Primary aldosteronism is characterized by high blood pressure, caused by increased retention of salt and water by the kidneys, and low serum potassium concentrations (hypokalemia), caused by excess excretion of potassium in the urine. The symptoms and signs of aldosterone excess include not only hypertension but also muscle weakness and cramps and increased thirst and urination. Primary aldosteronism is usually caused by a benign adrenal tumour (adenoma), but some patients have hyperplasia of both adrenal glands. Successful removal of the adrenal tumour usually results in reduction in blood pressure and cessation of potassium loss; patients with bilateral adrenal hyperplasia are treated with antihypertensive drugs.
Animal tests on the effect of mometasone furoate on embryonic development in rabbits revealed depressed body weight from mg/kg/BWT upwards. After topical treatment of rabbits, the progeny suffered various types of malformation, such as crooked front paws, cleft palate, gallbladder agenesis and umbilical hernia. In the rat, embryolethal effects from μg/kg/BWT (subcutaneous) and poor development from mg/kg/BWT (topical) (depressed body weight, delayed ossification) and substance-related increase in umbilical hernia were observed. When the drug was administered to mothers close to the birth date, protracted labour and difficult births were observed.
Another set of problems may arise if the disease is due to chemical poisoning. This happened to Simon Kelly as reported on his website . He had developed MG once before, apparently due to extensively working with oil paints in a confined space. Six years later he had another stressful period during which he painted his house and burned off old paint. Not only did he develop MG a second time, but his blood became very alkaline and his red blood cells ‘looked like sea urchins’, shriveled up, black, and full of spikes. He also believes that a high consumption of soymilk contributed to his condition by causing intestinal inflammation and diarrhea.