Severe postadenoidectomy bleeding revealing congenital alpha 2 antiplasmin deficiency in a child.
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Adenoidectomy↗
Biomedical subjects
R Favier
Publications and source records attributed to R Favier.
Fluid regulatory hormone response to exercise after coca-induced body fluid shifts.
To determine the effect of coca chewing on heart rate (HR), mean arterial blood pressure (MAP), and plasma volume and their relationship with the hormones regulating cardiovascular and body fluid homeostasis, 16 male volunteers were examined at rest and during 1 h of cycle exercise at approximately 75% of their peak oxygen uptake in two trials separated by 1 mo. One trial was performed after the subjects chewed a sugar-free chewing gum (Coca- trial), whereas the other was done after the subjects chewed 15 g of coca leaves (Coca+), with the order of the Coca- and Coca+ trials being randomized. Blood samples were taken at rest, before (R1) and after 1-h chewing (R2), and during the 5th, 15th, 30th, and 60th min of exercise. They were analyzed for hematocrit, hemoglobin concentration, red blood cell count, plasma proteins, and for the fluid regulatory hormones, including plasma catecholamines [norepinephrine (NE) and epinephrine], renin, arginine vasopressin, and the atrial natriuretic peptide (ANP). During the control trial (Coca-), from R1 to R2, there was no significant change in hematologic, hormonal, and cardiovascular status except for a small increase in plasma NE. In contrast, it can be calculated that coca chewing at rest induced a significant hemoconcentration (-3.8 +/- 1. 3% in blood and -7.0 +/- 0.7% in plasma volume), increased NE and MAP, and reduced plasma ANP. Chewing coca before exercise reduced the body fluid shifts but enhanced HR response during exercise. These effects were not accompanied by changes in NE, epinephrine, renin, and arginine vasopressin plasma levels. In contrast, plasma ANP response to exercise was lower during the Coca+ trial, suggesting that central cardiac filling was reduced by coca use. It is likely that the reduction in body fluid volumes is a major contributing factor to the higher HR at any given time of exercise after coca chewing.
Adult↗
[Paris-Trousseau thrombocytopenia: a new entity and a model for understanding megakaryocytopoiesis].
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Adult↗
Aerobic capacity and skeletal muscle properties of normoxic and hypoxic rats in response to training.
The aim of this study was to determine, in the rat, the effects of chronic exposure (7-9 weeks) to normobaric hypoxia (FIO2=0.13, equivalent to 3700 m altitude) on cardiac and skeletal muscle properties, on maximal oxygen uptake (VO2max), and endurance time to exhaustion (ETE). In addition, we evaluated the impact of endurance training (90 min of treadmill running per day, 5 days per week, for 9 weeks) on these parameters. The results were compared to normoxic rats fed ad libitum (NAL) and to normoxic pair-weight (NPW) animals in order to take into account the influence of hypoxia on growth rate. It was found that, in sedentary rats, hypoxia results in stunted growth, adrenal atrophy, a significant reduction of cross-sectional area of fast-twitch (type II) fibres, a reduced capillary-to-fibre ratio (C/F), and a reduced oxidative capacity (decreases in citrate synthase and 3-hydroxy-Acyl CoA dehydrogenase activities) of the plantaris muscle. These effects are mainly related to the anorexic effects of prolonged exposure to hypoxia. Nevertheless, hypoxic (H) rats displayed higher VO2max and ETE values when compared either to NAL or to NPW animals. Endurance training resulted, in all groups (H, NAL, NPW), in a significant change of the fibre type distribution of the plantaris which displayed an increased number of type IIA fibres and a decreased proportion of type IIB fibres. In addition, the C/F ratio and cross-sectional area of fast-twitch fibres were normalized by superimposition of training on hypoxia. Both VO2max and ETE were significantly higher in trained H rats than in NAL, but these improvements were mainly related to the reduced body weight induced by hypoxia. These data suggest that the greater aerobic capacity and tolerance for prolonged exercise induced by chronic exposure to hypoxia can be mainly accounted for by the anorexic effects of hypoxia, although other factors (e.g. increase in oxygen carrying capacity induced by hypoxia acclimatization) may play a significant role in some circumstances (e.g. in sedentary rats).
Acyl-CoA Dehydrogenase↗
Hormonal and metabolic adjustments during exercise in hypoxia or normoxia in highland natives.
In sea-level natives, exposure to hypoxia for a few weeks is characterized by an increased dependence on blood glucose and a decreased reliance on lactate for energy metabolism during exercise. These metabolic adjustments have been attributed to behavioral changes in the sympathoadrenergic and pancreatic systems. The aim of this study was to test the hypothesis of a reduced sympathoadrenergic activation and subsequent metabolic changes when high-altitude natives are acutely exposed to normoxia. Young Andean natives performed incremental exercise to exhaustion during hypoxia (arterial PO2 55.1 +/- 1.1 Torr) or during acute normoxia (arterial PO2 78.7 +/- 1.7 Torr). As a whole, oxygen uptake was increased in normoxia compared with hypoxia during graded exercise. This finding is not related to a decrease in anaerobic metabolism but rather is interpreted as a consequence of a shift in substrate utilization during exercise (increased contribution of fat as assessed by a reduction in the respiratory exchange ratio). These metabolic changes are not accompanied by modifications of glucoregulatory hormones (catecholamines, insulin, and glucagon). In particular, the exercise-induced catecholamine secretion was similar in chronic hypoxia and acute normoxia. As a consequence, blood lactate accumulation during incremental exercise was similar in both conditions. It is concluded that high-altitude natives do not display any sign of a greater sympathoadrenergic activation during chronic hypoxia and that the exercise-induced hormonal changes remained unaffected by acute inhalation of a normoxic gas mixture.
Adult↗
Effects of coca chewing on metabolic and hormonal changes during graded incremental exercise to maximum.
We examined the effects of 1 h of coca chewing on metabolic and hormonal responses during incremental exercise to exhaustion in traditional coca chewers (C; n = 8), and the results were compared with a group of nonchewers (n = 13). For 1 h, C chewed approximately 12 g of coca leaves that resulted in the apparition of cocaine in blood that reached 72 +/- 9 ng/ml. In resting conditions, even though sympathoadrenergic activity (as assessed by norepinephrine and epinephrine plasma levels) was similar in both groups, C displayed a higher level of plasma free fatty acids. Oxygen uptake measured at exhaustion and delta work efficiency during exercise were similar in both groups. During the incremental exercise, C displayed a significantly lower arterial oxygen saturation that cannot be explained by a reduced ventilatory response after coca chewing. In fact, even at maximal exercise, both ventilatory output and ventilatory equivalent were higher in C compared with nonchewers. It is concluded that the beneficial effects of coca chewing on exercise tolerance reported frequently by traditional coca users is not related to either an improved maximal exercise capacity or an increased work efficiency. However, during incremental exercise, coca chewing appeared to result in an increased free fatty acid availability that could be beneficial for prolonged submaximal exercise.
Adult↗
Effects of coca chewing on hormonal and metabolic responses during prolonged submaximal exercise.
The effects of coca chewing on prolonged submaximal exercise responses were investigated in chronic coca chewers and compared with a group of nonchewers. At rest, coca chewing during a 1-h period was followed by a significant increase in blood glucose, free fatty acid, and norepinephrine concentrations and a significant reduction in insulin plasma level. During prolonged (1-h) submaximal (65-70% peak O2 uptake) exercise, chewers displayed a significantly greater adrenergic activation (as evidenced by a higher level of plasma epinephrine) and an increased use of fat (as evidenced by a lower respiratory exchange ratio). The gradual increase in oxygen uptake (O2 drift) commonly observed during prolonged exercise was blunted in coca chewers. This blunting in O2 drift is not related to coca-induced changes in ventilatory or lactate responses to exercise but could possible be related to an enhanced glucose utilization by chewers during the late phase of exercise. The present results provide experimental evidence of the physiological effects of coca chewing that could explain the better ability of coca users to sustain strenuous work for an extended period of time.
Adolescent↗
Coca chewing for exercise: hormonal and metabolic responses of nonhabitual chewers.
To determine the effects of acute coca use on the hormonal and metabolic responses to exercise, 12 healthy nonhabitual coca users were submitted twice to steady-state exercise (approximately 75% maximal O2 uptake). On one occasion, they were asked to chew 15 g of coca leaves 1 h before exercise, whereas on the other occasion, exercise was performed after 1 h of chewing a sugar-free chewing gum. Plasma epinephrine, norepinephrine, insulin, glucagon, and metabolites (glucose, lactate, glycerol, and free fatty acids) were determined at rest before and after coca chewing and during the 5th, 15th, 30th, and 60th min of exercise. Simultaneously to these determinations, cardiorespiratory variables (heart rate, mean arterial blood pressure, oxygen uptake, and respiratory gas exchange ratio) were also measured. At rest, coca chewing had no effect on plasma hormonal and metabolic levels except for a significantly reduced insulin concentration. During exercise, the oxygen uptake, heart rate, and respiratory gas exchange ratio were significantly increased in the coca-chewing trial compared with the control (gum-chewing) test. The exercise-induced drop in plasma glucose and insulin was prevented by prior coca chewing. These results contrast with previous data obtained in chronic coca users who display during prolonged submaximal exercise an exaggerated plasma sympathetic response, an enhanced availability and utilization of fat (R. Favier, E. Caceres, H. Koubi, B. Sempore, M. Sauvain, and H. Spielvogel. J. Appl. Physiol. 80: 650-655, 1996). We conclude that, whereas coca chewing might affect glucose homeostasis during exercise, none of the physiological data provided by this study would suggest that acute coca chewing in nonhabitual users could enhance tolerance to exercise.
Adult↗
Muscle tissue adaptations of high-altitude natives to training in chronic hypoxia or acute normoxia.
Twenty healthy high-altitude natives, residents of La Paz, Bolivia (3,600 m), participated in 6 wk of endurance exercise training on bicycle ergometers, 5 times/wk, 30 min/session, as previously described in normoxia-trained sea-level natives (H. Hoppeler, H. Howald, K. E. Conley, S. L. Lindstedt, H. Claassen, P. Vock, and E. R. Weibel. J. Appl. Physiol. 59: 320-327, 1985). A first group of 10 subjects was trained in chronic hypoxia (HT; barometric pressure = 500 mmHg; inspired O2 fraction = 0.209); a second group of 10 subjects was trained in acute normoxia (NT; barometric pressure = 500 mmHg; inspired O2 fraction = 0.314). The workloads were adjusted to approximately 70% of peak O2 consumption (VO2peak) measured either in hypoxia for the HT group or in normoxia for the NT group. VO2peak determination and biopsies of the vastus lateralis muscle were taken before and after the training program. VO2peak in the HT group was increased (14%) in a way similar to that in NT sea-level natives with the same protocol. Moreover, VO2peak in the NT group was not further increased by additional O2 delivery during the training session. HT or NT induced similar increases in muscle capillary-to-fiber ratio (26%) and capillary density (19%) as well as in the volume density of total mitochondria and citrate synthase activity (45%). It is concluded that high-altitude natives have a reduced capillarity and muscle tissue oxidative capacity; however, their training response is similar to that of sea-level residents, independent of whether training is carried out in hypobaric hypoxia or hypobaric normoxia.
Acclimatization↗
Lactate and epinephrine during exercise in altitude natives.
We tested the hypothesis that the reported low blood lactate accumulation ([La]) during exercise in altitude-native humans is refractory to hypoxianormoxia transitions by investigating whether acute changes in inspired O2 fraction (FIo2) affect the [La] vs. power output (W) relationship or, alternatively, as reported for lowlanders, whether changes in [La] vs. W on changes in FIo2 are related to changes in blood epinephrine concentration ([Epi]). Altitude natives [n = 8, age 24 +/- 1 (SE) yr, body mass 62 +/- 3 kg, height 167 +/- 2 cm] in La Paz, Bolivia (3,600 m) performed incremental exercise with two legs and one leg in chronic hypoxia and acute normoxia (AN). Submaximal one- and two-leg O2 uptake (Vo2) vs. W relationships were not altered by FIo2. AN increased two-leg peak Vo2 by 10% and peak W by 7%. AN paradoxically decreased one-leg peak Vo2 by 7%, whereas peak W remained the same. The [La] vs. W relationships were similar to those reported in unacclimatized lowlanders. There was a shift to the right on AN, and maximum [La] was reduced by 7 and 8% for one- and two-leg exercises, respectively. [Epi] and [La] were tightly related (mean r = 0.81) independently of FIo2. Thus normoxia attenuated the increment in both [La] and [Epi] as a function of W, whereas the correlation between [La] and [Epi] was unaffected. These data suggest loose linkage of glycolysis to oxidative phosphorylation under influence from [Epi]. In conclusion, high-altitude natives appear to be not fundamentally different from lowlanders with regard to the effect of acute changes in FIo2 on [La] during exercise.
Adult↗
A new congenital dysmegakaryopoietic thrombocytopenia (Paris-Trousseau) associated with giant platelet alpha-granules and chromosome 11 deletion at 11q23.
This study characterizes a new congenital thrombocytopenia with mild hemorrhagic tendency occurring in a woman and her child with the following features. We found a deletion of the distal part of one chromosome 11 [del(11)q23.3-->qter] that was detected by cytogenetic analysis and confirmed by chromosome painting in the two patients and also an increased number of bone marrow megakaryocytes (MKs), including numerous micromegakaryocytes (mMKs) associated with a normal platelet life span. A normal number of MK colonies in culture was observed with one third of them containing a few large MKs; however, these were always associated with mMKs identified by immunologic staining. A massive cell lysis was observed at the end of the maturation. Fifteen percent of the platelets in the peripheral blood showed giant alpha-granules resulting from the fusion of alpha-granules. These giant granules, which appeared in red on giemsa stain, had a mean diameter of 1.5 microns and showed all markers (detected at electron microscopy by immunogold method) of matrix and alpha-granule membrane, ie, von Willebrand factor, fibrinogen, CD41, CD62P (P-selectin); however, they differed from lysosomes because acid phosphatases were not present. These giant alpha-granules were unable to release their contents after stimulation by thrombin, in contrast to platelets with normal morphology. Abnormalities in bone marrow MK maturation that were detected at the electron microscopic level and that led to lysis of numerous MKs were responsible for thrombocytopenia and were similar in both patients. MK abnormalities are probably the consequence of the chromosome aberration. ETS 1 and FLI, two proto-oncogenes that appear to be essential with GATA1 for the normal expression of MK-specific genes, map to 11q23-q24 and are, thus, deleted in this thrombocytopenia. In conclusion, the association of all these abnormalities constitutes a new familial platelet disorder and may present a valuable model for exploring the role of some genes involved in the regulation of thrombopoiesis.
Adult↗
[Transient correction of partial congenital factor V deficiency in nephrotic syndrome].
Plasma concentration of several hemostatic proteins may be modified during the acute phase of nephrotic syndrome. The case of such a syndrome in a patient with congenital factor V deficiency is presented. CASE REPORT--A 5 year-old girl with partial congenital factor V deficiency (level: 30%), was admitted for nephrotic syndrome complicating Henoch-Schönlein purpura. Urine protein excretion was 4 g/24 h. Initial plasma concentrations were: protein: 5.5 g/dl; albumin: 3.3 g/dl; factor II: 85%; factor V: 56%; factors VII + X: 80%. The patient was given methylprednisolone (1 g/1.73 m2) followed by prednisone (2 mg/kg/day). Under this treatment, the plasma concentrations were: protein: 4.5 g/dl; albumin: 2.0 g/dl; factor II: 180%; factor V: 84%; factors VII + X: 120%. Values at the onset of remission were: albumin: 3.4 g/dl; factor V: 49%. CONCLUSION--This observation suggests that hypoalbuminemia may enhance liver synthesis of factor V as known for some other coagulation factors, and transiently correct the hereditary deficiency.
Child, Preschool↗
Maximal exercise performance in chronic hypoxia and acute normoxia in high-altitude natives.
Maximal O2 uptake (VO2max) was determined on a bicycle ergometer in chronic hypoxia (CH) and during acute exposure to normoxia (AN) in 50 healthy young men who were born and had lived at 3,600 m altitude (La Paz, Bolivia). VO2max was significantly improved (approximately 8%) by AN. However, the difference in VO2max measured in CH and AN (delta VO2max) was lower than that reported in sea-level natives (SN) who exercised in chronic normoxia and acute hypoxia. It is shown that high-altitude natives (HN) and SN have a similar VO2max in normoxia, but highlanders can attain a greater VO2max when O2 availability is reduced by altitude exposure. In addition, in HN, the higher the subject's VO2max in hypoxia, the smaller his delta VO2max. These results contrast with the data obtained in 14 lowlanders acclimatized to high altitude who showed that their delta VO2max was positively related to their VO2max in hypoxia, as previously reported in SN who exercised in acute hypoxia (A. J. Young, A. Cymerman, and R. L. Burse. Eur. J. Appl. Physiol. Occup. Physiol. 54: 12-15, 1985). Furthermore, arterial O2 saturation of HN behaved differently from acclimatized lowland natives, inasmuch as it fell less during exercise both in CH and AN. HN with high aerobic capacity display a lower exercise ventilation and a reduced arterial saturation, which could explain their inability to improve VO2max with normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
Acclimatization↗
Training in hypoxia vs. training in normoxia in high-altitude natives.
To determine the interactions between endurance training and hypoxia on maximal exercise performance, we performed a study on sedentary high-altitude natives who were trained in normoxia at the same relative (n = 10) or at the same absolute (n = 10) intensity of work as hypoxia-trained subjects (n = 10). The training-induced improvement of maximal oxygen uptake (VO2max) in hypoxia-trained subjects was similar to that obtained in normoxia-trained sea-level natives submitted to the same training protocol (H. Hoppeler, H. Howald, K. Conley, S. L. Lindstedt, H. Claassen, P. Vock, and E. W. Weibel. J. Appl. Physiol. 59: 320-327, 1985). Training at the same absolute work intensity in the presence of increased oxygen delivery failed to provide a further increase in VO2max. VO2max was not improved to a greater extent by simultaneously increasing absolute work intensity and O2 delivery during the training sessions. In addition, training in normoxia is accompanied by an increased blood lactate accumulation during maximal exercise, leading to greater drops in arterial pH, bicarbonate concentration, and base excess. We conclude that, in high-altitude natives, 1) training at altitude does not provide any advantage over training at sea level for maximal aerobic capacity, whether assessed in chronic hypoxia or in acute normoxia; 2) VO2max improvement with training cannot be further enhanced by increasing O2 availability alone or in combination with an increased work intensity during the exercising sessions; and 3) training in normoxia in these subjects results in a reduced buffer capacity.
Adult↗
Peripheral-T-cell lymphoma with hemophagocytic histiocytosis localised to the bone marrow associated with inappropriate secretion of antidiuretic hormone.
A patient with high fever, loss of weight and profound pancytopenia is reported. Peripheral T-cell lymphoma with hemophagocytosis was diagnosed. Bone marrow was the only localisation of the lymphoma. At presentation there were (i) a coagulopathy consistent with hemophagocytic histiocytosis (ii) the features of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). These different abnormalities disappeared after chemotherapy and reappeared during each of the 2 periods of disease progression. The patient died 6 months after diagnosis without ever achieving complete remission. As far as we are aware this is the first case report of T-cell lymphoma with hemophagocytic syndrome localised to the bone marrow and associated with SIADH.
Aged↗
Glucoregulation and hormonal changes during prolonged exercise in boys and girls.
A group of 17 children, 8.5-11 years old, performed a 60-min cycle exercise at 60% of maximal oxygen uptake (VO2max) 2 h after a standardized breakfast. They were 10 young boys (pubertal stage = 1) and 7 young girls (pubertal stage < or = 2) of similar VO2max (respective values were 48.5 ml min-1 kg-1, SEM 1.8; 42.1 ml min-1 kg-1, SEM 2.4). Blood samples of 5 ml were withdrawn by heparinized catheter, the subjects being in a supine position, 30 min before the test, then after 0, 15, 30 and 60 min of exercise and following 30 min recovery. Haematocrit was immediately measured. Thereafter plasma was analysed for glucose, non-esterified fatty acid, glycerol, catecholamine (noradrenaline, adrenaline), insulin and glucagon concentrations. This study showed two main results. First, the onset of exercise induced a significant glucose decrease (of about 11.4%) in all the children. Secondly, both the glycaemic and the hormonal responses were obviously different according to the sex. In boys only, the initial glucose drop was significantly correlated to the pre-exercise insulin values. Whatever the time, the glycaemic levels and the catecholamine responses were lower in girls than in boys, whereas the insulin values remained higher. However, none of these two hormonal parameters seemed to be really responsible for the lower glucose values in girls. On the one hand, the great individual variability of noradrenaline and adrenaline and differences in their relative intensity at the end of the exercise between boys and girls might contribute to the lower catecholamine levels in girls.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Glucose↗
[For or against preoperative hemostatic evaluation in healthy children?].
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Child↗
A novel genetic thrombocytopenia (Paris-Trousseau) associated with platelet inclusions, dysmegakaryopoiesis and chromosome deletion AT 11q23.
We report a novel case of hereditary thrombocytopenia. A chronic thrombocytopenia was noted in a woman with mild hemorrhagic complications as well as in her very young son. A platelet fraction contained giant granules stained in red on blood smears. The number of bone marrow megakaryocytes was increased with many micromegakaryocytes. Since the platelet life span was normal, these results indicated an ineffective platelet production. A constitutional cytogenetic abnormality was detected in the two patients: a deletion of the long arm of chromosome 11. The association of these abnormalities constitute a new disorder: this never described cytological entity is a valuable model for exploring the role of some genes involved in the regulation of thrombopoiesis.
Adult↗