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  • Pk 700-704/ld/leg/92 1992

Get Pk 700-704/ld/leg/92 1992-2026

AZADGOVERNMENTOFTHESTATEOFJAMMU&KASHMIR LAWANDPARLIAMENTARYAFFAIRSDEPARTMENT MUZAFFARABAD Datedthe29thJune,1992 No.700704/LD/Leg/92. ThefollowingActoftheAssemblyreceivedtheassentofthePresidenton24thJune,1992isherebypublishedforgeneralinformation:.

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In the pediatric age group, malignancies, hypovitaminosis D, and endocrine disorders, mostly diabetes, were the most common causes of hypophosphatemia.

The acute effects of hypophosphatemia include neuromuscular symptoms and compromise. However, the dominant effects of chronic hypophosphatemia are the effects on musculoskeletal function including rickets, osteomalacia and impaired growth during childhood.

Low phosphorus disorders besides XLH include autosomal recessive and autosomal dominant hypophosphatemic rickets (very rare), tumor-induced osteomalacia, and Fanconi syndrome, which all cause bone problems. Poor kidney function can also lead to bone disease, including rickets.

Hypophosphatemia is a serum phosphate concentration 2.5 mg/dL (0.81 mmol/L). Causes include alcohol use disorder, burns, starvation, and diuretic use. Clinical features include muscle weakness, respiratory failure, and heart failure; seizures and coma can occur. Diagnosis is by serum phosphate concentration.

Hypophosphatemia is a condition in which your blood has a low level of phosphorous. Low levels can cause a host of health challenges, including muscle weakness, respiratory or heart failure, seizures, or comas. The cause of hypophosphatemia is always from some other underlying issue.

Congenital conditions of hypophosphatemia are part of the disorders that cause defective bone mineralization, manifesting with rickets and osteomalacia in childhood and osteomalacia in adulthood [1,2,3,4].

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