Alzheimer's Disease Slideshow Pictures Take the Alzheimer's Quiz Acetil-L-Carnitina, Acetyl Carnitine, Acétyl Carnitine, Acetyl L-Carnitine, Acétyl-L-Carnitine, Acetyl-L-Carnitine Arginate Dihydrochloride, Acetyl-L-Carnitine Arginate HCl, Acétyl-L-Carnitine Arginate HCl, Acetyl-L-Carnitine HCl, Acétyl-L-Carnitine HCl, Acetyl L-Carnitine Hydrochloride, Acetyl Carnitine, Acétyl-Carnitine, Acetyl-Levocarnitine, Acétyl-Lévocarnitine, ALC, Alcar, Carnitine Acetyl Ester, Dihydrochlorure d'Acétyl-L-Carnitine Arginate, Gamma-Trimethyl-Beta-Acetylbutyrobetaine, L-Acetylcarnitine, L-Acétylcarnitine, Levacecarnine, N-Acetyl-Carnitine, N-Acétyl-Carnitine, N-Acetyl-L-Carnitine, N-Acétyl-L-Carnitine, ST-200, Vitamin B(t) Acetate, 2-(acetyloxy)-3-carboxy-N,N,N-trimethyl-1-propanaminium inner salt; (3-carboxy-2-hydroxy-propyl)trimethylammonium hydroxide inner salt acetate. Acetyl-L-carnitine is an amino acid (a building block for proteins) that is naturally produced in the body.
It helps the body produce energy. Acetyl-L-carnitine is used for a variety of mental disorders including Alzheimer's disease, age-related memory loss, late-life depression, thinking problems related to alcoholism, and thinking problems related to Lyme disease. It is also used for Down syndrome, poor circulation in the brain, cataracts, nerve pain due to diabetes, nerve pain due to drugs used in the treatment of AIDS, and facial paralysis. Some men use acetyl-L-carnitine for infertility, symptoms of "male menopause" (low testosterone levels due to aging), and a disease of the penis called Peyronie's disease. The body can convert L-carnitine to acetyl-L-carnitine and vice versa. But, no one knows whether the effects of acetyl-L-carnitine are from the chemical itself, from the L-carnitine it can make, or from some other chemical made along the way. For now, don't substitute one form of carnitine for another. More evidence is needed to rate the effectiveness of acetyl-L-carnitine for these uses.
Natural Medicines Comprehensive Database rates effectiveness based on scientific evidence according to the following scale: Effective, Likely Effective, Possibly Effective, Possibly Ineffective, Likely Ineffective, and Insufficient Evidence to Rate (detailed description of each of the ratings). Next: How does Acetyl-l-carnitine work? Report Problems to the Food and Drug Administration You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.INTRODUCTIONHypocalcemia is a common problem after parathyroidectomy or thyroidectomy. The fall in serum calcium is primarily due to functional or relative hypoparathyroidism, leading to reductions in bone reabsorption and increases in bone formation, leading to an increased influx of calcium into bone and, in patients without end-stage renal disease, increased calcium excretion and decreased intestinal calcium absorption due to reduced parathyroid hormone (PTH)-mediated renal 1,25-dihydroxycholecalciferol (1,25(OH)2D) production.
A less frequent contributing factor is acute calcitonin release from the thyroid gland.The hypocalcemia is generally transient because the degree of bone disease is typically mild and normal parathyroid tissue recovers function quickly (usually within one week), even after long-term suppression.In some cases, however, the postoperative hypocalcemia is severe and prolonged, despite normal or even elevated levels of PTH. This phenomenon, called the hungry bone syndrome, most often occurs in patients who have developed bone disease preoperatively due to a chronic increase in bone resorption induced by high levels of PTH (osteitis fibrosa) [1,2]. The underlying hyperparathyroidism can either be primary or secondary due to end-stage renal disease. In addition to parathyroidectomy, a less severe hypocalcemic syndrome can occur in patients with end-stage renal disease who are treated with calcimimetics, which reduce PTH secretion by modulating the calcium-sensing receptor in the parathyroid glands [3].
(See "Indications for parathyroidectomy in end-stage renal disease".)In addition to reduced serum calcium, reduced serum phosphate and increased serum potassium levels may be observed in hungry bone syndrome. The decreased serum calcium and phosphate and increased potassium likely reflect increased bone influx and efflux, respectively. (See 'Clinical features' below.)Hungry bone syndrome has also been described after thyroidectomy in patients with hyperthyroidism [4,5]. In such patients, the preoperative bone disease is due to high bone turnover induced by excess thyroid hormone. A less common cause is estrogen therapy in patients with metastatic prostate cancer [6]. To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you: Medical Professional or Student The content on the UpToDate website is not intended nor recommended as a substitute
for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. use of this website is governed by the UpToDate Terms of Use Albright F, Reifenstein EC Jr. The parathyroid glands and metabolic bone disease, Williams & Wilkins, Baltimore 1948.Brasier AR, Nussbaum SR. Hungry bone syndrome: clinical and biochemical predictors of its occurrence after parathyroid surgery. Am J Med 1988; 84:654.Goodman WG, Frazao JM, Goodkin DA, et al. A calcimimetic agent lowers plasma parathyroid hormone levels in patients with secondary hyperparathyroidism. 58:436.DENT CE, HARPER CM. Hypoparathyroid tetany (following thyroidectomy) apparently resistant to vitamin D. Proc R Soc Med 1958; 51:489.Jones RM, Davidson CM. Thyrotoxicosis and the hungry bone syndrome: a cause of postoperative tetany. J R Coll Surg Edinb 1987; 32:24.Vogelgesang SA, McMillin JM. Hypocalcemia associated with estrogen therapy for metastatic adenocarcinoma of the prostate.
140:1025.Jofré R, López Gómez JM, Menárguez J, et al. Parathyroidectomy: whom and when? Kidney Int Suppl 2003; Felsenfeld AJ, Gutman RA, Llach F, et al. Postparathyroidectomy hypocalcemia as an accurate indicator of preparathyroidectomy bone histology in the uremic patient. Miner Electrolyte Metab 1984; 10:166.Falko JM, Bush CA, Tzagournis M, Thomas FB. Congestive heart failure complicating the hungry bone syndrome. Am J Med Sci 1976; 271:85.Shinoda T, Aizawa T, Shirota T, et al. Exacerbation of latent heart failure by mild hypocalcemia after parathyroidectomy in a long-term hemodialysis patient. 60:482.Benz RL, Schleifer CR, Teehan BP, et al. Successful treatment of postparathyroidectomy hypocalcemia using continuous ambulatory intraperitoneal calcium (CAIC) therapy. Perit Dial Int 1989; 9:285.Cruz DN, Perazella MA. Biochemical aberrations in a dialysis patient following parathyroidectomy. Am J Kidney Dis 1997; 29:759.Shpitz B, Korzets Z, Dinbar A, et al. Immediate postoperative management of parathyroidectomized hemodialysis patients.