Status of Serum calcium, phosphorus and Vitamin D

2012 ◽  
Vol 2 (7) ◽  
pp. 329-330
Author(s):  
Saira Baloch ◽  
◽  
Bikha Ram Devrajani ◽  
Aneela Atta-ur-Rahman
Keyword(s):  
Vitamin D ◽  
Serum Calcium ◽  
Calcium Phosphorus

Renal osteodystrophy

2013 ◽  
pp. 1274-1282
Author(s):  
Thomas Bardin ◽  
Tilman Drüeke
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Serum Calcium ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Osteitis Fibrosa ◽  
Alkaline Phosphatases ◽  
Calcium Phosphorus ◽  
Turnover Markers ◽  
25 Oh Vitamin D

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

Late Onset Hypocalcemic Seizures in Formula-Fed, Vitamin D Deficient Babies: Revisited

2020 ◽  
Vol 34 (1-2) ◽  
pp. 15-18
Author(s):  
Umar Amin Qureshi ◽  
Abdus Sami Bhat ◽  
Muzaffar Jan ◽  
Uruj Qureshi
Keyword(s):  
Vitamin D ◽  
Breast Feeding ◽  
Serum Calcium ◽  
Late Onset ◽  
Response To Treatment ◽  
Total Serum ◽  
Total Serum Calcium ◽  
Vitamin D Levels ◽  
Calcium Phosphorus ◽  
25 Oh Vitamin D

Purpose: Late onset neonatal hypocalcemia (LNH) is defined as hypocalcemia detected after day 3 of life. Its occurrence in babies fed with cow’s milk is well understood. Since the advent of modern-day formulas, the incidence has however decreased. Methods: A prospective descriptive study (January 2017 to December 2017) of LNH seizures in neonates was conducted. LNH was defined as the total serum calcium of less than 7 mg/dL in preterm or less than 8 mg/dL in term newborns after 72 h of life. Results: 14 neonates were presented with myoclonic and focal seizures due to late hypocalcemia. All were formula fed. Their mean serum calcium, phosphorus, alkaline phosphatase, magnesium, 25-OH vitamin D, intact PTH levels were 4.93 mg/dL, 9.19 mg/dL, 244 U/L, 1.2 mg/dL, 30 nmol/L, 38.6 pg/mL, respectively. Mean maternal vitamin D levels were 43 nmol/L. Mean hospital stay was 4 days. Clinical response to treatment was brisk in those who were able to shift to total breast feeding early. Conclusions: LNH in formula-fed and vitamin D deficient babies is not uncommon. Emphasis should be laid on exclusive breast feeding even in vitamin D deplete mothers. However, mothers at risk should be supplemented with vitamin D during pregnancy.

Extracellular cyclic AMP levels in osteomalacia

1980 ◽  
Vol 95 (2) ◽  
pp. 282-288 ◽  
Author(s):  
Jose A. Sisson de Castro ◽  
Joseph R. Tucci
Keyword(s):  
Vitamin D ◽  
Alkaline Phosphatase ◽  
Cyclic Amp ◽  
Serum Calcium ◽  
Serum Electrolytes ◽  
Calcium Phosphorus ◽  
Calcium Infusion ◽  
Appropriate Therapy ◽  
Urinary Cyclic Amp ◽  
Normal Increase

Abstract. Plasma and urinary cyclic AMP were measured in a 62-year-old man with severe osteomalacia due to a gluten-induced enteropathy. Before therapy, plasma cyclic AMP was normal and both urinary and nephrogenous cyclic AMP were markedly increased. A calcium infusion acutely diminished the elevated iPTH and urinary cyclic AMP levels. Following a bolus infusion of PTE, there was no phosphaturia despite a somewhat exaggerated increase in cyclic AMP excretion. With appropriate therapy, serum calcium, phosphorus, alkaline phosphatase, iPTH and 25-OHD3 and urinary and nephrogenous cyclic AMP gradually returned to normal. The response to PTE infusion after normalization of serum electrolytes, iPTH, and 25-OHD3 levels was similar to that seen before therapy. These results demonstrate that non-azotaemic malabsorptive osteomalacia is associated with elevations in urinary and nephrogenous cyclic AMP which gradually fall to normal with therapy. In contrast to studies in the vitamin D deficient rat, the maximal urinary cyclic AMP response to PTE is not diminished in the human with malabsorptive osteomalacia. The lack of a phosphaturic response to PTE depite a normal increase in urinary cyclic AMP excretion, as seen in our patient, is similar to that described in some patients with pseudohypoparathyroidism, suggesting that the response is not specific for the latter disorder. Finally, the data suggest that endogenous PTH does not modulate its renal receptors, at least in terms of cyclic AMP generation.

scholarly journals Study of serum calcium, phosphorus and vitamin D status in multitransfused β-thalassemia major children and adolescents of Jharkhand, India

2019 ◽  
Vol 6 (2) ◽  
pp. 598
Author(s):  
Zeeshan Ahmed ◽  
Pushpanjali . ◽  
Md. Shahnawaz Kausar ◽  
Doyel Sinha
Keyword(s):  
Vitamin D ◽  
Blood Transfusion ◽  
Serum Calcium ◽  
Thalassemia Major ◽  
Mean Values ◽  
Frequent Monitoring ◽  
Standard Population ◽  
Vitamin D Levels ◽  
Calcium Phosphorus ◽  
The Difference

Background: The pattern of levels of calcium, phosphorous and vitamin D levels among the patients with thalassemia major undergoing repeated blood transfusions remain unexplored. Only very few studies have been undertaken among Indian population. The present study was an attempt to determine the levels of calcium, phosphorous and vitamin D levels among thalassemia major patients undergoing repeated multiple transfusions.Methods: In a prospective observational study, 65 patients suffering from β-thalassemia major, aged 2-18 years, having undergone regular blood transfusion and chelation therapy, were evaluated for the levels of serum calcium, phosphorus and vitamin D and the values were compared to the standard values of the same.Results: The mean values of serum calcium (6.72±0.66), phosphorous (5.51±1.07) and vitamin D (13.12±2.9) were significantly lower in our patients as compared to that of standard population values, the difference in each being statistically significant (p<0.05).Conclusions: It is evident from the present study that the levels of calcium, phosphorous and vitamin D are deficient among β-thalassemia major patients on repeated blood transfusion. The deficiencies may be due to iron overload or due to nutritional deficiency. Frequent monitoring and supplementation in deficient states is recommended.

scholarly journals An Unusual Case of Hypercalcemia Associated with Graves’ Disease and Vitamin D Deficiency

2011 ◽  
Vol 4 ◽  
pp. CMED.S7116 ◽  
Author(s):  
Evgenia Korytnaya ◽  
Nagashree Gundu Rao ◽  
Jane V. Mayrin
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Vitamin D Deficiency ◽  
Serum Calcium ◽  
Graves Disease ◽  
Hydroxyvitamin D ◽  
Vitamin D Levels ◽  
Calcium Phosphorus ◽  
25 Hydroxyvitamin D ◽  
25 Oh Vitamin D

Objective To present a case of hypercalcemia associated with thyrotoxicosis in a patient with vitamin D deficiency and review biochemical changes during the course of treatment. Methods We report a case, describe the changes in serum calcium, phosphorus, parathyroid hormone in Graves’ disease and concomitant Vitamin D deficiency. We compare our findings to those reported in literature. Results Our patient had hypercalcemia secondary to thyrotoxicosis alone, which was confirmed by low parathyroid hormone level and resolution of hypercalcemia with treatment of thyrotoxicosis. The case was complicated by a concomitant vitamin D deficiency. Serum calcium elevation in patients with thyrotoxicosis occurs secondary to hyperthyroidism alone or due to concurrent hyperparathyroidism. Hypercalcemia from thyrotoxicosis is usually asymptomatic and is related to bone resorption. Vitamin D deficiency can be seen in patients with thyrotoxicosis because of accelerated metabolism, poor intestinal absorption and increased demand during bone restoration phase. Coexistence of hypercalcemia and Vitamin D deficiency in patients with thyrotoxicosis is rare, but possible, and 25-hydroxyvitamin D levels should be checked. The definite treatment for hypercalcemia in thyrotoxicosis is correction of thyroid function. Conclusion Hypercalcemia in thyrotoxicosis should be distinguished from concomitant hyperparathyroidism and confirmed by resolution of hypercalcemia with control of thyrotoxicosis. Patients with hypercalcemia and thyrotoxicosis may also have vitamin D deficiency and 25-OH Vitamin D levels should be checked.

scholarly journals Bilateral Basal Ganglia Calcification; An Unusual Initial Presentation of Pseudohypoparathyroidism

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A184-A185
Author(s):  
Ahmad Zare ◽  
Sara Choudhry
Keyword(s):  
Vitamin D ◽  
Basal Ganglia ◽  
Serum Calcium ◽  
Initial Presentation ◽  
Active Vitamin ◽  
Adequate Treatment ◽  
Basal Ganglia Calcification ◽  
Active Vitamin D ◽  
Calcium Phosphorus ◽  
History Of

Abstract Physiological intracranial calcification occurs in about 0.3–1.5% of cases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. A 21-year-old female who was initially evaluated by neurology team for headache and diplopia, underwent MRI of brain which revealed Calcifications involving the bilateral basal ganglia, thalami, dentate nuclei as well as juxtacortical frontal lobes. She reported Fatigue and muscle pain, usually in her arms especially after playing sports which had been going on for many years. She had no history of fractures, seizures, psychiatric disorders, developmental delay or obvious cognitive impairments. She denied any family history of calcium disorders or autoimmune diseases. As she had been generally healthy in her whole life, she never had any lab testing done. On examination, Height 5’1”, Chvostek’s sign was positive. Fundoscopy was normal. she had no dysmorphic features or shortened 4th metacarpal. Investigations revealed serum calcium less than 5.0 mg (N 8.3 - 10.1 mg/dl), PTH 205.1 pg/ml (N 18.4 - 80.1 pg/ml), phosphate 7.1 mg (N 2.5 - 5 mg), Vitamin-D 36.2 ng/ml (N 30.0 - 100.0 pg/ml),magnesium 2.0 m (N 1.6 - 2.6 mg/dl) with normal albumin, alkaline phosphatase and renal function test. She was diagnosed with pseudohypoparathyroidism and started on calcium and active vitamin D supplement and was referred for genetic testing study. She reported significant improvement in myalgia after a few weeks of starting calcium and active vitamin D supplementations and repeat lab testing showed improved hypocalcemia and hyperphosphatemia. This case illustrates unusual presentation of PTH resistance with basal ganglia calcification as initial presentation prompting further workup. She likely has pseudohypoparathyroidism type 1b. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, determination of serum calcium, phosphorus, and parathyroid hormone is mandatory in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism.

Vitamin D Provision in High-Yield Dairy Cows During the Winter Housing Period

2014 ◽  
Vol 1 (1) ◽  
pp. 42-46
Author(s):  
L. Yuskiv ◽  
V. Vlizlo
Keyword(s):  
Vitamin D ◽  
Alkaline Phosphatase Level ◽  
Mineral Metabolism ◽  
Physiological State ◽  
Blood Parameters ◽  
Postnatal Period ◽  
High Yield ◽  
Oral Supplementation ◽  
Calcium Phosphorus ◽  
Vitamin D 3

Aim. To investigate the vitamin D status in highly productive cows during winter housing period and effect of cholecalciferol by various ways of vitamin D 3 injection to cows in last days of gestation and after calving. Methods. Enzyme-linked immunoassay, spectrophotometry. Results. It has been stated that intramuscular injection of cholecalciferol into cows caused increase of the vitamin D 3 active metabolite – 25-OHD 3 , calcium, phosphorus and magnesium levels together with decrease of alkaline phosphatase level in pre- and post-natal periods. Oral supplementation makes little infl uence on the studied blood parameters of cows. Conclusions. Extrabuccal administration and oral supplementation of cholecalciferol in winter housing period to high-yield cows in the last days of gestation and after calving is accompanied by increased levels of its metabolites and their effect on mineral metabolism in the postnatal period. The nature of these changes depends on the mode of vitamin D administration and the physiological state of the cows.

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