Calcium prognosis

In chronic intoxication, the therapeutic objective is removal of the patient from the site of exposure and elimination of the noxa from the body (e. g. detoxification measures, infusions of calcium-disodium EDTA in cases of lead poisoning, etc.). There is no justification whatsoever for therapeutic nihilism. With the aid of dietetic measures (if necessary) and adjuvant therapy (N-acetylcysteine, antioxidants, ursodeoxycholic acid, S-adenosyl-methionine, etc.), the clinical course and hence the prognosis can be favourably influenced. Insufficient regression or inadequate normalization of laboratory parameters and histological changes despite removal of the patient from the area of exposure must arouse suspicion of a further, still existing noxa (alcohol, medicaments, other chemicals). 

Calcium channel blockers can cause parkinsonism. Of 32 patients with this complication, only three had made a full recovery 18 months after withdrawal patients under 73 years of age tended to have a better prognosis (57). It is not known if these patients would have developed parkinsonism in any case, and whether the drugs merely act as precipitants. 

Hyperkalemia carries a poor prognosis and is usually an indication for antidigoxin antibody. The suggestion that intravenous calcium should be used to treat the hjrper-kalemia that can occur in digitalis intoxication (173) has been challenged, on the grounds that it can increase the risk of cardiac dysrhythmias in such cases (174). 

Zaritsky AL, Horowitz M, Chemow B (1988) Glucagon antagonism of calcium channel blocker-induced myocardial dysfunction. Crit Care Med 16 246-251 Zeltser D, Justo D, HaUdn A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S (2004) Drug-induced atrioventricular block prognosis after discontinuation of the culprit drug. J Am Coll Cardiol 44 105-108... 

Patients with primary proximal tubular acidosis usually have stable serum HCO3 levels in spite of the reduced acid excretion. The compensatory mechanism is not known, but reduced endogenous acid production can probably be excluded. A more likely adaptation is the formation of additional bases at the expense of bone CaC03. Some patients with primary proximal acidosis present skeletal demineralization, reduced levels of CO3 in the hydroxyapatite crystals, and increased calcium losses in the feces. Patients with proximal renal acidosis are usually symptomless, and except in cases of acid overproduction, the prognosis is usually favorable. 

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