LABORATORY REPORT
Name : Ms MOUMITA ROY Sex/Age : Female / 32 Years Case ID : 50535100690
Ref. By : Dr. Manjari Chatterjee MBBS, DGO, DNB Reg Date : 03-May-2025 17:38 Pt. ID : 5714851
(Obs & Gyn)
Bill. Loc. : Neuberg Pulse Behala Chowrasta Mob.No : 9051749250
Sample Date and Time : 03-May-2025 17:40 Sample Type : Serum Ref Id1 :
Report Date and Time : 03-May-2025 22:43 Ref Id2 :
TEST RESULTS UNIT BIOLOGICAL REF RANGE REMARKS
Calcium 8.96 mg/dL 8.6-10
BAPTA
25 OH Cholecalciferol (D2+D3) 29.8 ng/mL Deficiency : 1 - 20
ECLIA Insufficiency : 20 - 29
Sufficiency: 30 - 100
25-OH-VitD plays a primary role in the maintenance of calcium homeostasis. It promotes intestinal calcium absorption and, in concert with PTH, skeletal
calcium deposition, or less commonly, calcium mobilization. Modest 25-OH-VitD deficiency is common; in institutionalised elderly, its prevalence may be
>50%. Although much less common, severe deficiency is not rare either. Reasons for suboptimal 25-OH-VitD levels include lack of sunshine exposure, a
particular problem in Northern latitudes during winter; inadequate intake; malabsorption (e.g, due to Celiac disease); depressed hepatic vitamin D 25-
hydroxylase activity, secondary to advanced liver disease; and enzyme-inducing drugs, in particular many antiepileptic drugs, including phenytoin,
phenobarbital, and carbamazepine, that increase 25-OH-VitD metabolism. Hypervitaminosis D is rare, and is only seen after prolonged exposure to
extremely high doses of vitamin D. When it occurs, it can result in severe hypercalcemia and hyperphosphatemia.
INTERPRETATION
• Levels <10 ng/mL may be associated with more severe abnormalities and can lead to inadequate mineralization of newly formed osteoid, resulting
in rickets in children and osteomalacia in adults. In these individuals, serum calcium levels may be marginally low, and parathyroid hormone (PTH)
and serum alkaline phosphatase are usually elevated. Definitive diagnosis rests on the typical radiographic findings or bone
biopsy/histomorphometry.
• Patients who present with hypercalcemia, hyperphosphatemia, and low PTH may suffer either from ectopic, unregulated conversion of 25-OH-VitD
to 1,25 (OH)2-VitD, as can occur in granulomatous diseases, particularly sarcoidosis, or from nutritionally-induced hypervitaminosis D. Serum 1,25
(OH)2-VitD levels will be high in both groups, but only patients with hypervitaminosis D will have serum 25-OH-VitD concentrations of >80 ng/mL,
typically >150 ng/mL.
• Patients with CKD have an exceptionally high rate of severe vitamin D deficiency that is further exacerbated by the reduced ability to convert 25-
OH- VitD into the active form, 1,25 (OH)2-VitD. Emerging evidence also suggests that the progression of CKD & many of the cardiovascular
complications may be linked to hypovitaminosis D.
• Approximately half of Stage 2 and 3 CKD patients are nutritional vitamin D deficient (25-OH-VitD, less than 30 ng/mL), and this deficiency is more
common among stage 4 CKD patients. Additionally, calcitriol (1,25 (OH)2-VitD) levels are also overtly low (less than 22 pg/mL) in CKD patients.
Similarly, vast majority of dialysis patients are found to be deficient in nutritional vitamin D and have low calcitriol levels. Recent data suggest an
elevated PTH is a poor indicator of deficiencies of nutritional vitamin D and calcitriol in CKD patients.CAUTIONS Long term use of anticonvulsant
medications may result in vitamin D deficiency that could lead to bone disease; the anticonvulsants most implicated are phenytoin, phenobarbital,
carbamazepine, and valproic acid.
------------------ End Of Report ------------------
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
Barun Jana Dr. Supratik Biswas
Verified by MBBS, MD
Consultant Biochemist
WBMC 64600 MC - 2167
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