Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liquorice extract has been claimed to induce inhibition of the activity of 11 beta-hydroxysteroid dehydrogenase which converts cortisol to cortisone. This enzyme is thought to protect the mineralocorticoid receptor from being occupied by endogeneous glucocorticoids in the kidney. Based on these hypotheses, we investigated the effect of low-dose glycyrrhizine on hyperkalemia due to hyporeninemic hypoaldosteronism in eight subjects with NIDDM. The mean serum potassium concentration decreased from 5.3 +/- 0.3 (SD) mEq/1 to 4.9 +/- 0.2 mEq/1 when 15 g of calcium polystyrene sulfonate, a potassium-binding resin, was given per day, and it decreased significantly to 4.4 +/- 0.4 mEq/1 with 150 mg/day of glycyrrhizine therapy. Changes in fasting plasma glucose and hemoglobin A1c were not significant. These data support the assumption that liquorice extract can be used safely in the therapy for treating hyperkalemia due to selective hypoaldosteronism in diabetes mellitus subjects.
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PMID:Effect of glycyrrhizine on hyperkalemia due to hyporeninemic hypoaldosteronism in diabetes mellitus. 833 14

During long-term treatment of arterial hypertension with calcium antagonists of the dihydropyridine type activation of the sympathetic nervous system and subsequently also of the renin-angiotensin-aldosterone system persists, while the haemodynamic reaction to vasodilatation, manifested by an elevated pulse rate and minute volume from the initial stage of therapy, recedes. In type II diabetics the basal and stimulated response of the renin-angiotensin-aldosterone system is reduced. The administration of calcium antagonists of the dihydropyridine type does not stimulate significantly the renin-angiotensin-aldosterone system as the starting function of the sympathetic nervous system is impaired within the framework of vegetative neuropathy. In almost 20% NIDDM plasma renin activity and aldosterone do not respond to furosemide administration and the vertical posture. In others the response is found but takes place at reduced levels. Hyporeninaemic hypoaldosteronism is thus manifested not so much by a drop of plasma renin and aldosterone beneath the lower range of reference values as by a reduced response to stimulation. Functional hyporeninaemic hypoaldosteronism is another, frequent late complication of diabetes. In advanced forms a further block of the renin-angiotensin-aldosterone system by ACE inhibitors can then produce, even in the absence of diabetic nephropathy, in the stage of chronic renal failure dangerous hyperkaliaemia which may threaten the patient. Dynamic examination of the sympathetic nerve and the renin-angiotensin-aldosterone system makes it possible to predict this condition. In practice it is necessary in diabetics with arterial hypertension after starting with ACE inhibitors during the first days to monitor repeatedly plasma potassium and creatinine. ACE inhibitors and calcium antagonists are otherwise for diabetics drugs of first choice which can arrest the progression of nephropathy, effectively reduced the blood pressure without causing deterioration of insulin resistance and hyperlipoproteinaemia and lead even to regression of hypertrophy of the vascular wall and left ventricle.
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PMID:[The effect of long-term treatment of arterial hypertension with Ca antagonists on the renin-angiotensin-aldosterone system in diabetics. Hyporeninemic hypoaldosteronism]. 857 95

Isolated hypoaldosteronism is found in 75% diabetics where the disease has persisted for 10 or more years. Sporadically it is found in congenital autonomous neuropathy, in acute glomerulonephritis, in gouty kidney, tubulointerstitial nephritis, after transplantation of the kidney, on mytomycin etc. During dynamic testing of the response of plasma renin activity and aldosterone to the administration of furosemide and a vertical position in diabetics a significantly reduced response was recorded as compared with non-diabetic hypertonic subjects. In 18.3% no response was observed (decompensated form of IHH). Diabetic hypertonics behaved like control hypertonics on long-term beta-blocker treatment. In the decompensated form of IHH after administration of drugs interfering with the activity of SNS-RAAS activity (ACEI, spirolactone etc.) a hyperkalaemic crisis may develop which threatens the patient with acidosis, dehydration, myoplegia, muscular spasms, however, in particular with fatal disorders of the cardiac rhythm. A similar effect may be exerted also by blockers of prostaglandin synthetase (non-steroid antirheumatics) and other drugs. The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. IHH is thus another serious but rarely diagnosed late complication of diabetes which depends only partly on the stage of DN. It must be, however, diagnosed and respected with regard to the selection of drugs for the treatment of arterial hypertension and the syndrome of insulin resistance and the 5H syndrome resp., i.e. the association of hyperinsulinism which compensates insulin resistance with hyperglycaemia (NIDDM), hypertension, hyperlipoproteinaemia and hirsutism in women (so-called Stein-Leventhal syndrome).
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PMID:[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]. 892 9

Type IV renal tubular acidosis (RTA) is the only RTA characterized by hyperkalemia, and it is caused by a true aldosterone deficiency or renal tubular aldosterone hyporesponsiveness. It is frequent among hospitalized patients as it is related to type 2 diabetes mellitus (T2DM) and common medications such as ACE-inhibitors (ACE-is) and trimethoprim-sulfamethoxazole (TMP-SMX). Drug-induced RTA commonly manifests in patients with predisposing conditions such as mild renal insufficiency and certain pharmacological therapies. ACE-i use and chronic adrenal insufficiency (cAI) are other significant risk factors. Chronic ACTH suppression is thought to induce global adrenal atrophy, including the zona glomerulosa, thus affecting aldosterone secretion as well. Furthermore, in the setting of cAI, treatment with ACE-is further suppresses aldosterone production. This case report describes a patient with cAI secondary to corticosteroid use for years who developed type IV RTA in the setting of lisinopril use. Potassium (K) elevation persisted despite removing underlying conditions and metabolic acidosis correction. The patient required long-term treatment with mineralocorticoids in addition to sodium bicarbonate to maintain normal K levels and acid-base status. Mineralocorticoid administration is a second-line treatment for type IV RTA, but it might be necessary for a subgroup of high-risk patients. In fact, it is important to consider patients with chronic adrenal insufficiency and on ACE-is treatment at increased risk for refractory hyperkalemia in the setting of type IV RTA. Indeed, this subgroup of patients can have severe hypoaldosteronism.
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PMID:Type IV RTA in Chronic Adrenal Insufficiency and Concomitant Lisinopril Treatment. 3313 4