java aztec barcode library See Table 26 10 for causes of osteoporosis in Objective-C

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Endocrine Disorders D Aluminum Toxicity
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Bone mineralization is inhibited by aluminum Osteomalacia may occur in patients receiving long-term renal hemodialysis with tap water dialysate or from aluminum-containing antacids used to reduce phosphate levels Osteomalacia may develop in patients being maintained on long-term total parenteral nutrition if the casein hydrolysate used for amino acids contains high levels of aluminum
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osteomalacia is typically asymptomatic at first Eventually, bone pain occurs, along with muscle weakness due to calcium deficiency Fractures may occur with little or no trauma
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Serum is obtained for calcium, albumin, phosphate, alkaline phosphatase, PTH, and 25[OH]D3 determinations Bone densitometry helps document the degree of osteopenia Radiographs may show diagnostic features In one series of biopsy-proved osteomalacia, alkaline phosphatase was elevated in 94% of patients; the calcium or phosphorus was low in 47% of patients; 25(OH)D3 was low in 29% of patients; pseudofractures were seen in 18% of patients; and urinary calcium was low in 18% of patients 1,25(OH)2D3 may be low even when 25(OH)D2 levels are normal Bone biopsy is not usually necessary but is diagnostic of osteomalacia if there is significant unmineralized osteoid
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E Hypophosphatasia
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Skeletal alkaline phosphatase is an enzyme that is necessary to form normal bone Alkaline phosphatase cleaves pyrophosphate, an inhibitor of mineralization, thereby allowing normal mineralization of the bone matrix There are four distinct alkaline phosphatase isomers; only one is found in bone and it is also in liver and kidney and is therefore known as tissue-nonspecific alkaline phosphatase ( bone alkaline phosphatase) Hypophosphatasia, a deficiency of bone alkaline phosphatase effect, is a rare genetic cause of osteomalacia that is commonly misdiagnosed as osteoporosis The incidence in the United States is about 1 in 100,000 live births; about 1 in 300 adults is a carrier Many different mutations in the gene (designated ALPL) encoding bone alkaline phosphatase have been described, and transmission can be either autosomal recessive or autosomal dominant The phenotypic presentation of hypophosphatasia is extremely variable At its worst extreme, it can present as a stillborn without dentition or calcified bones At its mildest, hypophosphatasia can present in middle age with premature loss of teeth, foot pain (due to metatarsal stress fractures), thigh pain (due to femoral pseudofractures), or arthritis (due to chondrocalcinosis) Serum alkaline phosphatase (collected in a non-EDTA tube) is low for age in patients with hypophosphatasia To confirm the diagnosis, a 24-hour urine should be assayed for phosphoethanolamine, a substrate for tissue-nonspecific alkaline phosphatase, whose excretion is always elevated in patients with hypophosphatasia Prenatal genetic testing, by way of chorionic villus biopsy, is available for the infantile form of hypophosphatasia There is no proven therapy for hypophosphatasia, except for supportive care Teriparatide, a useful therapy for osteoporosis, has been administered to some patients with hypophosphatasia, but its long-term efficacy is unknown
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Osteomalacia is often seen together with osteoporosis, and its presence can be inferred by finding low serum levels of 25(OH) vitamin D, low serum calcium, or low serum phosphate A high serum alkaline phosphatase may be present in severe osteomalacia but not osteoporosis The relative contribution of the two entities to diminished bone density may not be apparent until treatment, since a dramatic rise in bone density is often seen with therapy for osteomalacia Phosphate deficiency must be distinguished from hypophosphatemia seen in hyperparathyroidism Bone densitometry by DXA may give a misleadingly low reading for patients who are unusually slender with small bones It must also be remembered that bone density only approximates bone tensile strength
Prevention & Treatment
To obtain adequate sunshine vitamin D, the face, arms, hands, or back must have sun exposure without sunscreen for 15 minutes at least twice weekly The main natural food source of vitamin D is fish, particularly, salmon, mackeral, cod liver oil, and sardines or tuna canned in oil Most commercial cow s milk is fortified with vitamin D at about 400 IU per quart; however, skim milk and other dairy products contain much less vitamin D Vitamin supplements containing vitamin D are widely available, but contain plant-derived vitamin D2, which has less biologic availability than once believed In sunlight-deprived individuals (eg, veiled women, confined patients, or residents of higher latitudes during winter), the recommended daily allowance should be 1000 IU daily In such individuals, vitamin D supplements should be given prophylactically Patients receiving long-term phenytoin therapy may be treated prophylactically with vitamin D, 50,000 IU orally every 2 4 weeks Frank vitamin D deficiency is treated with ergocalciferol (D2), 50,000 IU orally once or twice weekly for 6 12 months, followed by 1000 2000 IU daily Ergocalciferol has a duration of action of 7 10 days, so by 2 weeks after a dose of ergocalciferol, the 25(OH) vitamin D level is back
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