Progress in clinical and biological research
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Prog. Clin. Biol. Res. · Jan 1989
Randomized Controlled Trial Comparative Study Clinical TrialUse of a 7.5% NaCl/6% Dextran 70 solution in the resuscitation of injured patients in the emergency room.
Animal studies and preliminary field patient trials suggest that hypertonic saline solutions can achieve resuscitation of hypovolemic shock with extremely small volumes. In the study reported here, we evaluated the effects of a hypertonic 7.5% NaCl/6% Dextran 70 (HSD) solution in the resuscitation of patients in the emergency room. Thirty-two patients were randomized into a prospective, randomized, placebo-controlled, double-blinded trial in which 250 ml of either HSD or, as a control, lactated Ringers (LR) was used as the initial fluid for resuscitation of patients with systolic blood pressures of 80 mmHg or less. ⋯ With the exception of one patient, the highest sodium concentration was 156 mEq/l, the highest chloride concentration was 126 mEq/1, and the highest osmolality was 401 mOsm/kg, and this value was obtained in a patient in the control LR group. Osmolality correlated far better with blood alcohol levels (Spearman's rank correlation coefficient = 0.81) than with any other variable, including sodium and chloride concentrations. The HSD solution was safe to use.(ABSTRACT TRUNCATED AT 250 WORDS)
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In this review, we have described the molecular bases accounting for beta, delta beta and gamma delta beta-thalassemias, discussed the molecular mechanisms responsible for the production of mild forms of thalassemia and presented a strategy for detecting beta-thalassemia mutations in each at risk population. The molecular bases of beta-thalassemia are very heterogeneous. The great majority of beta-thalassemias are caused by point mutations affecting the coding region or critical areas of the beta-globin gene and are only rarely produced by gross gene rearrangements. ⋯ Determinants recognized to date as able to produce mild forms of beta-thalassemias, are beta-thalassemia mutations with a high residual output of beta-globin chain production, coinheritance of alpha-thalassemia or nondeletion HPFH linked or not linked to the beta-globin gene cluster, delta beta thalassemias and specific beta-globin haplotype. Because in each population a restricted number of molecular defect occurs, strategies have been developed to detect the beta-thalassemia mutations in prospective parents in each at risk population. These strategies are based on the direct detection of the mutation by dot blot analysis on enzymatically amplified DNA using a limited number of oligonucleotide probes complementary to the most common mutations in each population.