Excessive erythrocytosis, chronic mountain sickness, and serum cobalt levels

  title={Excessive erythrocytosis, chronic mountain sickness, and serum cobalt levels},
  author={J. Ashley Jefferson and Elizabeth Escudero and Mar{\'i}a Elena Hurtado and J. Gim{\'e}nez Pando and Rosario Tapia and Erik R. Swenson and JosefT. Prchal and GeorgeE. Schreiner and Robert Blair Schoene and Abdias Hurtoado and Richard J. Johnson},
  journal={The Lancet},
High serum zinc and serum testosterone levels were associated with excessive erythrocytosis in men at high altitudes
Higher serum testosterone levels and Zn levels were associated with EE, and low scores of signs/symptoms of CMS wereassociated with higher Zn and nitric oxide levels.
Re-evaluation of excessive erythrocytosis in diagnosing chronic mountain sickness in men from the world's highest city.
Examination of individuals in La Rinconada, Peru, the highest city in the world, demonstrated that CMS at extreme altitude is not linked to elevation of hemoglobin, since CMS+ and CMS− individuals had similar levels of erythrocytosis.
Hyperuricemia, hypertension, and proteinuria associated with high-altitude polycythemia.
Hyperuricemia is common in subjects living at high altitude and associated with EE, hypertension, and proteinuria, and the increase in uric acid levels appears to be caused by increased urate generation secondary to systemic hypoxia, although a relative impairment in renal excretion also may contribute.
Ventilation, autonomic function, sleep and erythropoietin. Chronic mountain sickness of Andean natives.
The increased Epo production is mainly related to a greater ventilatory inefficiency, and not to altered sensitivity to hypoxia, cobalt or sleep abnormalities, suggesting improving oxygenation can represent a possible therapeutic option for this syndrome.
High altitude renal syndrome (HARS).
The frequent presentation of systemic hypertension and microalbuminuria with relatively preserved GFR coupled with the presence of polycythemia and hyperuricemia suggests a new clinical syndrome the authors term high altitude renal syndrome (HARS).
Intolerability of cobalt salt as erythropoietic agent.
New insights should keep athletes off taking Co(2+) to stimulate erythropoiesis, as the intake of inorganic cobalt can cause severe organ damage, concerning primarily the gastrointestinal tract, the thyroid, the heart and the sensory systems.
Hemoglobin Mass and Blood Volume in Patients With Altitude-Related Polycythemia
In CMS patients, the decreases in PV only partially compensated for the substantial increase in Hbmass, but it did not prevent an increase in BV; the decrease in PV contributed to an excessively high [Hb].
Chronic Mountain Sickness
In more advanced and severe stages, high-altitude pulmonary hypertension (HAPH) appears frequently, with related remodeling of pulmonary arterioles and right ventricular hypertrophy.
Genetic association analysis of chronic mountain sickness in an Andean high-altitude population.
This study does not find evidence of associations between the polymorphisms linked to the candidate genes and severe polycythemia; this does not, however, exclude that variations in these genes contribute to polycy Themia and possibly CMS.


Higher erythropoietin secretion in response to cobaltous chloride in post-hypoxic than in hypertransfused polycythemic mice.
It is demonstrated that EPO production in response to COC12 is depressed by polycythemia when induced by transfusion but not wheninduced by chronic exposure to hypobaric hypoxia, which confirms, but not explain, the nature of the conditioning effect of exposure to Hypoxia which makes the mechanism controlling EPO secretion either more sensitive to EPO-secreting stimuli or unable to recognize the polycythemic state.
LowTemperature Physics in the USSR: P~olmssop. duced by Peptic Digestion of Proteins: PRoiFssoR Low Tbemperatubre UJSSR£: PoROFSSOR H. CROxERTO and DR. R. CROXATTO. In Vitro GuiC. T. LANE . . . . . .
Assessment of risks in occupational cobalt exposures.
  • G. Nordberg
  • Medicine
    The Science of the total environment
  • 1994
Targeting of HIF-α to the von Hippel-Lindau Ubiquitylation Complex by O2-Regulated Prolyl Hydroxylation
It is shown that the interaction between human pVHL and a specific domain of the HIF-1α subunit is regulated through hydroxylation of a proline residue by an enzyme the authors have termed Hif-α prolyl-hydroxylase (HIF-PH).