G-cell hyperplasia

After the morphologic and immunocytochemical localization of these G cells, numerous investigators attempted to relate alteration of the numbers of these cells to various disease processes. The condition of G-cell hyperplasia was initially thought to represent a cause of peptic ulcer disease, whereas in conditions of achlorhydria, significant hyperplasia of the G cells was felt to be related to the hypergastrinemia that accompanied pernicious anemia and atrophic gastritis. 

T3. Tlirbat-Herrera, E. A., Hancock, C., Cabello-Inchausti, B., and Herrera, G. A., Plasma cell hyperplasia and monoclonal paraproteinemia in AIDS. Arch. Pathol. Lab. Med. 17(5), 497-501 (1993). 

A normal rate of thyroid hormone synthesis depends on an adequate dietary intake of iodine. Iodine is naturally present in water and soil, although some soils contain very low amounts. As a result, seafood is a more reliable source of iodine than crop plants. Approximately 1.6 billion people in more than 100 countries live in areas where natural sources of dietary iodine intake are marginal or insufficient. A minimum of 60 j.g of elemental iodine is required each day for thyroid hormone synthesis, and at least 100 j.g/day is required to eliminate thyroid follicular cell hyperplasia and thyroid enlargement (i.e., iodine deficiency goiter). 

Evidence for thyroid hormone involvement in PBDE toxicity includes observations in rats and mice that were orally exposed to commercial mixtures of deca-, octa-, or pentaBDE (see Section 3.2.2.2, Endocrine Effects). The main findings include (1) histological changes in the thyroid indicative of glandular stimulation (e.g., follicular cell hyperplasia similar to that induced by a hypothyroid state) (IRDC 1976 Norris et al. 1973, 1975b NTP 1986 WIL Research Laboratories 1984), and (2) decreased serum... 

Clegg, E.D., J.C. Cook, R.E. Chapin, P.M. Foster, and G.P. Daston. 1997. Leydig cell hyperplasia and adenoma formation Mechanisms and relevance to humans. Reprod. Toxicol. 11 (1) 107-121. 

Substances that have been associated with increases in Leydig cell tumours in mice are mainly chemicals with clear oestrogenic properties, e.g., diethylstilboestrol, methoxychlor, tri-p-anisylchloroethylene, stilboestrol, 17/3-oestradiol, oestradiol ester, tamoxifen and triphenylethylene [171-179]. Other compounds active in mice are finasteride, a 5a-reductase inhibitor that also induces Leydig cell hyperplasia, but not adenomas, in Sprague-Dawley rats [170,180] and M-nitrosodiethylamine [181]. In contrast to its effects in mice and Syrian and European hamsters [182], 17)d-oestradiol treatment of rats does not induce Leydig cell tumours and inhibits the appearance of the spontaneous tumours in the F344 strain [184]. 

Hooth, M.J., DeAngelo, A.B., George, M.H., Gaillard, E.T., Travlos, G.S., Boorman, G.A. Wolf, D.C. (2001) Subohronic sodium chlorate exposure in drinking water results in a ooncentration-dependent increase in rat thyroid follicular cell hyperplasia. Toxicol. Pathol. 29(2), 250-259,... 

Eissele R, Brunner G, Simon B, et al. Gastric mucosa during treatment with lansoprazole Helicobacter pylori is a risk factor for argyrophil cell hyperplasia. Gastroenterology 1997 112 707-717. 

G. Neuroendocrine Cell Hyperplasia with Bronchiolar Fibrosis... 

This is a condition in which there is excessive secretion of gastric juice as a result of gastrin secretion, usually by a pancreatic tumour or, less commonly, from hyperplasia of the G cells of the stomach. The continuous secretion of gastric juice results in... 

Borch K, Renvall H, Liedberg G (1985) Gastric endocrine cell hyperplasia and carcinoid tumors in pernicious anemia. Gastroenterology 88 638-648... 

G. R. Lankas and C. P. Peter, Induction of reversible urothelial cell hyperplasia in rats by clorsulon, a flukicide with weak carbonic anhydrase inhibitory activity. Food Chem. Toxicol., 1992, 30, 297-306. 

Komminoth, P., Roth, J., Saremaslani, P., Matias, G. X., Wolfe, H. J., and Heitz, P. U., 1994, Polysialic acid of the neural cell adhesion molecule in the human thyroid A marker for medullary thyroid carcinoma and primary C-cell hyperplasia. An immunohistochemical study on 79 thyroid lesions. Am. J. Surg. Pathol. 18 399-411. 

Renal Effects. Exposure to lead that results in PbB ranging from approximately 60 to >100 pg/dL has been associated with nephropathy in some studies of lead-exposed workers (e.g., Chia et al. 1995a). The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, few or no nuclear inclusion bodies,... 

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