For example, the fermented bean product miso is less likely to produce as much intestinal gas. Some legumes also stand up to prolonged cooking, which can help break down the oligosaccharides into simple sugars. Fermentative lactic acid bacteria such as Lactobacillus casei and Lactobacillus plantarum reduce flatulence in the human intestinal tract.Probiotics (live yogurt, kefir, etc.) are reputed to reduce flatulence when used to restore balance to the normal intestinal flora. Live (bioactive) yogurt contains, among other lactic bacteria, Lactobacillus acidophilus, which may be useful in reducing flatulence. L. acidophilus may make the intestinal environment more acidic, supporting a natural balance of the fermentative processes. L. acidophilus is available in supplements. Prebiotics, which generally are non-digestible oligosaccharides, such as fructooligosaccharide, generally increase flatulence in a similar way as described for lactose intolerance. Digestive enzyme supplements may significantly reduce the amount of flatulence caused by some components of foods not being digested by the body and thereby promoting the action of microbes in the small and large intestines. It has been suggested that alpha-galactosidase enzymes, which can digest certain complex sugars, are effective in reducing the volume and frequency of flatus. The enzymes alpha-galactosidase, lactase, amylase, lipase, protease, cellulase, glucoamylase, invertase, malt diastase, pectinase, and bromelain are available, either individually or in combination blends, in commercial products. The antibiotic rifaximin, often used to treat diarrhea caused by the microorganism E. coli, may reduce both the production of intestinal gas and the frequency of flatus events.
Renal management of phosphate is impaired in secondary hyperparathyroidism which results in hyperphosphatemia.Primary hyperplasia of the parathyroid gland, results from both hypocalcaemia and increased phosphate levels by decreasing expression of calcium sensing receptors and vitamin D receptors at the parathyroid gland. These decreases in receptor expression lead to hyperfunctioning of the parathyroid. Hyperfunction of the parathyroid gland is thought to exacerbate primary hyperplasia which evolves further to a secondary more aggressive hyperplasia. Histologically, these hyperplasic glands can be either diffuse or nodular. Primary hyperplasia, usually resulting in diffuse polyclonal growth is manly related to reversible secondary hyperparathyroidism. Secondary hyperplasia of the parathyroid gland is more often a nodular, monoclonal growth that sustains secondary hyperparathyroidism and is the catalyst in the progression to tertiary hyperparathyroidism. Nodular hyperplastic glands in tertiary hyperparathyroidism are distinctly larger in both absolute size and weight up to 20-40-fold increases have been reported. Parathyroid glands are normally composed of chief cells, adipocytes and scattered oxyphil cells. Chief cells are thought to be responsible for the production, storage and secretion of parathyroid hormone. These cells appear light and dark with a prominent Golgi body and endoplasmic reticulum. In electron micrographs, secretory vesicles can be seen in and around the Golgi and at the cell membrane. These cells also contain prominent cytoplasmic adipose. Upon onset of hyperplasia these cells are described as having a nodular pattern with enlargement of protein synthesis machinery such as the endoplasmic reticulum and Golgi. Increased secretory vesicles are seen and decreased intercellular fat is characteristic.