[PATHOLOGY OF THE THYMUS GLAND. (PRESENT-DAY KNOWLEDGE)].
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Differentiation of massive thymic hyperplasia from malignant lesions requires early resection. We report a case in which thoracoscopic thymectomy was performed for massive hyperplasia recurring 16 years after steroid therapy. This case provides additional information on the natural history, surgical management and histology of the disease.
Little is known about the immunotoxicity of the organophosphate pesticide, diazinon. This study aims at detailing the pathologies in the thymus, spleen, blood cells, and lymph nodes (brachial, mesenteric, and hind quarter gluteal nodes) during chronic oral exposure (300 mg diazinonkg-1 food for 45 days), and explore the combined toxicity with excess dietary protein (40%) or lipid (20% corn oil). Animals were allowed to recover on normal food for 2 weeks. All experimental treatments caused organ pathologies, including necrotic degeneration of the trabeculae (spleen and thymus), hyperplasia of the cortex and medulla (thymus and lymph nodes), hyperplasia of white and red pulp (spleen), and sometimes haemorrhage (all tissues). Blood smears often showed crenated/hypochromic red cells and vacuolated white cells with abnormal nuclei. The severity of lesions during exposure was generally in the following order: lipid<protein<diazinon alone<protein plus diazinon<lipid plus diazinon. Post-exposure recovery was limited, especially in the thymus and for lipid treatments. Quantitative image analysis revealed treatment and organ-specific changes in the proportions of fixed lymphocytes, PAS-positive carbohydrates, DNA, and protein staining. Histochemical changes were greatest after exposure. We conclude that the immunotoxicity of diazinon is exacerbated by excess dietary protein or lipid. The limited recovery and post-exposure histochemical changes imply deleterious effects on metabolism with oxidative stress after exposure.
Histological diagnosis of space-occupying lesions in the anterior mediastinum is rarely possible using conventional radiological diagnoses; computer tomography in our opinion often makes this possible. Our experience is based on 47 tumours which have been investigated histologically. In the anterior upper or middle mediastinum there were thymic tumours (thymona, thymus hyperplasia or persistence of the thymus), retrosternal thyroids, malignant lymphomas, teratoid cysts, one seminoma and one aneurysm. In the anterior inferior mediastinum, we found pericardial cysts, lipomas and one Morgagni hernia. The computer tomographic features of these various lesions are described. Some tumours can be defined histologically by computer tomography alone, whereas others (e.g. solitary lymphoma, benign thymoma) make it necessary to consider the clinical features in addition. Computer tomography is particularly valuable in the diagnosis of persistence of the thymus, since standard radiography in two planes fails to show the lesion.
Autoantibodies against the muscle acetylcholine receptor (AChR) play an essential role in the pathophysiology of autoimmune myasthenia gravis (MG). Their serum titers, however, vary considerably among patients. Our aim was to investigate whether their variation might be explained by genetic factors. Using different methods, we have obtained strong evidence for a three-locus association influencing autoantibody titers in MG patients with thymus hyperplasia or with a normal thymus. Two of the loci, one encoding the AChR alpha-subunit, the other encoding the alpha-chain of the class II antigen-presentation molecule, HLA-DQ, demonstrated interaction to determine high autoantibody titers. The third locus was associated with the 8.1 ancestral HLA haplotype. It exerted an additive effect and it is postulated to have a nonantigen specific immunoregulatory function. Our study demonstrates for the first time that polymorphism of an autoantigen gene may quantitatively modify the immune response against it. Altogether, the data lend support to a three-gene model to explain autoantibody expression in a subset of MG patients.
Four transgenic mice carrying the human activated c-Ha-Ras gene, the expression of which was driven into the thyroid gland by a bovine thyroglobulin promoter, have been produced. The M1 and M2 mice developed papillary thyroid carcinomas and the M2 mouse also developed a lung carcinoma, however none of them transmitted the transgene. Both the M3 and the M4 mice gave rise to transgenic lines. M3 progeny mice develop a goitre with morphological aspects of hyperplasia as well as a thymus hyperplasia. M4 developed a papillary thyroid carcinoma and a lung carcinoma. Lung tumors but not thyroid tumors were observed in M4 adult transgenic progeny. In this M4 line, thyroid dysgenesis leading to growth retardation and premature death was observed upon serial backcross that enhanced the DBA/2J genetic background. The development of thyroid tumors in M1, M2, M4 transgenic mice demonstrates the oncogenic potential of activated Ras gene in the thyroid gland. The M4 line raises interesting questions relative to the interference between the Ras-mediated signal transduction pathway and thyroid morphogenesis.
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The radioimmunological method was applied in the study of ACTH, STH, and prolactin content in thymomegaly combined with pneumonia, and in practically healthy children. A comparative analysis of hormonal parameters depending on the functional condition of the thymus demonstrated a directly proportional correlation between the STH, prolactin level, and the thymus hyperplasia; there proved to be a reverse relationship between the ACTH level and thymomegaly. Hypoadrenocorticotropinemia, hypersomatotropinemia, and hyperprolactinemia could be used as diagnostic criteria in thymomegaly.
INTRODUCTION: Celiac disease is an autoimmune enteropathy that appears on a predisposed genetic background. Its clinical presentation has been extended those last years by varied extradigestive manifestations. EXEGESIS: This is a case report of a twenty-year-old woman who presented simultaneously a celiac disease and pure red cell aplasia. The IgA and IgG antigliadin antibodies as well as antinuclear, anti-DNA, anti-SSA and anti-SSB antibodies were detected, without any clinical symptom supporting the diagnosis of systemic lupus erythematosus or Sjögren syndrome. Thoracic CT-scan reveals a thymus enlargement and biopsy concludes to thymus hyperplasia at histological examination. Pure red cell aplasia regressed after gluten-free diet, corticoid therapy and thymectomy. CONCLUSION: This observation, added to the three others paediatric cases previously published in the literature concern an uncommon association between pure red cell aplasia and celiac disease. However, they are not enough to conclude to a direct link between these two disorders. Pure red cell aplasia could represent un new dysimmune manifestation occurring in celiac disease, but this will need to be confirmed with others cases.
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The so-called lymphofollicular hyperplasia, which is caused by the occurrence of hyperplastic lymph follicles within the organ, is constantly associated with autoimmune diseases (e.g., myasthenia gravis) and in rare instances with malignant tumors. The architecture of lymphofollicular hyperplasia was studied immunohistochemically using antibodies against epithelial, vascular, lymphocytic, and histiocytic antigens. There is evidence, that the configuration, microtopography, cellular composition, and immunohistological findings of the lymph follicles with germinal centers in the myasthenic thymus are essentially the same as in those occurring in lymph nodes and in other lymphatic tissue. Furthermore it could be shown that the follicles originate in the interlobular septal space and displace the thymic parenchyma by extension.
Potentialities of the modulation of thymus function with thymalin and the hormonal-immunological status in simulated hypo- and hyperplasia of the thymus. The advisability of the use of the drug was shown.
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