL. Both direct and indirect Coombs’ tests were negative. As her laboratory test results indicated nonimmune hemolytic anemia, an osmotic fragility test was performed, which was found to be negative. In addition, Hb electrophoresis revealed 89.8% HbA, 1.4% HbA2, and 8.8% HbF. Her laboratory test results suggested that she suffered from a type of congenital hemolytic anemia; however, the likelihood of hereditary spherocytosis seemed low. Thereafter, multiplex enzyme assay for six major erythrocyte metabolic enzymes based on ion paring ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS)1 were performed, which showed average activity values compared with those of control; the activity of glucose-6-phosphate dehydrogenase was 1.97 mg/min/gHb (2.16 mg/min/gHg in control, reference value, 1.06–3.31 mg/min/gHg), pyruvate kinase was 1.83 mg/min/gHg (1.75 mg/min/gHg in control, reference value, 1.02–2.46 mg/min/gHg), pyrimidine 5′-nucleotidase was 63.5 μg/min/gHg (38.3 ug/min/gHg in control, reference value, 10.4–56.4 μg/min/gHg), hexose kinase was 97.02 μg/min/gHg (35.0 μg/min/gHg in control, reference value, 123–488 μg/min/gHg), triosephosphate isomerase was 11.2 mg/min/gHg (7.9 mg/min/gHg in control, reference value was not reported), and adenosine deaminase was 510.6 μg/min/gHb (188.7 μg/min/gHg in control, reference value, 76.9–249.7 μg/min/gHg).
Acquired Hemophilia A and urothelial carcinoma
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Fadi Taza, Nawar Suleman, Robert Paz, Christopher Haas
Five months later, the patient was admitted to our hospital non-traumatic ecchymosis. He reported usual health until approximately one week prior to presentation at which time he noted the spontaneous development of multiple discrete areas of bruising localized to his hands and upper extremities that appeared in a successive fashion over the course of the week and demonstrated various stages of ecchymosis-related changes. He noted no new exposures, trauma, nor medications, and denied a history of prior bruising. He denied bleeding from his gums, bright red blood per rectum, and melena. Physical examination demonstrated a hemodynamically stable elderly Caucasian male in no acute distress with multiple discrete areas of bruising along the abdomen, entire left forearm with varying degrees of healing as well as the left hand and a lesion along the right elbow. Laboratory diagnostics demonstrated a microcytic anemia (hemoglobin 6.3 g/dL (RV 12.5–16.5 g/dL)), MCV 76 (RV 81–100)), elevated RDW (21.2 (RV 11.5–15.5)), reticulocyte hypoproliferation (reticulocyte index 0.89), and a hematocrit of 22.1%, for which he was transfused a single unit of packed red blood cells. His platelet count remained preserved (245 k/uL) and peripheral smear demonstrated an absence of schistocytes. The metabolic panel was unremarkable except for an elevated total bilirubin of 2.2 mg/dl (RV 0.2–1.3) and direct bilirubin of 0.61 mg/dl (RV 0–0.30), likely reflecting hematoma resorption. Coagulation studies revealed a mildly prolonged PT of 17.4 s, a markedly prolonged aPTT of 117s, INR of 1.4 and a preserved fibrinogen level of 416 mg/dL (RV 213–536 mg/dL). Mixing studies revealed an elevated PTT (89.4s) with failure to correct to the normal range upon 1:1 mixing of patient to normal pooled plasma (PTT 65s), suggesting the presence of an inhibitor. To determine whether the etiology was secondary to an autoimmune or viral etiology an extensive diagnostic workup was sent and resulted negative (Table 1). The coronavirus-19 Polymerase chain reaction was negative. Given the patients clinical presentation and abnormal mixing studies, the presence of a coagulation factor inhibitor was suspected. While Factor V, IX, and vWF levels were 60% (RV 70–140), 76% (RV 60–150), and 484% (RV 50–130) respectively, Factor VIII levels were found to be 1% (RV 55–175%). The Bethesda assay confirmed the diagnosis, demonstrating the presence of a Factor VIII inhibitor at 57 Bethesda Units (BU)/mL (RV < 0.5 BU). The patient was diagnosed with Acquired Hemophilia A.