Calcium rebound

Discuss calcium rebound with respect to antacids. 

Calcium-containing antacids—rebound hyperacidity, metabolic alkalosis, hypercalcemia, vomiting, confusion, headache, renal calculi, and neurologic impairment... 

Antacids containing calcium carbonate have the greatest neutralising capacity but tend to cause acid rebound with long-term use. Calcium carbonate may also lead to hypercalcaemia and the milk-alkali syndrome, which is characterised by nausea, headache and renal damage. 

NaHCOs and CaCOs can neutralize HCl rapidly, depending on particle size and crystal structure, and effectively. NaHCOs acts rapidly but absorption of unneutralized NaHCOs produces risks for alkalosis and sodium retention which may lead to edema, hypertension or heart failure. Also neutralized antacids may cause alkalosis by permitting the absorption of endogenous NaHCOs. Ca + may stimulate the secretion of gastrin and HCl and calcium-containing antacids have been associated with rebound acid hypersecretion. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

The physician is concerned with at least three factors when prescribing antacids (1) Acid rebound (associated with calcium carbonate) (2) milk-alkali syndrome (caused by ingestion of large quantities of alkali) and (3) phosphorus depletion (by aluminum salts). The mechanism of add rebound, especially in the long-term use of caldum carbonate, is poorly understood. It has been established that there is an excessive re-addification of the antrum (pylonc gland area) a number of hours after ingestion of calcium caibonate. 

T-type calcium channels play critical roles in shaping the electrical and plastic properties of neurons and are also implicated in hormone secretion, differentiation and muscle development (Huguenard, 1996 Perez-Reyes, 2003). In thalamic reticular and relay neurons, T-type channels contribute to rhythmic rebound burst firing and spindle waves associated with slow-wave sleep. T-type channels also play crucial roles in dendritic integration and calcium-mediated spiking in hippocampal pyramidal cells, and in synaptic release at olfactory dendrodendritic... 

Hade JE, Spiro HM. Calcium and acid rebound a reappraisal. J Clin Gastroenterol. 1992 15 37-44. 

Simoneau G. Absence of rebound effect with calcium carbonate. Eur J Dmg Metab Pharmacokinet 1996 21(4) 351-7. 

Freedman SB, Daxini BV, Noyce D, Kelly DT. Intermittent transder-mal nitrates do not improve ischemia in patients taking beta-blockers or calcium antagonists Potential role of rebound ischemia during the nitrate-free period. J Am Coll Cardiol 1995 25 349-355. 

Recall that calcium is a factor in the stimulation of the release of gastric acid. Thus, a calcium-containing antacid will first neutralize stomach acid, bringing the pH up, but the calcium may then produce a "rebound effect by stimulating release of additional acid. 

Antacids continue to be used by patients for a variety of indications. Many factors, including palata-bility, determine the effectiveness and choice of antacid (Table 36-1). Although sodium bicarbonate effectively neutralizes acid, it is very water-soluble and rapidly absorbed from the stomach, and the alkali and sodium loads may pose a risk for patients with cardiac or renal failure. Depending on particle size and crystal structure, CaCO rapidly and effectively neutralizes gastric H+, but the release of COj from bicarbonate- and carbonate-containing antacids can cause belching, nausea, abdominal distention, and flatulence. Calcium also may induce rebound acid secretion, necessitating more frequent administration. 

Calcium carbonate is most effective in neutralizing acid, however one third to one half of the dmg can be systemically absorbed resulting in acid rebound. Hypercalcemia and milk-alkah syndrome can result from excessive use of calcium carbonate. Calcium carbonate is intensified if taken with milk products. 

E. Treatment courses should be separated by a minimum of 2 days, and an interval of 2 or more weeks may be indicated to assess the extent of posttreatment rebound in blood lead levels. An additional course of calcium EDTA treatment may be considered based on posttreatment blood lead concentrations and the persistence or recurrence of symptoms. 

The toxicity of vitamin C is very low and doses of 10 g/day appear to be quite safe. The major concern at high doses is the risk of the formation of calcium oxalate kidney stones and it might be wise not to take calcium supplements with vitamin C. The increase of oxalate levels, even at high doses, only increases by about 50%. The evidence for rebound effects where, following withdrawal of high-dose therapy, vitamin C levels fall and for in vivo mutagenicity is not conclusive. The worst effects of vitamin C at high dose appear to be GI disturbances and diarrhoea. 

---