PubMed Health⌕ Search

Biomedical subjects

R Vautrin

Publications and source records attributed to R Vautrin.

15 recordsLinked to original sources
PubMed2001

[Cervical and pharyngeal inflammatory pseudo-tumors, a report of two cases: clinical course and treatment].

The authors report two new cases of inflammatory pseudotumours, sited in the pharynx and neck--sites in which no previous cases have so far been reported in the literature. The aetiology and clinical course of these rare benign tumours remain little understood even today. Their treatment is also not clearly described. This is most often surgical, although medical treatment is often very effective, and is sometimes appropriate. The authors begin by describing these two clinical cases, and then use the literature to give an account of the clinical course and treatment of inflammatory pseudotumours.

Adult↗
PubMed1998

[Diagnostic criteria for progressive necrotizing external otitis. Are scintigraphic findings reliable?].

OBJECTIVES: Determine the role of 99m technetium scintigraphy for diagnosis in progressive necrotizing external otitis and assess the diagnostic criteria of this disease. METHOD: A retrospective study was conducted in 16 patients hospitalized for suspected progressive necrotizing external otitis. Patient characteristics, clinical features, imaging findings and disease course were recorded in order to evaluate the classical criteria of diagnosis. RESULTS: The clinical course and complementary test results showed that 99m technetium scintigraphy lacked specificity for progressive necrotizing external otitis. These findings are in disagreement with those reported in the literature. CONCLUSION: Patient characteristics and clinical course are key elements for early diagnosis of this disease. Scintigraphy findings are contributive only when bone lysis (which occurs late) can be evidenced. A prospective study would be required to confirm the lack of specificity of scintigraphy in progressive necrotizing external otitis.

Adult↗
PubMed1998

[Oto-neuro-surgical approach and accessibility to the cochlear nuclei. Significance in auditory brain stem implant].

The auditory brainstem implant (ABI) is now used to stimulate the cochlear nucleus to obtain auditory perception in patients with type 2 neurofibromatosis. Only electrical stimulation of the cochlear nucleus complex, in the lateral recess of the fourth ventricle, can achieve auditory rehabilitation of these profound bilateral retrocochlear deafness. With 20 standard translabyrinthine approaches, our personal anatomical study propose to describe surgical landmarks of the cochlear nuclear complex and surgical accessibility of the lateral recess of the fourth ventricle. The root of vestibulocochlear nerve, the glossopharyngeal nerve and the choroid plexus of the fourth ventricle might have surgical significance because of their reliability.

Brain Stem↗
PubMed1987

The effect of topical agents on haematopoiesis following thermal injury: studies on an animal model.

Several investigators have described 'toxins' in the serum of burned patients that result in systemic alterations and in an overall breakdown of host defences. One of these toxins isolated from the burn eschar resulted in 80 per cent mortality when injected into non-burned mice. However, if the eschar was pretreated with cerium before isolating the toxin, the mortality in the recipients decreased. This experiment suggested that the cerium neutralized the toxin. We have partially isolated from the serum of burned patients and mice a substance that inhibits erythroid colony formation in vitro. To test if cerium neutralized this erythroid inhibitor, we applied cerium or silver nitrate to the eschar of a mouse model of thermal injury. We found that neither agent altered the level of inhibitor or any of the granulocyte or erythroid parameters measured.

Analysis of Variance↗
PubMed1987

The haematopoietic response to burning: studies in a splenectomized animal model.

Several haematopoietic changes occur following burning. These changes are important because they may effect a patient's ability to fight infection and to heal wounds. Studies of haematopoiesis in burned humans are difficult because of the complexity of these patients and because of the difficulty of collecting specimens. We therefore established a mouse model of these haematopoietic events; however, this model differed from the human situation as all three haematopoietic cell lines were being produced by the murine spleen. In this paper, we modified the model by removing the spleen and then repeating our previous studies. After splenectomy, granulocyte production, murine mortality and body weight did not change. Compared with the original model, the modified splenectomy model could not expand erythropoiesis. The result was greater anaemia. This model is, now, a closer simulation of the human situation and will prove useful in studies of haematopoiesis after thermal injury.

Animals↗
PubMed1987

The anemia of thermal injury: partial characterization of an erythroid inhibitory substance.

Anemia is one of a large number of systemic changes occurring in severely burned patients and has a multifactorial etiology including hemorrhage, hemolysis, and depression of the rate of erythropoiesis. In previous studies, it was found that serum of burned humans and animals contained a substance(s) capable of interfering with red cell colony formation in vitro. Here are reported studies done in an attempt to characterize further the inhibitory activity. The molecular weight was more than 50,000 daltons by ultrafiltration. By gel filtration an inhibitory region was identified with an approximate molecular weight range of 140-290,000. Treatment of sera with proteolytic enzymes resulted in loss of activity suggesting that the inhibitory substance(s) was a protein. Ion exchange chromatography indicated that the inhibitor was an acidic protein. It is suggested that this material participates in the pathophysiology of the anemia of thermal injury by depressing red cell production.

Adult↗
PubMed1986

The anemia of thermal injury: mechanism of inhibition of erythropoiesis.

The anemia of thermal injury is a multifactorial process and includes hemorrhage and hemolysis. Much evidence suggests that a reduced rate of erythropoiesis contributes to this anemia. Prior studies show that this anemia is temporally related to the appearance in burn patients sera of a substance(s) capable of inhibiting erythropoiesis in vitro. Four experiments were done to elucidate the mechanism of action of this inhibitor. In all experiments sera from burn patients previously shown to be inhibitory to erythropoiesis in vitro were studied. In the first, inhibitory sera were exposed to erythropoietin solutions without loss of erythropoietic activity. Second, mouse marrow cells were preincubated with serum without loss of their ability to form erythroid colonies. Third, the inhibitory effect could not be overcome with increasing amounts of erythropoietin. Finally, erythroid colony formation was effected only if the inhibitory serum was present during the first 8 to 12 hr of culture. The data suggest that the erythropoietic inhibitor in these sera acts directly on erythroid stem cells in vitro and not by inactivating or interference with erythropoietin.

Anemia↗
PubMed1984

The haematopoietic response to burning: studies in an animal model.

Changes in haematopoiesis which occur in humans after burning injury may have important effects on morbidity and mortality. Because of the heterogeneity of burn patients we studied the regulation of blood cell formation which occurs in an animal using an established mouse model. Mice received a 20 per cent third degree scald injury on the back. Serial studies of a variety of haematopoietic parameters including stem cell, bone marrow and peripheral blood findings were done post burn. Although anaemia occurred frequently after injury red blood cell survival studies and examination of the stool for occult blood showed that neither haemolysis nor blood loss were primary causes of the anaemia. Bone marrow erythroid stem cells fell markedly post burn and this was associated with the development of a substance in serum capable of inhibiting red cell colony formation but not white cell colony formation of normal marrow cells. Reticulocytosis occurred but was mild and the anaemia was primarily of the aregenerative type. Partial compensation for the depressed marrow erythropoiesis occurred in the spleen with an increase in erythroid colony-forming cells and erythroblasts. Marked granulocytosis occurred in the peripheral blood and bone marrow. There was an increase in splenic granulocytic stem cells post burn. Megakaryocytosis was striking in the bone marrow and spleen and there was an increase in peripheral blood platelet count. Evidence of immune stimulation included an increase in the size of the spleen and an increase in peripheral blood and splenic lymphocytes. Correlations of many of these findings suggested that the events were not occurring at random but that the changes in haematopoiesis were linked together. We speculate that the anaemia was the result of the increase in granulopoietic and thrombopoietic effort seen post burn.

Anemia↗
PubMed1977

The effect of serum from uremic patients on erythropoietin.

Serum from patients with chronic renal failure (CRF serum) contains a substance inhibitory to erythropoiesis in vitro. This paper explores the mechanism of the inhibition. Four experiments were performed to evaluate the effects of CRF serum on erythropoietin (EP). In the first 2 experiments, the effect of exposure of EP solutions to CRF serum was evaluated using the plethoric mouse EP assay system and a tissue culture system containing normal dog marrow cells. In the third study, dog marrow cells were preincubated with CRF serum before being stimulated with EP. Finally, EP-dose response curves were constructed in the dog marrow tissue culture system and analyzed using an enzyme kinetic model. The results show no evidence of inhibition or inactivation of EP by CRF serum, although in vitro heme synthesis is clearly depressed in the presence of CRF serum. We conclude that CRF serum inhibits erythropoiesis by directly, although reversibly, impairing the ability of erythroblasts to synthesize heme.

Aged↗
PubMed1977

Granulopoietic and erythropoietic activity in patients with anemias of iron deficiency and chronic disease.

The serum levels of granulocyte colony-stimulating factor (CSF) and erythropoietin (Ep) were measured in 16 patients with iron-deficiency anemia and 15 patients with the anemia of chronic disease. Levels of both CSF and Ep in the serum of patients with iron-deficiency anemia had an inverse linear relationship to the level of the packed cell volume (PCV). There was no correlation between PCV and the levels of CSF or Ep in the serum of patients with the anemia of chronic disease. The similarity in the behavior of CSF and Ep in iron-deficiency anemia suggests that they may be influenced by similar control mechanisms or have a common cellular or molecular source.

Anemia↗
PubMed1976

The anemia of chronic renal failure and chronic diseases: in vitro studies of erythropoiesis.

The presence of a serum factor in chronic renal failure (CRF) which inhibits erythropoietin-stimulated erythropoiesis was studied, using a technique in which dog marrow cells were stimulated to produce heme in the presence of human serum. In the total series comparing 27 normal sera with 52 CRF sera, less heme was synthesized when the system contained CRF sera (total series, p = 0.0001). There was no evidence of inhibition of heme synthesis by serum from 12 patients with the anemia of chronic diseases (CD). Mixing experiments with normal and CRF sera suggested that this defect in CRF serum was not due to lack of a factor necessary for heme synthesis. Addition of urea, creatinine, and guanidinosuccinic acid to normal serum did not impair its ability to support erythropoiesis in this system. These data demonstrated that serum from patients with CRF contains a material inhibiting erythropoiesis in vitro, We propose that the material is responsible, in part, for the clinically severe anemia seen in these patients.

Adolescent↗
PubMed1975

The anemia of chronic renal failure: in vitro response of bone marrow to erythropoietin.

Bone marrow cells of patients with chronic renal failure were studied in short-term in vitro cultures to determine erythropietin responsiveness. Seven normals and fourtheen patients on hemodialysis were studied. Bone marrow cells of normal subjects and of patients with chronic renal failure responded similarly to erythropoietin. Total heme synthesis was significantly lower in cultures prepared with uremic serum than normal serum. We conclude that there is a substance in the serum of uremic patients which suppresses general heme synthesis and that this "uremic toxin" may be responsible, in part, for the clinically severe anemia seen in these patients.

Adult↗