Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study reports the benefits and side effects of conventional treatment, phosphate and calcitriol supplementation in patients with heritable hypophosphatemic rickets and a long-term follow-up, median of 60.9 months. The group is composed of 17 patients (ten girls). Sixteen patients presented with bone pain and/or deformities, and in one patient the diagnosis was radiological. All the patients had increased alkaline phosphatase, hypophosphatemia, decreased fractional phosphate tubular reabsorption (TRP) and maximum tubular phosphate reabsorption/glomerular filtration rate ratio (TPO4/GFR). Ten of 17 patients had metabolic acidosis, which was corrected only with the conventional treatment. Potassium citrate was prescribed to the patients who developed hypercalciuria. Excluding one patient with pulmonary dysfunction, the remaining 16 patients were divided into two groups according to the age at treatment onset (T0): group I (GI) > or =4 years (n =9) and GII <4 years (n =7). GI and GII had similar follow-up periods and treatment protocols. Seven out of nine GI patients underwent orthopedic surgery, in contrast to none of GII. Anthropometric data results showed that within each group there is no difference in weight and stature z -score at T0 and at the end of the observation (Tf), but, when both groups are compared, GII shows higher z-score for stature at T0 (p <0.05) and at Tf (p <0.05). Nephrocalcinosis developed in three cases and correlated with hypercalciuria (p <0.001) and dose of calcitriol (p =0.03). In conclusion, higher stature z-score is associated with early treatment. A careful protocol is recommended to detect such complications as nephrocalcinosis. We suggest potassium citrate for patients with hypercalciuria to avoid calcium precipitation.
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PMID:Hypophosphatemic rickets: results of a long-term follow-up. 1625 97

Both K and Ca supplementation may have beneficial effects on bone through separate mechanisms. K in the form of citrate or bicarbonate affects bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and bone metabolism in young women. Twelve healthy women aged 22-30 years were randomised into four controlled 24 h study sessions, each subject serving as her own control. At the beginning of each session, subjects received a single dose of calcium carbonate, calcium citrate, potassium citrate or a placebo in randomised order. The diet during each session was identical, containing 300 mg Ca. Both the calcium carbonate and calcium citrate supplement contained 1000 mg Ca; the potassium citrate supplement contained 2250 mg K. Markers of Ca and bone metabolism were followed. Potassium citrate decreased the bone resorption marker (N-terminal telopeptide of type I collagen) and increased Ca retention relative to the control session. Both Ca supplements decreased S-PTH concentration. Ca supplements also decreased bone resorption relative to the control session, but this was significant only for calcium carbonate. No differences in bone formation marker (bone-specific alkaline phosphatase) were seen among the study sessions. The results suggest that potassium citrate has a positive effect on the resorption marker despite low Ca intake. Both Ca supplements were absorbed well and decreased S-PTH efficiently.
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PMID:Acute effects of calcium carbonate, calcium citrate and potassium citrate on markers of calcium and bone metabolism in young women. 1953 11