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Radiation Syndromes and Their Modifications
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
Table 8.5 summarizes the laboratory findings in persons exposed to a bone marrow syndrome dose: initial granulocytosis within the first 2–4 days after exposure, followed by leukopenia during the fourth and fifth weeks. Recovery of leukocytes was observed at day 36. The lymphocyte changes were less variable. Within 3–4 days, the lymphocytes reached their minimum and remained at this level for at least 5 weeks. The lymphocyte count remained about 800–900/mm3 during this period. However, the number increased slightly thereafter, but did not return to normal values for weeks and months. The severe decline in platelets was not seen until about 28 days after exposure. After 24 days, the number of platelets dropped below 50,000/mm3. Recovery started at day 32, and the values returned to a normal level after about 7 weeks of exposure. A transient mild anemia associated with reticulocytosis was found in most cases. A “late critical phase,”which generally occurs during the fourth and fifth weeks, is characterized by a severe granulocytopenia and thrombocytopenia. The “late critical phase”is initiated by nausea, vomiting, fever, and diarrhea. About 50% of the Hiroshima and Nagasaki population exposed to bone marrow syndrome doses died during this “late critical phase.”The survival of the exposed individual depends upon recovery of the bone marrow.
Transient Erythroblastopenia of Childhood
Published in Stephen A. Feig, Melvin H. Freedman, Clinical Disorders and Experimental Models of Erythropoietic Failure, 2019
The absolute reticulocyte count (normal 50 to 150,000/|μl) is almost always low, although the percent reticulocytes may be elevated if the patient is seen at the beginning of recovery. In our patients we have observed that the reticulocyte count has a bimodal distribution. The majority (42 of 56 cases) had less than 1% reticulocytes and in many patients no reticulocytes were seen. A small fraction (14 of 56 cases) had a mean reticulocytosis of 7%, ranging from 1.6 to 15.8%. The presence of significant reticulocytosis can confuse the diagnosis with other disorders, such as the recovery from bleeding.32
Hemolytic Anemias: General Considerations
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
4. Reticulocytosis. There are several ways to utilize the reticulocyte count (typically expressed as the percentage of red cells which are reticulocytes) to evaluate red cell production by the marrow. The reticulocyte count may be expressed as an uncorrected percentage, or as the absolute reticulocyte count (percent reticulocytes multiplied by the red cell count per cubic millimeter), or as the corrected reticulocyte count (percent reticulocytes multiplied by patient’s hematocrit/45), or as the reticulocyte production index (corrected reticulocyte count multiplied by a factor which reflects the increased shift of less mature cells to the peripheral blood) (8). All of these modifications are efforts to remind the clinician that a reticulocyte count of 1%, which is perfectly adequate to maintain a hematocrit of 45%, is too low if the patient’s hematocrit is 25% (see Table 4 for normal values of reticulocyte evaluations). An elevated reticulocyte count is considered a hallmark of hemolytic anemia. However, as many as 37% of patients with autoimmune hemolytic anemia can present with reticulocytopenia (as defined by a reticulocyte production index <2%), and it is important to remember that absence of reticulocytosis does not rule out a hemolytic anemia (9, 10). Individuals with mild chronic hemolysis (particularly patients with hemoglobinopathies or thalassemia) often have a relatively normal hemoglobin concentration and hematocrit but have an elevated reticulocyte count: The shortened red cell survival requires extra marrow production in order to maintain a near-normal hematocrit/hemoglobin. The phenomenon of transient aplastic crises in chronic hemolysis due to B19 parvovirus infection will be discussed elsewhere.
Nutritional deficiency presenting as acute pain, fatigue and bruising in a college health clinic
Published in Journal of American College Health, 2022
Adam Pallant, Tanya Sullivan, Andrew Kaluzny
A review of the patient’s exam with a dedicated eye toward vitamin deficiency now enables fine focus. The petechiae all surround hair follicles of the lower legs with several corkscrew hairs present. The hemorrhage is exclusively in the lower extremities and fails to show any signs of healing over time. His gums bleed easily, although this is reported as longstanding. A serum vitamin C level is drawn and the patient is immediately prescribed 1 gram of vitamin C orally twice daily. The day after starting vitamin C, the patient’s hemoglobin drops to 8.6, the platelet count remains normal, total bilirubin increases to 3.3 mg/dl (direct bilirubin of 0.4 mg/dl) with an increased LDH of 258 IU/L. Clinically worse, the patient is hospitalized. By day three after hospitalization his hemoglobin dropped to a low of 8.4 g/dl yet there was concomitant evidence of robust reticulocytosis within three days of beginning vitamin C supplementation. Ongoing evidence of hemolysis lasts two weeks after initiation of vitamin supplementation. Lymphopenia persists beyond one month of vitamin C supplementation with the lowest measured ALC of 0.7 × 109/l. He does not receive transfusion and is not placed onto prophylaxis for opportunistic infection. His symptoms of malaise begin to resolve within 24 hours of vitamin C supplementation. Joint pains disappear by one week of treatment, and skin hemorrhage clears by three weeks of daily supplementation of vitamin C at 1 gram per day.
Mild erythrocytosis as a presenting manifestation of PIEZO1 associated erythrocyte volume disorders
Published in Pediatric Hematology and Oncology, 2019
Tristan Knight, Ahmar Urooj Zaidi, Shengnan Wu, Manisha Gadgeel, Steven Buck, Yaddanapudi Ravindranath
Case 1: Patient 1 was evaluated at age 17 years for mild polycythemia and reticulocytosis. Medical history included anxiety, depression, and attention-deficit hyperactivity disorder (ADHD), and medications included sertraline, methylphenidate, and minocycline. Family history was significant for heart failure of unknown etiology in the father and paternal grandfather. Peripheral blood smear showed both spherocytes and stomatocytes (Figure 1D), Osmoscan was consistent with mild spherocytosis and EMA MCF was reduced, suggesting reduced band 3 content (Figure 1E). Laboratory values are listed in Table 1. No abnormal hemoglobins were noted on hemoglobin evaluation; Hb p50 was 25.6 mmHg (reference range (RR) 24–28 mmHg). Serum erythropoietin was 18.7 mIU/mL (RR 4.3–29.0), giving a normalized value of +58.35.
Severe acute kidney injury owing to rhabdomyolysis and intravascular haemolysis in an 11-year-old child with G6PD deficiency
Published in Paediatrics and International Child Health, 2019
Milan Talwar, Sriram Krishnamurthy, Narayanan Parameswaran, C. G. Delhikumar, Satish Haridasan, Bheemanathi Hanuman Srinivas
Haemoglobin was 3.3 g/dL, total leucocyte count 3.3 × 109/L and platelet count 260 × 109/L. Red blood cells were normocytic and normochromic with moderate anisopoikilocytosis. Blood film demonstrated many fragmented red blood cells and reticulocytosis (corrected reticulocyte count 5%). Blood urea was 68.2 mmol/L (2.9–8.2), serum creatinine 610 μmol/L (53–106), sodium 136 mmol/L and potassium 4.1 mmol/L. Urinalysis showed no RBCs but tested positive for blood by multistix on several occasions. Lactate dehydrogenase was 114.7 μkat/L (1.7–3.4) and creatinine kinase total (CPK) 136 μkat/L (0.67–2.5). The investigations were consistent with severe intravascular haemolysis in association with rhabdomyolysis, resulting in haemoglobinuria and myoglobinuria. Rhabdomyolysis was diagnosed on the basis of high levels of LDH, elevated blood CPK and the presence of myoglobin casts in the renal tubules demonstrated in the renal biopsy on immunohistochemistry.