Differentiation of nutritional rickets and VDDR1A was made by normal/high 25-OHD levels, low/inappropriately normal 1,25-[OH.sub.2] D levels and improvement in the clinical, biochemical and radiological findings of rickets after replacement with calcitriol
. All patients received calcitriol
and patients with hypocalcaemia received calcium replacement.
For a nursing mother, the calcitriol
dose should be decreased (to half of the pre-pregnancy dose) since endogenous calcitriol
production is stimulated by prolactin and increased production of PTH-related peptide.
A total of 40 female BALB/c mice were randomly divided into five groups (n = 8): (1) normal control group, (2) asthma model group, (3) budesonide treatment group, (4) calcitriol
treatment group, and (5) combined treatment group.
During subsequent clinic visits, doses of calcium supplements and calcitriol
were titrated and she was started on magnesium oxide.
Seven out of 8 patients had additional factors that could potentially contribute or worsen denosumab-related hypocalcaemia including use of noncalcium based phosphate binders (1 case), absence of or use of low doses of calcitriol
(less than daily doses) supplementation (5 cases), low levels of vitamin D (4 cases), concomitant treatment with loop diuretics (2 cases), history of parathyroidectomy (1 case), and presence of an acute medical illness with reduced oral intake (1 case).
Phase I studies revealed that pulse administration may allow higher calcitriol
oral or subcutaneous doses without major toxicities (Smith et al., 1999; Beer et al., 2001).
The purpose of this study was to: 1) observe the in vitro effects of 10, 100, and 1000 nM concentrations of calcitriol
on VSMC calcification in the presence of normal and high phosphate, 2) examine the surface morphology and protein expression of VSMCs given 100 nM calcitriol
in the presence of normal and high phosphate, and 3) observe the in vitro effects of combinations of calcitriol
, FGF-23, and soluble klotho on VSMC calcification in the presence of high phosphate.
Moreover, the increased FGF23 markedly inhibits the action of the proximal tubular 1a-hydroxylase enzyme responsible for the conversion of calciferol to calcitriol
Certain recent studies have shown how calcitriol
enhances the antimicrobial effects of macrophages and monocytes, which are important effector cells, fighting against pathogens such as Mycobacterium tuberculosis.
Hypercalcemia is a common clinical problem and is most commonly caused by malignancy, or primary hyperparathyroidism.[sup],, Hypercalcemia has also been associated with granulomatous diseases, such as sarcoidosis and TB.[sup] Risk factors for hypercalcemia include intake of Vitamin D and calcium as well as sun exposure.[sup] The etiology of hypercalcemia might be related to elevated serum calcitriol
concentrations due to activated macrophages in granulomas.[sup] Patients with hypercalcemia may be asymptomatic or may exhibit constipation, anorexia, muscle weakness, and fatigue.