Increased MCV.

Alcoholism (chronic), anemia (acquired hemolytic, aplastic, immune hemolytic, macrocytic induced by megaloblastic anemias, pernicious [early]), benzene exposure, cigarette smokers, cirrhosis, chronic lymphocytic leukemia, cytomegalovirus, diabetic ketoacidosis, diabetes mellitus, DNA synthesis disorders (inherited), folate deficiency, hepatic disease, infants, leukocytosis (pronounced), methanol poisoning, newborns, obese, pancreatitis, peripheral arterial disease, preleukemia, reticulocytosis, sprue, and vitamin B12 deficiency. Drugs include capecitabine, hydroxyurea, zidovudine (AZT).

Decreased MCV.

Anemia (chronic, dyserythropoietic, hypochromic, iron deficiency, microcytic, pyridoxine responsive, sickle cell), alpha- or beta-thalassemia, Brunner's gland hamartoma, chlorosis, chronic disease, colorectal cancer, diverticulitis, diverticulosis, endocarditis, G6PD deficiency, gangrene, hemoglobin E, hemoglobin H, leukocytosis (pronounced), malaria, myocarditis, nephropathy (nonimmune), pruritus, radiation therapy, red blood cell fragmentation, subacute bacterial endocarditis, and warm autoantibodies. Drugs include stavudine.

Increased Total Alkaline Phosphatase.

May also be caused by alcoholism, carbohydrate ingestion (large quantities), children, cholelithiasis in persons with sickle cell disease, diabetes mellitus, Fanconi syndrome, fat ingestion, fibrous dysplasia, histiocytosis, Hodgkin's disease, hyperalimentation, hyperparathyroidism (with bone disease), hyperthyroidism, hypophosphatemia, kidney tissue rejection, liver abscess, liver disease, lung cancer, lymphoma, mononucleosis (infectious), multiple myeloma, myocardial infarction, osteosarcoma, primary biliary cirrhosis, pulmonary infarction, renal infarction, rheumatoid arthritis, rickets, sarcoidosis, and sickle cell crisis. Drugs include acetaminophen, acetohexamide, acyclovir, albumin, allopurinol, aluminum nicotinate, amiodarone, amitriptyline, ampicillin, anabolic steroids, androgens, asparaginase, aspirin, aurothioglucose, azathioprine, baclofen, barbiturates, bromocriptine mesylate, carbamazepine, carmustine, cephalexin, cephaloridine, chlordiazepoxide, chlorpromazine hydrochloride, chlorpropamide, cholestyramine resin, cimetidine, cinchophen, clindamycin, clonazepam, colchicine, diltiazem, ergosterol, erythromycin, estrogens, floxuridine, flurazepam, fosinopril, gold sodium, N-hydroxyacetamide, imipramine, imipramine pamoate, indomethacin, isoniazid, lincomycin, meclofenamate sodium, methotrexate, methyldopa, methyldopate hydrochloride, methyltestosterone, metoprolol tartrate, minoxidil, mithramycin, naproxen sodium, niacin, nifedipine, nitrofurantoin, novobiocin, oral contraceptives, oxacillin sodium, oxyphenisatin, papaverine hydrochloride, penicillamine, pertofrane, phenobarbital, phenothiazines, phenylbutazone, phenytoin, procainamide hydrochloride, propranolol, propylthiouracil, rifampin, salicylates, sildenafil, sulfamethoxazole, sulfisoxazole, sulfisoxazole acetyl, sulfobromophthalein sodium, tetracycline, thiomalate, thiothixene, thyroid hormone replacement, tolazamide, tolbutamide, tolmetin sodium, valproic acid, and vitamin D. Herbal or natural remedies include Echinacea (taken for 8 weeks or longer).

Decreased.

Anemia (pernicious), blood transfusions (massive), celiac disease, cretinism, hypophosphatasia, hypothyroidism, malnutrition, milk-alkali syndrome (Burnett's syndrome), nephritis (chronic), osteolytic sarcoma, scurvy, vitamin D intoxication, and zinc depletion. Drugs include aminobiphosphonates (Neridronate), edetate disodium, fluorides, oxalates, phosphates, and propranolol.

Description.

Alkaline phosphatase is an enzyme found in bone, liver, intestine, and placenta that rises during periods of bone growth (osteoblastic activity), liver disease, and bile duct obstruction. It is made up of bone, liver, placental, biliary, and intestinal isoenzymes that can be separated by electrophoresis. Alkaline phosphatase isoenzymes should be measured for any client who has an elevated alkaline phosphatase level.

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 bettersensitivity.[10][11] 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.[11] More recently, slightly elevated serum GGT has also been found to correlate with cardiovascular diseases and is under active investigation as a cardiovascular risk marker. GGT in fact accumulates inatherosclerotic plaques,[12] suggesting a potential role in pathogenesis of cardiovascular diseases,[13] and circulates in blood in the form of distinct protein aggregates,[14] some of which appear to be related to specific pathologies such as metabolic syndrome, alcohol addiction and chronic liver disease. High body mass index is associated with type   2 diabetes  only in persons with high serum GGT.[15]

GGT is elevated by large quantities of alcohol ingestion. Determination of total serum GGT activity is however not specific to alcohol intoxication,[16]and the measurement of selected serum forms of the enzyme offer more specific information.[14] Isolated elevation or disproportionate elevation compared to other liver enzymes (such as ALP or ALT) may indicate alcohol abuse or alcoholic liver disease.[17] 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.[18]

Numerous drugs can raise GGT levels, including barbiturates and phenytoin.[19] GGT elevation has also been occasionally reported following NSAIDs,St. John's wort, and aspirin. Elevated levels of GGT may also be due to congestive heart failure.[2

ESRIncreased.

Anemia, ankylosing spondylitis, arteritis (temporal), arthritis (rheumatoid), cat-scratch disease, cholesterol, coccidioidomycosis, colon cancer, Crohn's disease, dermatomyositis, endocarditis, fever of undetermined origin, fibrinogen elevation, hemolytic anemia, hyperfibrinogenemias, industry-related diseases, infection, inflammation, macroglobulinemia, malignancy, multiple myeloma, obstructive hepatic disease, osteomyelitis, pain (acute, chronic, abdominal, pelvic),

paraproteinemia, pelvic inflammatory disease, pericarditis, peritonitis, polyclonal hyperglobulinemias, polymyalgia rheumatica, pregnancy, pulmonary embolism, sickle cell disease, sinusitis, Sjögren's syndrome, subacute bacterial endocarditis, systemic lupus erythematosus, and tissue destruction. Drugs include dextran, fat emulsion, oral contraceptives, and vitamin A.

Decreased.

Congestive heart failure and poikilocytosis. Drugs include albumin, corticotropin, cortisone, and lecithin.

Description.

The erythrocyte sedimentation rate (ESR) is the most widely used lab test to monitor the course of inflammatory disease, as well as infections. When a tube of well-mixed venous blood is positioned vertically, the red blood cells will tend to fall to the bottom. The rate at which they fall is the ESR. The ESR is a reflection of acute-phase reaction in inflammation and infection. A limitation of this test is that it lacks sensitivity and specificity for disease processes. In addition, ESR cannot detect inflammation as quickly or early as can the C-reactive protein test. Thus C-reactive protein is sometimes used preferentially over ESR as a marker of inflammation (see C-reactive protein—Serum or plasma ). Various methods are used to measure the ESR. The Westergren method is used most often because of the simplicity of the procedure. The Wintrobe method is more accurate for borderline elevations in the ESR. The zeta sedimentation ratio is a sedimentation rate calculation that provides more accurate data than the ESR in clients with anemia, requires the smallest amount of blood for testing, and provides the fastest results.

CRP

Usage.

Monitoring of rheumatoid arthritis and rheumatic fever inflammatory processes, differentiation of Crohn's disease from ulcerative colitis, predictor of myocardial infarction (plasma levels >1.6 mg/L predict future coronary events) in women and coronary heart disease in middle-aged men, marker for existing arterial disease, detection of the presence or exacerbation of inflammatory processes (high preoperative levels indicate increased risk for postoperative infection), and monitoring response to therapy for inflammatory conditions. More reliable than ESR in evaluating inflammatory conditions.

Description.

C-reactive protein (CRP) is an abnormal serum glycoprotein produced by the liver during acute inflammation. CRP is detectable within 6–10 hours after the body's inflammatory response is stimulated and may rise as high as 4000 times when the acute phase inflammatory response is peaking. Because it disappears rapidly when inflammation subsides, its detection signifies the presence of a current inflammatory process. It is the best indicator of the severity of pancreatitis when measured 48 hours after the onset of symptoms. C-reactive protein has been linked to metabolic syndrome, a group of signs that include abdominal obesity, hypertriglyceridemia, low

HDL-C, hypertension, and high fasting blood glucose levels. It is now suspected that chronic inflammation as evidenced by an chronically elevated C-reactive protein level may be an additional component of the syndrome. Its contribution is hypothesized to be regulation of the adverse lipid profile seen in metabolic syndrome. The American Heart Association and The Centers for Disease Control in 2003 jointly issued recommendations for use of CRP as a “discretionary tool” for use in evaluating clients with moderate risk of heart disease, but not for use in widespread screening for heart disease. Wakugawa et al. (2006) found that elevated high-sensitivity CRP was an independent risk factor for future ischemic stroke in Japanese males, and when combined with at least one other risk factor for stroke indicates an extreme increase in the risk. C-reactive protein interacts with the complement cascade and is detected by antiserum by means of immunoassays.

Professional Considerations