Severe Metabolic Complications in a Cross-Country Runner With Sickle Cell Trait

Helzlsouer, Kathy J.

doi:10.1001/jama.1983.03330300061037

Cited by 40 publications

(10 citation statements)

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“…These haematological changes corresponded with gradual increases in plasma haemoglobin due to increased red cell breakdown as well as gradual elevation of potassium ions and lactate dehydrogenase during storage. These observations could be as a result of haemoglobin S erythrocytes fragility subsequent to polymerization of haemoglobin S and reduced deformability and loss of red cell elasticity during storage due to low oxygen tension and low pH storage medium [38–40] on the one hand, as well as metabolically active intra-erythrocytic Plasmodium parasites could account for these haematological changes. Malaria parasites have been found to be viable in stored blood for at least the first 14 days [41].…”

Section: Discussionmentioning

confidence: 99%

Storage related haematological and biochemical changes in Plasmodium falciparum infected and sickle cell trait donor blood

et al. 2018

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BackgroundIn sub-Saharan Africa where sickle cell trait (SCT) and malaria is prevalent, significant proportions of blood donors may be affected by one or more of these abnormalities. The haemato-biochemical properties of SCT and asymptomatic malaria in donor blood have not been evaluated. This study evaluated the haemato-biochemical impact of SCT and asymptomatic malaria infections in citrate-phosphate-dextrose-adenine (CPDA-1) stored donor blood units.MethodsFifty-milliliters of sterile CPDA-1 anti-coagulated blood were drained into the sample pouch attached to the main blood bag. Ten units each of sickle cell/malaria negative, sickle cell and malaria positive blood were analyzed. Baseline and weekly haematological profiling and week 1, 3 and 5 concentrations of plasma haemoglobin, % haemolysis, sodium, potassium and chloride and lactate dehydrogenase (LDH) were assayed. Differences between baseline and weekly data were determined using one-way analysis of variance (ANOVA) and Kruskal-Wallis test, whereas differences between baseline parameters and week 1–3 data pairs were determined using paired t-test. P-value < 0.05 was considered statistically significant.ResultsStorage of SCT and malaria infected blood affected all haematological cell lines. In the SCT donors, red blood cells (RBC) (4.75 × 1012/L ± 1.43baseline to 3.49 × 1012/L ± 1.09week-5), haemoglobin (14.45 g/dl ± 1.63baseline to 11.43 g/dl ± 1.69week-5) and haematocrit (39.96% ± 3.18baseline to 33.22% ± 4.12week-5) were reduced. In the asymptomatic malaria group, reductions were observed in RBC (5.00 × 1012/L ± 0.75baseline to 3.72 × 1012/L ± 0.71week-5), haemoglobin (14.73 g/dl ± 1.67baseline to 11.53 g/dl ± 1.62week-5), haematocrit (42.72% ± 5.16baseline to 33.38% ± 5.80week-5), mean cell haemoglobin concentration (35.48 g/dl ± 1.84baseline to 35.01 g/dl ± 0.64week-5) and red cell distribution width coefficient of variation (14.81% ± 1.54baseline to 16.26% ± 1.37week-5). Biochemically, whereas plasma LDH levels significantly increased in asymptomatic malaria blood donors (319% increase at week 5 compared to baseline), SCT blood donors had the most significant increase in plasma potassium levels at week 5 (382% increase). Sodium ions significantly reduced in SCT/malaria negative and sickle cell trait blood at an average rate of 0.21 mmol/L per day. Moreover, elevations in lymphocytes-to-eosinophils and lymphocytes-to-neutrophils ratios were associated with SCT and malaria positive blood whilst elevation lymphocytes-to-basophils ratio was exclusive to malaria positive blood.ConclusionSevere storage lesions were significant in SCT or malaria positive donor blood units. Proper clinical evaluation must be done in prospective blood donors to ensure deferral of such donors.Electronic supplementary materialThe online version of this article (10.1186/s12878-018-0128-x) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Storage related haematological and biochemical changes in Plasmodium falciparum infected and sickle cell trait donor blood

et al. 2018

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“…However, greater RBC lactate transport activity in AS should also lead to greater lactate and H ϩ accumulation in RBCs, resulting in severe intra-erythrocytic lactic acidosis (14). As suggested by Smith et al (30), a greater lactate influx into the RBCs of AS than of AA could be involved in the reported cases of sudden death in SCT carriers after strenuous exercise (8).…”

Section: Discussionmentioning

confidence: 99%

Faster lactate transport across red blood cell membrane in sickle cell trait carriers

Farhang¹,

Connes²,

Hue³

et al. 2006

Journal of Applied Physiology

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“…Previous population studies on this subject have shown no evidence of increased mortality in sickle-cell trait [Petrakis et al, 1970;Heller et al, 1979;Janerich et al, 19731. Nevertheless reports of morbidity and mortality in Hb AS carriers continue to appear in the current literature [Sateriale and Hart, 1985;Helzlsouer et al, 1983;Lane and Githens, 1985;Nussbaum and Rice, 1984;Pastorek and Seiler, 1985;Magnuson et al, 19801. Therefore, in an attempt to estimate the longevity of persons with sickle-cell trait we analyzed its prevalence at various ages in a large nonhospitalized population.…”

Section: Introductionmentioning

confidence: 99%

“…In nonmalarious areas such as in the United States, questions have arisen as to whether significant morbidity is associated with the carrier state for the sickle-cell gene [Sears, 1978;Diggs, 1984;Knasel 19821. The variety and severity of medical problems attributed to Hb AS are such that one wonders whether people with this genetic trait might have a shorter lifespan than those without it [Sateriale and Hart, 1985;Helzlsouer et al, 1983;Lane and Githens, 1985;Nussbaum and Rice, 1984;Pastorek and Seiler, 1985;Magnuson et al, 19801. Previous population studies on this subject have shown no evidence of increased mortality in sickle-cell trait [Petrakis et al, 1970;Heller et al, 1979;Janerich et al, 19731.…”

Section: Introductionmentioning

confidence: 99%

“…Sickle-cell trait (Hb AS) is one of the most common genetic traits in American blacks with prevalence figures ranging from 5.8 to 10.2% [Winter, 19861. In spite of the serious manifestations in homozygous individuals the sickle-cell gene pool has increased in Africa and other geographic areas because of the protection provided against falciparum malaria (balanced polymorphism) [Livingston, 197 1 ;Luzzatto, 1979;Colombo and Felicetti, 19851. In nonmalarious areas such as in the United States, questions have arisen as to whether significant morbidity is associated with the carrier state for the sickle-cell gene [Sears, 1978;Diggs, 1984;Knasel 19821. The variety and severity of medical problems attributed to Hb AS are such that one wonders whether people with this genetic trait might have a shorter lifespan than those without it [Sateriale and Hart, 1985;Helzlsouer et al, 1983;Lane and Githens, 1985;Nussbaum and Rice, 1984;Pastorek and Seiler, 1985;Magnuson et al, 19801. Previous population studies on this subject have shown no evidence of increased mortality in sickle-cell trait [Petrakis et al, 1970;Heller et al, 1979;Janerich et al, 19731. Nevertheless reports of morbidity and mortality in Hb AS carriers continue to appear in the current literature [Sateriale and Hart, 1985;Helzlsouer et al, 1983;Lane and Githens, 1985;Nussbaum and Rice, 1984;Pastorek and Seiler, 1985;Magnuson et al, 19801.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Age and prevalence of sickle‐cell trait in a large ambulatory population

Castro

Rana

Bang

et al. 1987

Genetic Epidemiology

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We performed hemoglobin electrophoresis in 30,400 apparently healthy black individuals in the Washington D.C. Metropolitan area, who were participating in a community based sickle-cell screening program during the period 1978-1985. The overall prevalence of sickle-cell trait was 6.7%. The frequency of sickle-cell trait in various age groups, which included young children, adults, and individuals over 65 years of age, ranged from 6.4 to 7.4%. There were no statistically significant differences in the prevalence of sickle-cell trait among the various age groups, nor did we detect a significant trend for increasing or decreasing sickle cell frequency with advancing age (P = 0.418). Thus, in this population sickle-cell trait appears to have no effect on longevity. If the various complications of sickle-cell trait reported in the literature are not fortuitous, their frequency and/or severity must be too low to affect prevalence figures.

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Severe Metabolic Complications in a Cross-Country Runner With Sickle Cell Trait

Cited by 40 publications

References 8 publications

Storage related haematological and biochemical changes in Plasmodium falciparum infected and sickle cell trait donor blood

Storage related haematological and biochemical changes in Plasmodium falciparum infected and sickle cell trait donor blood

Faster lactate transport across red blood cell membrane in sickle cell trait carriers

Age and prevalence of sickle‐cell trait in a large ambulatory population

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