Haemoglobin is a readily available major protein in the human body and responsible for the transport of oxygen from the lungs to the peripheral tissues and carbon dioxide from the peripheral tissues back to the lungs.
The transport of oxygen is based on a chemical interaction between molecular O2 and heme, a tetrapyrrole porphyrin ring containing ferrous (Fe2+) iron.
Haemoglobin levels are decreased in all varieties of anaemia, resulting from haemorrhage, or from deficiency of iron, folic acid or vitamin B.
Red cell haemolysis resulting from autoimmune process or due to enzyme abnormality (G6PD) may also result in anaemia.
The defective globin chain synthesis as in all Thallassaemias or structural abnormalities of the haemoglobin molecule may result in severe anaemia.
Increased levels of haemoglobin concentration are observed in Polycythaemia Vera, Congenital Heart Diseases and in Haemo-concentration due to various clinical causes e,g. heatstroke and dehydration.
Exercise has been reported to lead to a reversible increase of about 3 – 10%.
Male: 14.0 – 18.0 gm/dL
Female: 12.0 – 16.0 gm/dL
The level of blood glucose depends on a dynamic equilibrium- intake of carbohydrate and endogenous glucose synthesis versus glucose storage, utilization & excretion.
The most common impairment associated with abnormal carbohydrate metabolism is Diabetes Mellitus, with its accompanying high blood glucose levels.
Other conditions which may also result in abnormal blood glucose levels include disorders of the pituitary gland, hyperthyroidism, Cushing’s syndrome, traumatic injury, convulsive disorders, mental stress and phoeochromocytoma.
Acute and chronic infections, eclampsia, hypertension and severe liver disease may also exhibit transitory elevations of blood glucose levels. On the other hand hyperinsulinism from either exogenous insulin overdose or from pancreatic lesions can result in low levels of blood glucose.
Fasting: 60 – 110 mg/dL
Post Prandial : Upto 150 mg/dL
Glycosylated Haemoglobin (HbA1c):
Elevated glycohaemoglobin levels are found in diabetic patients. Even though blood & urine glucose determinations are useful, they do not give all the necessary information to assess carbohydrate control to a doctor. However Glycohaemoglobin measurement offers more convenient and accurate measurement to the overall glucose metabolism of the patients.
The unique ability of Glycohaemoglobin is to measure retrospectively the mean glucose concentration for the previous 6 – 8 weeks which makes it a useful indicator for assessing the long term control of diabetic patients.
Normal: 4.5 – 5.90 %
Good Control: 5.91 – 6.80 %
Fair Control: 6.81 – 7.65 %
Poor Control: More than 7.65 %
Calcium has numerous functions in the body. It functions as an important factor in structure of bones and teeth, in neuromuscular activity and in clotting of blood.
Increased serum calcium levels are observed in primary hyperparathyroidism, hypervitaminosis D and multiple myeloma.
In addition some neoplastic diseases of bones may be associated with increased serum calcium levels.
Decreased serum calcium levels are observed in hypoparathyroidism, tetany, steatorrhoea and nephritis.
8.5 – 10.5 mg/dL
Liver Function Tests:
Bilirubin is the breakdown product of haemoglobin. Bilirubin formed in the reticulo-endothelial system is transported (bound to albumin) to the liver. This bilirubin is water soluble and is known as indirect or unconjugated bilirubin. In the liver bilirubin is conjugated to glucuronic acid to form direct or conjugated bilirubin. Conjugated bilirubin is excreted via the biliary system into the intestine where it is metabolized by bacteria to urobilinogen and stercobilinogen. Total and Direct Bilirubin estimation in serum is used for the diagnosis, differentiation and follow up of Jaundice. Jaundice is classified mainly into three types- Haemolytic (Prehepatic), Hepato-cellular (Hepatic) and Obstructive (Post Hepatic) Total Bilirubin is eleveted in obstructive conditions of the bile duct, hepatitis, cirrhosis, haemolytic disorders and several inherited enzyme deficiencies. Indirect Bilirubin is elevated by prehapatic causes such as haemolytic disorders or liver diseases resulting in impaired entry, transport or conjugation within the liver. Monitoring of Indiredct Bilirubin in neonates is of great importance as it is in the indirect (Free) bilirubin bound to albumin that is able to pass the blood brain barrier more easily, increasing the danger of cerebral damage. The direct (Conjugated bilirubin increases in hepatic causes. Ie. Parenchymal liver diseases (Hepatitis)- infective, toxic atc and obstructive causes- gall stones, any type of growth or due to regurgitation of bile into hepatic circulation.
Serum Glutamic Pyruvic Tranaminase (SGPT) (ALT)
It is also called as Alanine Amino Transferase.
GPT is widely distributed in various tissues of the body. GPT activity is maximum in liver tissue followed by relatively lower levels in kidney, heart and skeletlal muscles.
It is useful in evaluating liver function in viral, bacterial or chemical hepatitis.
A moderate increase is also found in obstructive jaundice, metastatic carcinoma and myocardial infarction.
GPT levels may be decreased in patients undergoing long term haemodialysis without supplemental vitamin therapy.
5 – 35 U/L
Serum Glutamic Oxaloacetic Transaminase (SGOT)
It is also called as Aspartate Amino Transferase (AST)
GOT is widely distributed in various organs of the body.
GOT activity is maximum in heart tissue followed by relatively lower levels in the kidney and muscles.
When any of these organs is damaged or diseases Serum GOT levels rises in proportion of the severity of damage. GOT is particularly useful in the diagnosis of Myocardial Infarction.
The level increases after 3- 8 hours of onset of attack, reaches to peak value after 48 hours and returns to normal on 4th to 6th day after infarction.
Other cardiac conditions like Rheumatic conditions and Acute CCF may also show elevated GOT levels.
Slight to moderate increase in enzyme activity is also seen in liver and skeletal muscle degenerative disorders.
8 – 40 U/L
Serum Alkaline Phosphatase:
The increase of serum or plasma Alkaline Phosphatase activity is related to bone regeneration and is increased in Rickets and Osteomalacia.
The activity is also found to be increased in Post Hepatic (Obstructive) as well as Infective or Toxic Hepatitis.
A physiological increase is observed in pregnancy and in active bone growth in children.
Alkaline Phosphatase is present in high concentration in liver, bone, placenta, intestine and certain tumors.
Decrease in serum Alkaline phosphatase activity is found in Severe Anaemia, Scurvy, Kwashiorkor and Cretinism.
80 – 270 U/L
Increased Levels are found I dehydration, Multiple Myeloma, Chromic liver diseases and Chronic Infections.
While decreased levels are found in renal disease, malnutrition, albuminuria and terminal liver failure.
Total Protein is useful for monitoring gross changes in protein levels caused by various disease states.
It is usually performed in conjunction with other tests such as serum Albumin, Liver Function Testa or Protein Electrophoresis.
6.0 – 8.5 gm/dL
Gamma Glutamyl Transpeptidase:
Also called as Gamma Glutamyl Transferase It is found in many tissues, the most notable one being the liver, and has significance as a diagnostic marker. Elevated serum GGT activity can be found in diseases of the liver, biliary system, and pancreas. In this respect, it is similar to alkaline phosphatase (ALP) in detecting disease of the biliary tract. Indeed, the two markers correlate well, though there is conflicting data about whether GGT has better sensitivity. In general, ALP is still the first test for biliary disease. The main value of GGT over ALP is in verifying that ALP elevations are, in fact, due to biliary disease; ALP can also be increased in certain bone diseases, but GGT is not. More recently it has also been found to be elevated in persons with cardiovascular diseases and is under active investigation as a cardiovascular risk marker. GGT is elevated by large quantities of alcohol ingestion.It is however,not specific to alcohol intoxication. Isolated elevation or disproportionate elevation compared to other liver enzymes (such as ALP or ALT) may indicate alcohol abuse or alcoholic liver disease. It may indicate excess alcohol consumption up to 3 or 4 weeks prior to the test. The mechanism for this elevation is unclear. Alcohol may increase GGT production by inducing hepatic microsomal production, or it may cause the leakage of GGT from hepatocytes. Numerous drugs can raise GGT levels, including barbiturates and phenytoin. Elevated levels of GGT may also be due to congestive heart failure.
Renal (Kidney) Function Tests:
Urea is the major end and waste product of protein nitrogen metabolism in humans. It constitutes the largest fraction of the non protein nitrogen component of the blood. Urea is produced in the liver and excreted through the kidneys in the urine. Consequently, the circulating levels of urea depend upon the protein intake, protein catabolism and kidney function. Elevated blood urea levels are found in various renal disorders like glomerulo-nephritis, pyelo-nephritis, nephritic syndrome and due to obstruction in occurring at any level in the urinary tract. Blood Urea level may also be raised in severe dehydration and in massive gastrointestinal bleeding. Elevated urea levels can also be seen in liver diseases, Congestive Cardiac Failure (CCF), Diabetes Mellitus, infections, adreno-cortical insufficiency, acute intestinal occlusion, various poisonings & shock.
Creatinine is a waste product formed in muscle from high energy storage compound, creatine phosphate. The amount of creatinine produced is fairly constant and is primarily a function of muscle mass. Creatinine is removed from plasma by glomerular filtration and then excreted in urine without any appreciable resorption by the tubules. Creatinine is used to assess renal function. Serum Creatinine levels do not start to rise until renal function has decreased by at least 50%. An elevated serum creatinine level may rapidly fall when the obstruction in the urinary tract is removed by surgery. Congestive Cardiac Failure (CCF), shock and mechanical obstruction of urinary tract also contribute to an elevated Serum Creatinine.
Uric acid is the main end product of nucleic acids and purine metabolism. Characteristic increase in Serum Uric Acid concentration is seen in Gout in which salts of Uric Acid are deposited in and around joints. In case of Renal Failure or urinary obstruction, uric acid is retained (ie. Cannot be excreted because of obstruction) and its level in serum rises. Estimation of uric acid in serum is also of great importance in diagnosis of Eclampsia.
Sodium , Potassium and Chloride are the majoe electrolytes that play an important role in maintaining normal water distribution in the cells of the body and osmotic pressure and cation- anion balance in extracellular fluid compartment. Sodium and Chloride are filtered by glomeruli in the kidney and reabsorbed at the proximal and distal tubules. The reabsorption is governed by the adrenocortical hormone aldosterone. Hence sodium and chloride assays help in the diagnosis and prognosis of hyper and hypo adrenalism. Low potassium levels are associated with apathy and muscle weakness, paralysis, severe vomiting and diarrhea. Chloride estimation is import ant in the diagnosis of Meningitis.
Serum Sodium levels are low in GIT fluid loss, burns, salt losing renal disorders and Diuretic Overdose. Serum sodium levels are raised in acute renal failure with superimposed water-load, Congestive Cardiac Failure (CCF), Liver Cirrohis and Nephrotic Syndrome.