This test measures the total amount of the various types of proteins in the liquid portion (serum or plasma) of blood. Two classes of proteins are found in blood, i.e., albumin (ALB) and globulin. Albumin represents approximately 60% of the total protein content in healthy people. The remaining 40% of proteins in the plasma are referred to as globulins. The albumin/globulin (A/G) ratio is the amount of albumin in the serum divided by the globulins. The A/G ratio is used to try to identify causes of change in total serum protein. It will go out of the normal range if one component increases or decreases relative to the other. It is important to look at changes in the individual components (albumin and globulins) as well as the A/G ratio because the A/G ratio remains in the normal range or may change whenever the proportions of albumin and other proteins increase or decrease.
Hemoglobin A1c (HbA1c) is considered the gold standard for monitoring long-term (2~3 months) glycemic control in patients with diabetes mellitus. Circulating glucose nonenzymatically attaches to hemoglobin A in red blood cells and remains attached throughout the red blood cells life span (~120 days). High levels of glycated Hb are associated with cardiovascular disease, nephropathy, retinopathy etc. The presence of some hemoglobin (Hb) variants interferes either positively or negatively with the HbA1c quantitation and consequently would adversely affect the interpretation of HbA1c results. HbA1c, however, is not suitable in health conditions with altered red cell turnover, such as some hemoglobinopathies and thalassemia, chronic kidney disease, or hemolytic anemia. HbA1c is not appropriate for evaluating short-term variations in glycemic control due to the long lifespan of erythrocytes.
Serum proteins also undergo irreversible glycation. Albumin is the most abundant serum protein which contains multiple lysine residues susceptible to glycation. It is estimated that glycated albumin (GA) concentrations account for ~90% of glycated serum proteins. Albumin (ALB) reacts with glucose 10 times more rapidly than hemoglobin (Hb), it is not influenced by hematologic disorders and it has a shorter half-life (~14 days), thus reflecting patient short-term glycemic status (2 to 3 weeks). Glycated serum proteins (GSP) will most accurately reflect glycemic control in the above-mentioned conditions, or when monitoring the effects of changes in therapy in patients with diabetes or gestational diabetes. Alternative testing, such as GSP or GA, assist physicians with the monitoring of glycemic control in those conditions where glycated hemoglobin measurements are inaccurate.
Preliminary tests are designed to assess glycated hemoglobin (HbA1c), total protein and albumin (ALB). Sufficient volume is required for the quantitation of glycated albumin (GA). The patient would be classified as diabetic, according to the 2010 American Diabetes Association position statement, by using a level of HbA1c >6.5% whereas for the %GA, we use the reference intervals calculated for the population. Clinical concordance is evaluated by creating a 2 by 2 contingency table according to whether the patient would be classified as diabetic by using the tests: HbA1c >6.5% or %GA >17.5%. The distribution of the results obtained for HbA1c, and %GA would be very similar since both quantities are a reflection of glycemic control. Glycated albumin is not impacted by stage 3 or stage 4 chronic kidney disease, and among all interfering substances tested lipemia was found to have the greatest effect.
Insulin deficiency causes a lack of glucose utilization in insulin-dependent tissues such as muscle and adipose, and therefore leads to hyperglycemia. Lack of insulin also stimulates hyperglycemia by increasing hepatic gluconeogenesis. This is a common mechanism in diabetic ketoacidosis and a hyperosmolar hyperglycemic state. Deprived of glucose utilization, the body must look elsewhere for "fuel" to survive. In addition to hyperglycemia, lack of insulin increases the degradation of triglycerides into free fatty acids in adipose tissue, which travel to the liver and are converted to the ketoacids: β-hydroxybutyric acid, acetone, and acetoacetate. Unopposed counterregulatory hormone effect (glucagon & cortisol) causes further increases in glucose production from the liver and degradation of triglycerides. Together, these factors promote hyperglycemia, which leads to an osmotic diuresis resulting in dehydration, metabolic acidosis, and a hyperosmolar state.
There is overwhelming evidence that, an elevated LDL-C concentration in blood plasma is atherogenic, whereas a high HDL-C level is cardioprotective. We propose that in addition to the well-established conventional risk factors, the total cholesterol / HDL ratio may represent an important cumulative index of the presence of an atherogenic dyslipidemia that is associated with insulin resistance. The importance of measuring and properly interpreting the total cholesterol / HDL ratio (rather than the LDL-C / HDL-C ratio) is emphasized. We contend that calculation of the LDL-C / HDL-C ratio may underestimate Ischemic Heart Disease risk in some patients, if compared to — the accuracy of the estimation which is achieved through the simple use of the total cholesterol / HDL ratio. Additional metabolic markers, such as apolipoprotein (Apo) levels and markers of inflammation (e.g., C-reactive protein levels), could be used to predict coronary heart disease.
Diabetic ketoacidosis develops when the surge of ketoacid production (ketone bodies) is so powerful that a metabolic acidosis results. Patients with type 1 diabetes are more likely to exhibit diabetic ketoacidosis (DKA) because of their absolute deficiency of insulin secretion. Considerable electrolyte loss may result — especially potassium depletion. Frequently, one can identify a precipitating factor leading to diabetic ketoacidosis. Such factors can include the inappropriate use of insulin (non-compliance), cardiovascular disease, or infection which may be the most common cause of diabetic ketoacidosis. Myocardial infarction may precipitate hyperglycemia and ketoacidosis through an increase in counterregulatory hormones, such as epinephrine. Drugs such as thiazides, sympathomimetics, second-generation antipsychotics, and corticosteroids may also precipitate hyperglycemia and diabetic ketoacidosis.
This include blood glucose >250 – 200 mg/dL, arterial or venous pH <7.3, serum bicarbonate <18 – 15 mEq/L, and moderate degrees of ketonemia or ketonuria >2+. Symptoms include polyuria and polydipsia, weight loss, fatigue, dyspnea, vomiting, preceding febrile illness, abdominal pain, and polyphagia. Serum potassium levels are typically elevated in response to the presence of acidosis and insulin deficiency, but total body potassium is depleted. Both amylase and lipase may be elevated in the setting of diabetic ketoacidosis and are not necessarily indicative of pancreatitis. Patients exhibit hyperkalemia as a result of insulin deficiency and acidosis despite total body potassium depletion. Acetone is sensed as a fruity smell on the patient's breath, and β-hydroxybutyrate (D3H) is the primary ketone in serum. In the above-mentioned case, monitoring the biochemical changes caused by treatment is very necessary.