Report
Report
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
Page 1 of 14
Final Laboratory Report PID : 9720590
Differential Counts
Neutrophils 58.9 % 40 - 75
Flowcytometry
Lymphocytes 26.6 % 20 - 45
Flowcytometry
Monocytes 7.6 % 2 - 10
Flowcytometry
Absolute Counts
Absolute Neutrophil Count 5219 Cells/cmm 2000-7000
Calculated
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
According to ICSH guideline (international Council for Standardisation in Hematology), the differential counts should be
reported in absolute numbers.
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
BIOCHEMICAL INVESTIGATIONS
Plasma Glucose - F 81 mg/dL Normal : 70 - 99
HEXOKINASE/G-6-PDH Impaired Fasting : 100 -
125
Diabetic : =>126
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO [Link] R
Consultant Biochemist MC-5972
Verified by Page 6 of 14
Final Laboratory Report PID : 9720590
Lipid Profile
Interpretation
LDL Cholesterol:
LDL-C estimated using the modified Sampson (NIH) equation,preferred over Direct & Friedewald methods as per
ACC/AHA 2026 guidelines". TGL >800, direct LDL is preferred.
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO [Link] R
Consultant Biochemist MC-5972
Verified by Page 7 of 14
Final Laboratory Report PID : 9720590
BIOCHEMICAL INVESTIGATIONS
Free T3 2.36 pg/mL 1.58 - 3.91
CMIA
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO Dr K Vinodini
MBBS., M.D(Micro)
MC-5972
Verified by Page 8 of 14
Final Laboratory Report PID : 9720590
BIOCHEMICAL INVESTIGATIONS
TSH 1.02 µIU/mL 0.35 - 4.94
CMIA PREGNANCY:
First trimester : 0.1 - 2.5
Second trimester : 0.2 -
3.0
Third trimester : 0.3 - 3.0
INTERPRETATIONS
• Circulating TSH measurement has been used for screening for euthyroidism, screening and diagnosis for
hyperthyroidism & hypothyroidism. Suppressed TSH (<0.01 µIU/mL) suggests a diagnosis of hyperthyroidism
and elevated concentration (>7 µIU/mL) suggest hypothyroidism. TSH levels may be affected by acute illness
and several medications including dopamine and glucocorticoids. Decreased (low or undetectable) in Graves
disease. Increased in TSH secreting pituitary adenoma (secondary hyperthyroidism), PRTH and in
hypothalamic disease thyrotropin (tertiary hyperthyroidism). Elevated in hypothyroidism (along with decreased
T4) except for pituitary & hypothalamic disease.
• Mild to modest elevations in patient with normal T3 & T4 levels indicates impaired thyroid hormone reserves &
incipent hypothyroidism (subclinical hypothyroidism).
• Mild to modest decrease with normal T3 & T4 indicates subclinical hyperthyroidism.
• Degree of TSH suppression does not reflect the severity of hyperthyroidism, therefore, measurement of free
thyroid hormone levels is required in patient with a supressed TSH level.
CAUTIONS
Sick, hospitalized patients may have falsely low or transiently elevated thyroid stimulating hormone.
Some patients who have been exposed to animal antigens, either in the environment or as part of treatment or
imaging procedure, may have circulating antianimal antibodies present. These antibodies may interfere with the
assay reagents to produce unreliable results.
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO Dr K Vinodini
MBBS., M.D(Micro)
MC-5972
Verified by Page 9 of 14
Final Laboratory Report PID : 9720590
BIOCHEMICAL INVESTIGATIONS
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO Dr K Vinodini
MBBS., M.D(Micro)
MC-5972
Verified by Page 10 of 14
Final Laboratory Report PID : 9720590
Electrolytes
Sodium 144.00 mmol/L 136 - 145
ISE, Indirect
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO [Link] R
Consultant Biochemist
Verified by Page 11 of 14
Final Laboratory Report PID : 9720590
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 [Link] 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.
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
AUTO [Link] R
Consultant Biochemist MC-5972
Verified by Page 12 of 14
Final Laboratory Report PID : 9720590
Chemical Examination
Protein Negative mg/dL Negative
Reflectance Photometry (Protein Error of
Principle indicator)
Microscopic Examination
Red Blood Cells 0 /HPF 0-2.3 cells/hpf
Phase Contrast Microscopy (Sedimentation
based with AIEM)
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)
Crystals
Calcium oxalate Monohydrate H 2.70 /HPF 0-1.4 p/hpf
Phase Contrast Microscopy (Sedimentation
based with AIEM)
Note:(LL-VeryLow,L-Low,H-High,HH-VeryHigh,A-Abnormal)