Cardiac Biomarkers, Electrolytes, and Other Analytes in Collapsed Marathon Runners:
Implications for the Evaluation of Runners Following Competition
Siegel AJ, et al.
Am J Clin Pathol, June 208; 129(6):948-51.
We measured analytes in collapsed Boston Marathon runners to compare with changes in asymptomatic runners.
Of collapsed runners at the 2007 marathon, 18.2% had a measurable cardiac troponin T (cTnT) value with a mean
post race level of 0.017 ng/mL (0.017 mug/L; SD, 0.02 ng/mL [0.02 mug/L)). Three subjects had cTnT values
above the cutoff (0.10 ng/mL [0.10 mug/L]) typically used for the diagnosis of acute myocardial infarction. The
mean and median N-terminal proB-type natriuretic peptide levels were 73 ng/L (SO, 77.3 ng/L) and 54.3 ng/L
(interquartile range, 22.8-87.3 ng/L), respectively, in collapsed runners. Only 4.9% had values more than the
age-specific normal value (<125 ng/L for subjects younger than 75 years). In collapsed subjects at the 2006
marathon, 18.0% had an abnormal sodium value, including 18 cases of hypernatremia and 7 cases of
hyponatremia. The ionized calcium level was low in 49% of subjects, and the ionized magnesium level was low in
19.5% and elevated in 1 subject. The blood lactate level was elevated in 95% of subjects. The frequency of
elevated post race cTnT levels in collapsed athletes after endurance exercise is similar to that in asymptomatic
runners. Other metabolic abnormalities, including hypernatremia, hyponatremia, low ionized calcium and
magnesium levels, and lactic acidosis may contribute to muscle fatigue and collapse.
Iron and Anemia in Human Biology: A Review of Mechanisms
Handelman GJ, et al.
Heart Fail Rev, June 2008; 13(4):393-404.
The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of
iron for erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia,
storage iron declines until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be
monitored with clinical indicators, beginning with low plasma ferritin, followed by decreased plasma iron and
transferrin saturation, and culminating in red blood cells with low-Hb content. When adequate dietary iron is
provided, these markers show return to normal, indicating a response to the dietary supplement. Anemia of
inflammation (also known as anemia of chronic disease, or ACD) follows a different course, because in this form
of anemia storage iron is often abundant but not available for erythropoiesis. The diagnosis of ACD is more
difficult than the diagnosis of iron-deficiency anemia, and often the first identified symptom is the failure to show a
response to a dietary iron supplement. Confirmation of ACD is best obtained from elevated markers of
inflammation. The treatment of ACD, which typically employs erythropoietin (EPO) supplements and
intravenous iron (IV-iron), is empirical and often falls shorts of therapeutic goals. Dialysis patients show a complex
pattern of anemia, which results from inadequate EPO production by the kidney, inflammation, changes in
nutrition, and blood losses during treatment. EPO and IV-iron are the mainstays of treatment. Patients with heart
failure can be anemic, with incidence as high as 50%. The causes are multifactorial; inflammation now appears to
be the primary cause of this form of anemia, with contributions from increased plasma volume, effects of drug
therapy, and other complications of heart disease. Discerning the mechanisms of anemia for the heart failure
patient may aid rational therapy in each case.
Hematological Manifestations of Copper Deficiency: A retrospective Review
Halfdanarson TR, et al.
Eur J Haematol; June 2008; 80(6):523-31.
Copper deficiency is an established cause of hematological abnormalities but is frequently misdiagnosed. Copper
deficiency can present as a combination of hematological and neurological abnormalities and it may masquerade as a
myelodysplastic syndrome. We reviewed the records of patients with hypocupremia and hematologic abnormalities
identified between 1970 and 2005. Patients with hypocupremia unrelated to copper deficiency (e.g. Wilson's disease)
were excluded. Forty patients with copper deficiency and hematological abnormalities were identified. Ten patients
(25%) had undergone bariatric (weight reduction) surgery and an additional 14 patients (35%) had undergone surgery
on the gastrointestinal tract, most commonly gastric resection. In 12 cases, no cause for copper deficiency was
identified. Anemia and neutropenia were the most common hematologic abnormalities identified and the majority of
the patients also had neurologic findings, most commonly due to myeloneuropathy. Abnormalities observed on bone
marrow examination including vacuoles in myeloid precursors, iron-containing plasma cells, a decrease in granulocyte
precursors and ring sideroblasts may be valuable clues to the diagnosis. Copper deficiency is an uncommon but very
treatable cause of hematologic abnormalities.
The Use of Intravenous Iron in Patients with Cancer-Related Anaemia
Lopez V.
Biol Trace Elem Res; June 2008: 122(3):238-55.
Intravenous iron has become the standard of care in patients with renal failure receiving treatment with erythropoiesis
stimulating agents (ESAs) to treat true and functional iron deficiency and to prevent its development in haemodialysis
patients. In cancer-related anaemia, several recently published, randomized studies suggested that intravenous iron
improved haemoglobin response rates in ESA-treated patients compared to those treated with oral iron or placebo.
The data supporting the efficacy of intravenous iron instead of oral iron in this setting are increasingly persuasive but
larger randomized trials are needed before definitive recommendations are made.
Zinc in Human Health: Effect of Zinc on Immune Cells
Prasad AS.
Mol Med: May 2008; 14(5-6):353-7.
Although the essentiality of zinc for plants and animals has been known for many decades, the essentiality of zinc for
humans was recognized only 40 years ago in the Middle East. The zinc-deficient patients had severe immune
dysfunctions, in as much as they died of intercurrent infections by the time they were 25 years of age. In our studies in
an experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia,
severe immune dysfunctions mainly affecting T helper cells, hyperammonemia, neurosensory disorders, and decreased
lean body mass. It appears that zinc deficiency is prevalent in the developing world and as many as two billion subjects
may be growth retarded due to zinc deficiency. Besides growth retardation and immune dysfunctions, cognitive
impairment due to zinc deficiency also has been reported recently. Our studies in the cell culture models showed that
the activation of many zinc-dependent enzymes and transcription factors were adversely affected due to zinc
deficiency. In HUT-78 (T helper 0 [Th(0)] cell line), we showed that a decrease in gene expression of interleukin-2
(IL-2) and IL-2 receptor alpha (IL-2Ralpha) were due to decreased activation of nuclear factor-kappaB (NF-kappaB) in
zinc deficient cells. Decreased NF-kappaB activation in HUT-78 due to zinc deficiency was due to decreased binding
of NF-kappaB to DNA, decreased level of NF-kappaB p1 05 (the precursor of NF-kappaB p50) mRNA, decreased
kappaB inhibitory protein (IkappaB) phosphorylation, and decreased Ikappa kappa. These effects of zinc were cell specific. Zinc also is an antioxidant and has anti-inflammatory actions. The therapeutic roles of zinc in acute infantile
diarrhea, acrodermatitis enteropathica, prevention of blindness in patients with age-related macular degeneration, and
treatment of common cold with zinc have been reported. In HL-60 cells (promyelocytic leukemia cell line), zinc
enhances the up-regulation of A20 mRNA, which, via TRAF pathway, decreases NF-kappaB activation, leading to
decreased gene expression and generation of tumor necrosis factor-alpha (TNF-alpha), IL-1 beta, and IL-8. We have
reported recently that in both young adults and elderly subjects, zinc supplementation decreased oxidative stress
markers and generation of inflammatory cytokines.
Response of Selenium Status Indicators to Supplementation of Healthy North
American Men with High-Selenium Yeast
Hawkes WC, et al.
Biol Trace Elem Res; April 2008; 122(2):107-21.
The essential nutrient selenium is required in microgram amounts [recommended dietary allowance (RDA) = 55
mug/day, 699 nmol/day] and has a narrow margin of safety (upper tolerable intake limit = 400 mug/day, 5
mumol/day). We conducted a randomized placebo-controlled study of high-selenium yeast, the form used in most
supplements (300 mug/day, 3.8 mumol/day), administered to 42 free-living healthy men for 48 weeks. Dietary
intakes of selenium, macronutrients, and micronutrients were not different between groups and did not change during
the study. Supplementation more than doubled urinary selenium excretion from 69 to 160 mug/day (876 to 2,032
nmol/day). Urinary excretion was correlated with recent selenium intake estimated from 3-day diet records: urinary
selenium excretion = 42 mug/day (533 nmol/day) + 0.132 x dietary selenium intake, p < 0.001. Dietary selenium
intake was not significantly correlated with the other indicators of selenium status, presumably because urinary
selenium excretion reflected recent intake, and tissue selenium was homeostatically controlled. After 48 weeks of
supplementation, plasma selenium was increased 60% from 142 to 228 mug/I (1.8 to 2.9 mumol/I), and erythrocyte
selenium was approximately doubled from 261 to 524 mug/l (3.3 to 6.6 mumol/I). Selenium concentrations
increased more modestly in hair (56%) and platelets (42%). Platelets were the only blood component in which
glutathione peroxidase activity was significantly related to selenium content. Selenium levels decreased rapidly after
the end of supplementation, and there were no significant differences in selenium status indicators between groups by
week 96. The absorption, distribution, and excretion of selenium from high-Se yeast were similar to selenium in
foods.
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