Search PubMed⌕ Search

Biomedical subjects

G Chomette

Publications and source records attributed to G Chomette.

At least 181 records · Page 10Linked to original sources
PubMed1984

Histoenzymological and ultrastructural study of a bifocal calcifying epithelial odontogenic tumor. Characteristics of epithelial cells and histogenesis of amyloid-like material.

A calcifying epithelial odontogenic tumor, simultaneously located in the two jaws (maxilla and mandible) was examined by histochemical and electron microscopic methods. Squamous tumor cells without secretory polarity were different from those of common ameloblastoma. High activities of alkaline phosphatase and ATPases were demonstrated by light and electron microscopy on the cytoplasmic membrane, findings similar to those in the stratum intermedium cells of the normal dental germ from which these tumor cells seem to arise. The tumor cells, like preameloblasts of the dental germ, also produce a granulo-filamentous material in intracytoplasmic vesicles and discharge it into the stroma. This "pseudo-amyloid" substance represents an abnormal protein of the enamel matrix and calcification, mainly occurring in that substance, might be an attempt at mineralization.

Adenosine Triphosphatases↗
PubMed1984

Renal immunopathology in renal cell carcinoma.

Signs of glomerulopathy, especially a nephrotic syndrome can occur in cancer patients, but the exact frequency of glomerular lesions is not well known in these patients. To define this frequency in a given type of malignancy we have studied the nephrectomy kidneys in 40 patients with renal cell carcinoma. Proteinuria, which was present in 7 cases, ranged from 0.15 to 1.5 g per 24 h. Reduction of the creatinine clearance greater than 50% was observed in 5 patients. Circulating immune complexes were detected in 11 of the 15 patients studied. Carcinoembryonic antigens were noted in 2 of 9 patients investigated. Research of alpha 1 foetoprotein carried out in 12 patients was always negative. HBs antigen or Hbs antibodies were detected in 6 of 29 patients studied. Light microscopic examination of the normal uninvolved kidney tissue showed obvious glomerular lesions (mesangial hypertrophy with or without deposits, with or without cell proliferation) in 7 patients (17.5%). Amyloid deposits were never observed. Immunofluorescence study revealed mesangial deposits in 35% of patients versus 5.4% of control subjects (P less than 0.0001). These deposits included C3 and/or IgM in 13 cases, IgA and C3 in one case. No fixation was observed, neither on tubules of normal tissue nor on carcinoma lesions. This report demonstrates that glomerular deposits are usually found in approximately one third of patients with renal cell carcinoma and that these deposits are located in the mesangial areas and not in the subepithelial space as it is often observed when glomerulonephritis is expressed by clinical symptoms.

Adenocarcinoma↗
PubMed1984

Iodine-induced thyrotoxicosis: analysis of eighty-five consecutive cases.

Iodine-induced thyrotoxicosis was documented in eighty-five cases. Eighty per cent occur in apparently normal thyroid glands; 60% among them occur in males. Amiodarone accounted for 50% of iodine-induced thyrotoxicosis. Mean thyroid hormone levels at diagnosis were: FT1: 21.7 (normal mean: 7.5, arbitrary units); T3: 4.53 nmol 1(-1) (normal: 2.30 nmol 1(-1). Mean 131I- 24-h uptake was 3.5% (normal range in France 25-45%) and was activated by exogenous TSH (mean 27%). The spontaneous cure in nontreated cases was observed within an average 6 months. A phase of biological hypothyroidism (mean FT1: 3.7, T3: 1.23 nmol 1(-1), TSH: 9.6 microU ml-1 (normal TSH range: 1-7 microU ml-1] preceded the return to euthyroidism. Intrathyroid iodine content measured by X-ray fluorescence was high, then fell gradually. Thyroid tissue study showed a large quantity of intrathyroid iodine and the overiodination of thyroglobulin. Histological and electron microscopic studies are reported. Prednisone and in some cases propylthiouracile were found to be effective.

Adolescent↗
PubMed1984

Arrhythmogenic right ventricular dysplasia: a clinical model for the study of chronic ventricular tachycardia.

Arrhythmogenic right ventricular dysplasia (ARVD) is a recently individualised clinical entity which sometimes presents with episodes of ventricular tachycardia (VT). These attacks may be resistant to anti-arrhythmic therapy and new therapeutic approaches have been developed for the treatment of this condition. These new methods are mainly surgical, based on the analysis of the electrical activation of the heart in sinus rhythm and during VT. This approach has increased our understanding of the physiopathology of VT, not only in the context of ARVD, but also in the most commonly encountered clinical setting of VT, after myocardial infarction. Electrophysiological study of the epicardial activation of the dysplastic zones has demonstrated the presence of delayed potentials recorded after the end of the QRS complex. This can be explained by the histopathology of these tissues. ARVD is characterised histologically by partial degeneration of the myocardial wall. Most of the muscle fibers are replaced by fatty tissue in the middle of which some healthy fibers survive. These changes are mainly observed in the intramyocardial and subepicardial layers, the subendocardium being almost normal. Strands of isolated muscle fibers within the non-conducting fatty degeneration may lead to very delayed activation with respect to the adjacent healthy tissues. The propagation of activation is delayed as it passes through this plexiform structure and in the zones adjacent to healthy muscle were reentry phenomena may arise. In ARVD, these changes are mainly located over the right ventricle, so explaining the right ventricular origin of most forms of VT observed in this condition. However, we have also observed a case which suggested an isolated arrhythmogenic left ventricular dysplasia. Epicardial mapping localizes the point of origin of VT in zones situated between the slow and normally conducting tissues. Simple ventriculotomy, a full thickness section of the ventricular wall, at the point of epicardial breakthrough of the VT prevents recurrence in the great majority of patients. The same pathophysiological concepts may be applied to VT complicating myocardial infarction but in this situation the myocardial fibers capable of slowly conducting the activation are isolated within the fibrous tissue in the border zone of the infarct. The point of origin of VT is usually within the interventricular septum with a point of epicardial breakthrough which could be located some distance away. Different surgical techniques have been developed to deal with this condition. Encircling endocardial ventriculotomy isolates the arrhythmogenic zone from the rest of healthy tissues by tracin

Adult↗
PubMed1984

[Significance of intraventricular conduction disorders observed in arrhythmogenic right ventricular dysplasia].

Correlations between surface ECGs, epicardial mapping and histological data in 15 cases of arrhythmogenic right ventricular dysplasia (ARVD) provide information about the possible mechanism of intraventricular conduction defects in about one third of cases. Two cases in this series had complete right bundle branch block and 4 cases showed diffuse intraventricular conduction defects. The other cases had normal ECGs. The point of origin of the activation in 11 cases was situated in the left ventricle, even in 6 of the 9 cases with normal ECGs. The points of latest activation were located over the right ventricular free wall near the atrio-ventricular groove. However, in all cases but one, a normal right ventricular point of origin was observed, suggesting participation of the right bundle within a free wall showing delayed activation. This activation showed very irregular delayed propagation due to the zones of dysplasia. These results suggest that in ARVD, the mechanism of the conduction defects is not disease of the bundle branch itself but a distal block probably situated in the right ventricular wall. This hypothesis is supported by the histological appearances of the dysplastic zones.

Adult↗
PubMed1984

Histoenzymological features of epithelial cells in epidermoid carcinomas of oral mucosa and in ameloblastomas of jaws.

An histoenzymological study comprising oxidative enzymes, diaphorases, acid and alkaline phosphatases, naphtolesterases, referred to 60 biopsy and operation specimens. It showed interesting arguments for diagnosis and understanding of precancerous and cancerous lesions of the oral mucosa and also of ameloblastomas of jaws. The enzymatic activities of precancerous and cancerous oral lesions were compared with those of normal buccal mucosa and epidermis, benign hyperkeratosis (activities similar to those of the epidermis) and lichen planus. In severe dysplasia and epidermoid carcinoma, numerous variations of oxidative, esterase and acid phosphatase activities were seen from one cell to another. But this pattern was non conclusive for the diagnosis, a similar one being found in inflammatory lesions and especially in the lichen planus. In lobules of invasive carcinoma, the strong enzymological activities (particularly acid phosphatases, naphtolesterases) were correlated with a high degree of differentiation of the tumor and these enzymatic methods offered an interesting contribution for the fine evaluation of histoprognosis in malignant epithelial tumors. Among the lesions of jaws, radicular and dentigerous cysts had low enzymatic activities similar to those of normal buccal epithelium. The epidermoid cysts (keratocysts), because of their highly differentiated keratinization, like benign hyperkeratosis, had the same enzymatic activities as epidermis. Peculiar were the enzymatic activities of common ameloblastoma; they differed from those of other lesions of squamous tissues (low oxidative activities without decreasing gradient). Besides, round epithelial clumps, the stroma showed a high and widespread alkaline phosphatase activity. Thus, this peculiar stromal activity may be useful to differentiate ameloblastoma from the other epidermoid cysts of the jaws. In the other hand, such a constatation suggests a low degree of odontogenic induction.

Ameloblastoma↗
PubMed1984

[Visceral scleroderma].

Visceral involvement in systemic scleroderma is frequent, the most commonly affected organs being the kidney, the lung, the heart and the gastro-intestinal tract; associating different degrees of sclerosis and vasculitis depending on which organ is involved. However, this is not always clinically obvious, and angiospastic phenomena may be assumed to be responsible for certain ischaemic lesions. The diagnosis is also difficult because some visceral lesions may occur at an early stage and appear to be of primary origin. Extensive investigation, including biopsies to demonstrate small vascular changes then becomes essential.

Digestive System Diseases↗
PubMed1984

[Hemangiopericytoma of the orofacial region].

Prognosis in 11 cases of hemangiopericytoma of the orofacial region (9 buccal and 2 parotid tumors) was, as with these lesions in other zones, an uncertain entity: 4 local recurrences within 8 months to 7 years; one fatal outcome after 3 years from pulmonary micrometastases. Histologic classification of these tumors into 3 cytologic groups of increasing malignancy (I to III) is a function of the number of their cytologic anomalies. They are also divided according to their overall morphology into poorly differentiated, differentiated and sclerous types. Positive correlations between structure and cytologic criteria of malignancy and structure and clinical course have been demonstrated. Ultrastructural examination in 2 cases showed polymorphic endothelial, fibroblastic and smooth muscle cells in contact with adult tumoral pericytes. This suggests the origin of the tumor from young cells of multiple potency rather than from adult pericytes.

Adolescent↗
PubMed1984

Acinic cell tumors of salivary glands. Frequency and morphological study.

Among 873 salivary gland tumors, 15 cases of acinic cell tumors were found (frequency of 1.6%). They occurred approximately evenly in man and women, the mean age being 41 years. They were located principally in the major salivary glands (12 cases in the parotid and 1 case in the submandibular gland) and only twice in accessory glands. Histologically, these tumors were divided into two groups: group I = highly differentiated tumors (less than 20% undifferentiated cells) and group II = poorly differentiated tumors (more than 20% undifferentiated cells). These histological feature seems to play a role in the clinical behaviour of these neoplasms. Thus, the 9 patients with highly differentiated tumors were alive and well 5 to 22 years after the treatment. On the other hand, 5 of the 6 patients with poorly differentiated tumors had local recurrences (4 cases) and lethal metastases to distant lymph nodes and bone (3 cases). The ultrastructural study corroborated the analogy of differentiated tumoral cells with normal acinic cells (numerous secretory granules and ergastoplasmic cisternae). Moreover, the undifferentiated cells had numerous ribosomes and their morphological structure was similar to that of intercalated duct cells. The histogenesis of this rare tumor is discussed. The acinic cell tumor seems more likely to arise from immature cells of intercalated ducts than from adult acinic cells.

Adult↗
PubMed1984

[Bifocal odontogenic calcified epithelial tumor (Pindborg's tumor). A morphologic and ultrastructural study].

Histoenzymologic and ultrastructural examinations were conducted on a doubly located calcified odontogenic epithelial tumor. The cells of the tumor, developing in both the maxilla and mandible, differed from those of the common ameloblastoma, being all of the malpighian type without any secretory polarity. Furthermore, optical and electronic microscopy showed evidence of marked alkaline phosphatases and ATPases activity in their numerous peripheral microvilli. These identical activities to those of the stratum intermedium could suggest the origin of the tumor from these latter cells. But, like the preameloblasts of the dental germ, these tumoral cells produce in their intracytoplasmic vesicles and then excrete into the stroma, a granulofilamentous substance, pseudo-amyloid, which could thus represent an abnormal protein of the enamel matrix. The calcifications, mainly present in this amyloid-like substance, are the expression of an attempt to mineralize this abnormal matrix. Stromal calcifications may result from a sketchy odontogenetic induction, as shown by the intense activity of ATPases and alkaline phosphatases on the fibroblastic cytoplasm membranes.

Adult↗