Type: F

Test 282

SuperUser Account — Tue, 16 Sep 2008 21:43:14 GMT

Test: Fecal Fat, Quantitative
Number: 001354
CPT: 82710
Synonyms: Fat, Quantitative ; Fecal Lipids ; Quantitative Fecal Fat ; Stool Fat, Quantitative ; Total Fat, Quantitative
Test Includes: Stool weight and fat content (in g/24 hours)
Special Instructions: The request form must state collection time (in hours). Collections of 24 or 48 hours are not recommended since results are subject to greater variability. Also state patient´s age on the request form.
Specimen: Stool (72-hour)
Volume: Entire collection or homogenized aliquot
Container: One or more clean LabCorp-approved stool collection kits (order LabCorp N^o 03192) containing a 1-gallon can, absorbent sheet, Armlock O-ring, and a leak-proof plastic bag
Collection: Collect stool directly into can. Do not fill any can more than 2/3 full. Secure lid with pressure and firmly attach the O-ring. State collection time on the can label. Place the can and the absorbent sheet into the leak-proof plastic bag and seal. Send the entire can, or if submitting aliquot, follow this procedure: (1) Weigh specimen and collection container and subtract the weight of an empty container of same type (1-gallon can weight with lid: 360 g metal or 320 g plastic container). This is the ?net weight? to be recorded on the request form. (2) Open the container and observe if the contents are liquid. If liquid stool, secure the lid, mix, and submit an aliquot of the total collection. If solid stool, add deionized water (approximately 500 mL) to the specimen container and mix thoroughly to create a homogenous specimen. Submit an aliquot of the total collection. (3) Record on the request form the amount of water added to liquefy the stool or if no water was required.
Storage Instructions: Refrigerate specimen during collection and store at 2°C to 8°C.
Patient Preparation: Adult patients should be on a standard diet containing 50-150 g of fat per day for at least 3 days before test is started and during the 72-hour collection. In children, the amount of fat in the diet should be constant for 1 day before the test and during the test. The patient should not have had mineral oil as a laxative prior to specimen collection.
Causes for Rejection: Container more than 2/3 full; container leaking; improper container (ie, non-LabCorp-approved paint can, paper cartons, coffee cans, plastic bags, etc); foreign matter other than feces inside of container (ie, spoons, tongue depressors, plastic bags, toilet paper, etc); patient not on special diet; improper labeling of container or request form; specimen on outside of container; specimen contaminated with urine
Reference Interval:

Pediatrics (0-6 years): <2.0 g/24 hours
Adults: <7.0 g/24 hours

Use: In malabsorption syndromes, notably pancreatic insufficiency and Whipple disease, steatorrhea is a prominent feature. Fecal fats can be useful in diagnosis of cystic fibrosis, chronic pancreatitis, neoplasia, or stone obstruction. Also useful in regional enteritis, celiac disease, sprue, and the atrophy of malnutrition.
Limitations: C8 and C10 saturated fatty acids are not quantitated with this method.
Methodology: Extraction/spectrophotometry

Test 350

SuperUser Account — Tue, 16 Sep 2008 21:44:19 GMT

Test: Fibrinogen Activity
Number: 001610
CPT: 85384
Synonyms: Clottable Fibrinogen ; Factor I Activity
Special Instructions: If the patient´s hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer Coagulation Collection Procedures for directions.
Specimen: Whole blood
Volume: 4.5 mL, 2.7 mL, 1.8 mL
Minimum Volume: 90% of full draw
Container: Blue-top (sodium citrate) tube; do not open tube.
Collection: Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.¹ Evacuated collection tubes must be filled to completion to ensure a proper blood to anticoagulant ratio.^2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples.^4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red top) tubes prior to citrate (blue top) tubes. Any tube containing an alternate anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

Please print and use the Specimen Collection Bulletin as a tube-filling guide.
Storage Instructions: Specimens are stable at room temperature for up to 24 hours. If testing cannot be completed within 24 hours, specimens should be centrifuged for at least 10 minutes at 1500xg. Plasma should then be transferred to a LabCorp PP transpak frozen purple tube with screw cap (LabCorp N^o 49482). Freeze immediately and maintain frozen until tested. Refer to Coagulation Collection Procedures for directions.
Causes for Rejection: Clotted specimen; gross lipemia or hemolysis; tubes <90% full; improper labeling; specimen collected in tube other than 3.2% citrate
Use: Diagnosis of homozygous and heterozygous fibrinogen deficiency as well as dysfibrinogenemia; diagnosis of disseminated intravascular coagulation;^6,7,8 fibrinogen levels can be used to assess the effectiveness of thrombolytic therapy.⁹
Limitations: Fibrinogen is an acute-phase reactant and can often become significantly increased in conditions involving tissue damage, infection, or inflammation.⁶ Increased levels may be seen in smokers, during pregnancy, and in women taking oral contraceptives.⁶ Fibrinogen levels can be diminished in advanced liver disease.⁹ Very high levels of heparin or fibrin breakdown products may falsely reduce fibrinogen levels because they interfere with the rate of clot formation.⁶ Lipemia or hemolysis may interfere with this assay.
Methodology: Prothrombin reagent (thromboplastin) is mixed with the patient sample. This activates the extrinsic pathway and converts endogenous prothrombin to thrombin. Thrombin, in turn, converts fibrinogen to fibrin. Clot formation monitored by light transmittance is compared to a calibration curve to produce a functional fibrinogen concentration.
Additional Information: Fibrinogen, also referred to as factor I, is a 340 kilodalton glycoprotein that is produced by the liver.⁶ Fibrinogen has a plasma half-life of about 4 days. Proteolytic conversion of fibrinogen to fibrin occurs through both the extrinsic and intrinsic pathways.⁶ Fibrinogen deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT).^7,8

Congenital afibrinogenemia, a condition associated with the complete absence of fibrinogen, is rare with only about 150 cases reported in the literature.^6,7 Fibrinogen deficiency is inherited as an autosomal recessive trait.^7,8 Afibrinogenemia occurs in individuals who are homozygous or doubly heterozygous for mutations. These individuals have infinite protime and aPTT results due to the inability to produce fibrin. Approximately 25% of patients with afibrinogenemia have mild thrombocytopenia.⁷

Individuals who are heterozygous for congenital fibrinogen deficiency are usually asymptomatic unless their fibrinogen levels fall to <50 mg/dL.⁷ Both functional (activity) and antigenic levels are diminished in these individuals.⁷ Fibrinogen deficiency affects both males and females with a prevalence that is equal in all ethnic groups.⁷ Acquired deficiencies occur in individuals with significant hepatic dysfunction, renal disease, and after L-asparaginase therapy.⁶ Diminished levels can also be seen in patients with disseminated intravascular coagulation (DIC) or who are undergoing thrombolytic therapy.⁶ Fibrinogen is one of the major determinants of the erythrocyte sedimentation rate and individuals with afibrinogenemia typically have greatly extended sedimentation rates.⁷

Individuals with dysfibrinogenemia have fibrinogen that is qualitatively defective with low functional fibrinogen levels (activity) and normal or decreased antigenic levels.⁶ Congenital dysfibrinogenemia is inherited as an autosomal dominant mutation.⁶ A number of disfibrinogenemic defects have been identified with a variety of manifestations including abnormal fibrin polymerization, impaired fibrinopeptide release, abnormal fibrin stabilization, and abnormal fibrin clot lysis.^6,7 Fibrinogen activity and antigen levels are useful in the diagnosis of dysfibrinogenemia since these individuals often have diminished activity relative to antigen levels.⁸

Individuals with afibrinogenemia have a bleeding tendency of varying severity.⁷ Symptoms often start in early infancy with umbilical cord bleeding, intracerebral hemorrhage, or bleeding at circumcision.^6,7,8 Individuals with afibrinogenemia also suffer from deep muscle and joint bleeding and other mucous membrane bleeding throughout life.⁶ Women with afibrinogenemia typically do not experience menorrhagia.⁸ Patients with heterozygous hypofibrinogenemia usually have a minimal history of bleeding with symptoms only observed after major surgery or trauma.^6,7 Approximately 50% of individuals with dysfibrinogenemia are asymptomatic.^6,7 These individuals are usually detected when prolonged clotting times are discovered as a result of routine laboratory testing. However, about one in four will suffer prolonged bleeding after surgery and approximately 20% will have an increased tendency toward thrombosis.⁶

A number of clinical and epidemiological studies have revealed a consistent association between elevated fibrinogen levels and increased risk for atherosclerotic vascular disease.¹⁰ However, it remains to be determined whether increased fibrinogen acts as a mediator of arterial thrombosis or simply reflects the inflammation associated with atherosclerosis.¹⁰

Footnotes:

Adcock DM, Kressin DC, and Marlar RA, “Effect of 3.2% vs 3.8% Sodium Citrate Concentration on Routine Coagulation Testing,” Am J Clin Pathol, 1997, 107(1):105-10.
Reneke J, Etzell J, Leslie S, et al, “Prolonged Prothrombin Time and Activated Partial Thromboplastin Time Due to Underfilled Specimen Tubes With 109 mmol/L (3.2%) Citrate Anticoagulant,” Am J Clin Pathol, 1998, 109(6):754-7.
“National Committee for Clinical Laboratory Standardization: Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline,” Third Edition, Villanova: NCCLS Document H21-A3:11(23), 1999.
Gottfried EL and Adachi MM, “Prothrombin Time and Activated Partial Thromboplastin Time Can Be Performed on the First Tube,” Am J Clin Pathol, 1997, 107(6):681-3.
McGlasson DL, More L, Best HA, et al, “Drawing Specimens for Coagulation Testing: Is a Second Tube Necessary?” Clin Lab Sci, 1999, 12(3):137-9.
Adcock DM, Jensen R, Johns CS, et al, Coagulation Handbook, Esoterix Coagulation, 2002.
Roberts HR and Escobar MA, “Less Common Congenital Disorders of Hemostasis,” Consultative Hemostasis and Thrombosis, Kitchens CS, Alving BM, and Kessler CM, eds, Philadelphia, PA: WB Saunders Co, 2002, 57-71.
Triplett DA, “Coagulation Abnormalities,” Clinical Laboratory Medicine, 2nd ed, McClatchey KD, ed, Philadelphia, PA: Lippincott Williams and Wilkins, 2002, 1033-49.
Van Cott EM and Laposata M, “Coagulation,” Laboratory Test Handbook With Key Word Index, Jacobs DS, DeMott WR, and Oxley DK eds, Hudson, OH: Lexi-Comp, 2001, 327-58.
Chandler WL, Rodgers GM, Sprouse JT, et al, “Elevated Hemostatic Factor Levels as Potential Risk Factors for Thrombosis,” Arch Pathol Lab Med, 2002, 126(11):1405-14

Test 361

SuperUser Account — Tue, 16 Sep 2008 21:44:29 GMT

Test: Fecal Fat, Qualitative
Number: 001677
CPT: 82705
Synonyms: Fatty Acid, Stool ; Fecal Fat Stain ; Neutral Fat, Stool ; Qualitative Fat ; Sudan IV Stain, Stool
Test Includes: Neutral and total fats
Specimen: Stool (fresh random)
Volume: Approximately 3 g
Minimum Volume: 0.5 g
Container: Plastic screw-cap vial
Collection: Do not contaminate outside of container; do not overfill container.
Storage Instructions: Refrigerate at 2°C to 8°C.
Patient Preparation: Patient should be on a diet containing at least 60 g of fat. The patient should not use suppositories or mineral oil before the specimen is collected. Oily material (eg, creams, lubricants, etc) should be avoided prior to collection of the specimen.
Causes for Rejection: Specimen contaminated with urine and/or water; specimen on outside of container; specimen containing interfering substances (eg, castor oil, bismuth, Metamucil®, barium)
Reference Interval:

Total fats (neutral fats, soaps, and fatty acids): normal (<100 droplets/hpf)
Neutral fats: normal (<60 droplets/hpf)

Use: Detect the presence of fecal fatty acids and neutral fat. Increases in neutral fat are commonly associated with pancreatic exocrine insufficiency. Increase in stool total fats (neutral fats, soaps, and fatty acids) is likely to be associated with small bowel disease.
Methodology: Microscopic examination following staining with Sudan IV
Contraindications: Administration of barium, bismuth, Metamucil®, castor oil, mineral oil, or ingestion of oily salad dressing within 1 week prior to collection of the specimen

Test 414

SuperUser Account — Tue, 16 Sep 2008 21:45:27 GMT

Test: Fructose, Semen Analysis
Number: 001875
CPT: 82757
Specimen: Semen, frozen
Volume: Entire specimen
Container: Clean screw-cap container
Collection: To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Storage Instructions: Freeze at -20°C.
Patient Preparation: Follow physician´s instructions.
Causes for Rejection: Thawed specimen
Reference Interval: Positive
Use: Congenital absence of vas deferens; blocked ejaculatory ducts, either congenital or acquired
Methodology: Resorcinol

Test 448

SuperUser Account — Tue, 16 Sep 2008 21:46:06 GMT

Test: Folate (Folic Acid)
Number: 002014
CPT: 82746
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.4 mL (Note: This volume does not allow for repeat testing.)
Container: Red-top tube or gel-barrier tube
Collection: If a red-top tube is used, transfer separated serum immediately to a plastic transport tube. Avoid hemolysis.
Storage Instructions: Refrigerate
Causes for Rejection: Plasma specimen; hemolysis
Reference Interval:

Normal: >5.4 ng/mL
Deficit: <3.4 ng/mL
Intermediate: 3.4-5.4 ng/mL

Use: Detect folate deficiency; monitor therapy with folate; evaluate megaloblastic and macrocytic anemia; evaluate alcoholic patients and those with prior jejunoileal bypass for morbid obesity or those with intestinal blind-loop syndrome
Limitations: May be decreased in patients on oral contraceptives. Frequently measured with red cell folate and vitamin B₁₂ levels.
Methodology: Immunochemiluminometric assay (ICMA)
Additional Information: Naturally occurring folates are present widely in plant and animal foods taken in the diet and absorbed in the small intestine. Folic acid (pteroylglutamic acid) has a number of biologically active forms (largely conjugates of glutamic acid, eg, N-5-methyltetrahydrofolic acid and N-5-formyltetrahydrofolic acid - folinic acid) that function as coenzymes. Lack of folic acid inhibits DNA synthesis in rapidly dividing cells, thus producing megaloblastic anemia. While a specific folate-binding protein is present in the serum, some 90% of folate is unbound. The binding protein increases with folate deficiency and returns to normal with treatment.

Serum levels are affected by present dietary intake. Drugs that are folate antagonists, such as methotrexate and pentamidine, may induce a deficiency state. Some drugs, such as oral contraceptives, phenytoin, and ethanol impair absorption of folate. In the pH range of physiologic significance, folate binds to aluminum hydroxide. Chronic use of antacids or H₂-receptor antagonists by patients with diets marginal in folate has been considered as a cause of folic acid deficiency.¹ Levels are commonly high in patients with B₁₂ deficiency since this vitamin is needed to allow incorporation of folate into tissue cells. Folate (folic acid) deficiency is present in some 33% of pregnant women, many alcoholics, patients with a wide variety of malabsorption syndromes including celiac disease, sprue, Crohn disease, and jejunal/ileal bypass procedure.

Measurement of both serum and red cell folate levels constitutes a reliable means of determining the existence of folate deficiency. These tests are recommended for all patients who have megaloblastic anemia, as well as for patients who have anemia, hypersegmentation of the granulocytic nuclei, and coincident evidence of iron deficiency. The finding of a low serum folate means that the patient´s recent diet has been subnormal in folate content and/or that recent absorption of folate has been subnormal, but does not prove that the patient either has or will develop tissue folate depletion requiring folate therapy. Therefore, serum folate assays have a very poor predictive value in diagnosis and should be interpreted with caution. A low red cell folate can mean either that there is tissue folate depletion due to folate deficiency requiring folate therapy, or alternatively, that the patient has primary vitamin B₁₂ deficiency blocking the ability of cells to take up folate. In the latter case, the proper therapy would be with vitamin B₁₂ rather than with folic acid. It is for these reasons that it is advisable to determine red cell folate in addition to serum folate, and thereby definitively determine that the diagnosis is folate deficiency for which the proper treatment is folic acid. For thoroughness, the serum vitamin B₁₂ level should also be determined, since >50% of all patients with significant megaloblastic anemia have primary deficiency of vitamin B₁₂ rather than of folic acid.²

Folate deficient diets have been proposed for methotrexate responsive malignancy. It has also been suggested that plasma folate concentrations in patients who do and do not respond to folate deprivation/antagonism be compared and ratioed to methotrexate levels as part of tumor therapy regimes.³ The levels of serum and RBC folate may be significantly increased in hyperthyroidism.⁴

Footnotes:

Russell RM, Golner BB, Krasinski SD, et al, “Effect of Antacid and H₂ Receptor Antagonists on the Intestinal Absorption of Folic Acid,” J Lab Clin Med, 1988, 112(4):458-63.
Bauer JD, Clinical Laboratory Methods, 9th ed, St Louis, MO: Mosby-Year Book Inc, 1982, 95-6.
Cohen P and Dix D, “On the Role of Folate Deficiency in Cancer Therapy,” Clin Chem, 1988, 34(9):1945-6 (letter).
Ford HC, Carter JM, and Rendle MA, “Serum and Red Cell Folate and Serum Vitamin B₁₂ Levels in Hyperthyroidism,” Am J Hematol, 1989, 31(4):233-6

References:

Chanarin I, “Megaloblastic Anaemia, Cobalamin, and Folate,” J Clin Pathol, 1987, 40(9):978-84 (review).

Craig GM, Elliot C, and Hughes KR, “Masked Vitamin B₁₂ and Folate Deficiency in the Elderly,” Br J Nutr, 1985, 54(3):613-9.

Davis RE and Nicol DJ, “Folic Acid,” Int J Biochem, 1988, 20(2):133-9 (review).

Test 658

SuperUser Account — Tue, 16 Sep 2008 21:51:09 GMT

Test: Follicle-Stimulating Hormone (FSH), Serum
Number: 004309
CPT: 83001 (per specimen)
Synonyms: FSH ; FSH, Serum ; Pituitary Gonadotropin
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.3 mL (Note: This volume does not allow for repeat testing.)
Container: Red-top tube or gel-barrier tube
Collection: If a red-top tube is used, transfer separated serum to a plastic transport tube. Avoid hemolysis.
Storage Instructions: Refrigerate
Causes for Rejection: Plasma specimen
Reference Interval: See table.^1,2

Age	Male (mIU/mL)	Female (mIU/mL)
5th d	<0.2-4.6	<0.2-4.6
2 mo - 3 y	0.2-2.7	1.4-9.2
4-6 y	0.2-2.7	0.4-6.6
7-9 y	0.2-2.7	0.4-5.0
10-11 y	0.4-5.0	Not established
12-13 y	0.4-6.6	Not established
14-15 y	0.7-13.2	Not established
>15 y	1.4-18.1	Follicular: 2.5-10.2
Midcycle: 3.4-33.4
Luteal: 1.5-9.1
Pregnant: <0.2
Postmenopausal: 23.0-116.3
Tanner Stage
I & II	0.3-4.6	0.7-6.7
III & IV	1.2-15.4	1.0-7.4
V	1.5-6.8	1.0-9.2

Use: Excessive FSH and LH are found in hypogonadism, anorchia, gonadal failure,³ complete testicular feminization syndrome, menopause, Klinefelter syndrome, alcoholism, castration. FSH and LH are pituitary products, useful to distinguish primary gonadal failure from secondary (hypothalamic/pituitary) causes of gonadal failure, menstrual disturbances and amenorrhea. Useful in defining menstrual cycle phases in infertility evaluation of women and testicular dysfunction in men. FSH is commonly used with LH, which also is a gonadotropin. Both are low in pituitary or hypothalamic failure. FSH and LH levels are high following menopause.
Limitations: Secretion of both LH and FSH are pulsatile, in response to the normal intermittent release of gonadotropin releasing hormone (GnRH). In addition, in females both FSH and LH vary over the course of the menstrual cycle, with peaks at time of ovulation. Thus, interpretation of a single determination may be difficult. It has been suggested that samples be obtained at 15-30 minute intervals and equal volumes of serum be pooled to decrease the effect of pulsatile secretion.
Methodology: Immunochemiluminometric assay (ICMA)
Additional Information: FSH and LH are glycoprotein pituitary hormones which have unique β-subunits, and α-subunits in common with TSH and hCG. They are under complex regulation by hypothalamic GnRH and by gonadal sex hormones, estrogen and progesterone in females, and testosterone. On the simplest level, FSH and LH are high in conditions in which sex hormones cannot be elaborated, and low in conditions of primary pituitary dysfunction. FSH acts on granulosa cells of the ovary and the Sertoli cells of testis. LH acts on Leydig (interstitial) cells of the gonads. Normally FSH increase occurs at an early stage of puberty, 2-4 years before LH reaches the same levels.

FSH is elevated in Klinefelter syndrome and in some subjects with precocious puberty. It is decreased with precocious puberty related to adrenal tumors or congenital adrenal hyperplasia. Normal FSH in an adult nonovulating female, represents dysfunction at the central nervous system hypothalamic/pituitary level, and a “normal” value should in such a setting be considered pseudonormal.

High LH:FSH ratio (over 1.5) is found in the polycystic ovary syndrome.⁴

Footnotes:

Murthy JN, Hicks JM, and Soldin SJ, “Evaluation of the Technicon Immuno I Random Access Immunoassay Analyzer and Calculation of Pediatric Reference Ranges for Endocrine Tests, T-Uptake, and Ferritin,” Clin Biochem, 1995, 28(2):181-5.
Tietz NW, ed, Clinical Guide to Laboratory Tests, 3rd ed, Philadelphia, PA: WB Saunders Co, 1995, 220.
Layman LC, Wilson JT, Huey LO, et al, “Gonadotropin-Releasing Hormone, Follicle-Stimulating Hormone Beta, Luteinizing Hormone Beta Gene Structure in Idiopathic Hypogonadotropic Hypogonadism,” Fertil Steril, 1992, 57(1):42-9.
Watts NB and Keffer JH, Practical Endocrine Diagnosis, 4th ed, Philadelphia, PA: Lea & Febiger, 1989

References:

Jaakkola T, Ding YQ, Kellokumpu-Lehtinen P, et al, “The Ratios of Serum Bioactive/Immunoreactive Luteinizing Hormone and Follicle-Stimulating Hormone in Various Clinical Conditions With Increased and Decreased Gonadotropin Secretion: Re-evaluation by a Highly Sensitive Immunometric Assay,” J Clin Endocrinol Metab, 1990, 70(6):1496-505.

Test 689

SuperUser Account — Tue, 16 Sep 2008 21:52:02 GMT

Test: Ferritin, Serum
Number: 004598
CPT: 82728
Special Instructions: Values obtained with different assay methods should not be used interchangeably in serial testing. It is recommended that only one assay method be used consistently to monitor each patient´s course of therapy. This procedure does not provide serial monitoring; it is intended for one-time use only. If serial monitoring is required, please use the serial monitoring number 480111 (see test below) to order.
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.3 mL (Note: This volume does not allow for repeat testing.)
Container: Red-top tube or gel-barrier tube
Collection: If a red-top tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions: Refrigerate
Causes for Rejection: Plasma specimen; hemolysis
Reference Interval: Male: 22-322 ng/mL; female: 10-291 ng/mL
Use: Diagnose hypochromic, microcytic anemias. Decreased in iron deficiency anemia and increased in iron overload. Ferritin levels correlate with and are useful in evaluation of total body storage iron. In hemochromatosis, both ferritin and iron saturation are increased. Ferritin levels in hemochromatosis may be >1000 ng/mL.
Limitations: Ferritin escapes from necrotic hepatocytes. In the presence of liver disease, inflammatory diseases such as rheumatoid arthritis, with malignancy or with iron therapy, iron deficiency may not be reflected by low serum ferritin. Ferritin determinations are not reliable in infants on iron therapy. Bone marrow aspiration may be needed in some settings, such as low-normal ferritin and low serum iron in the presence of apparent anemia of chronic disease, low-normal ferritin in the presence of liver disease.¹
Methodology: Immunochemiluminometric assay (ICMA)
Additional Information: The serum ferritin is, other than a bone marrow examination, the most reliable indicator of total body iron stores. When combined with the serum iron and percent saturation of iron binding capacity/transferrin, it can usually differentiate the microcytic hypochromic anemias into iron deficiency anemia (ferritin low, iron low, saturation low, TIBC high, transferrin high), the anemia of chronic disease (ferritin normal or high, iron low, normal to low transferrin or TIBC), or thalassemia (ferritin normal or high). Ferritin is low with combined iron deficiency and thalassemia. In adults, serum ferritin level ≤10 ng/mL indicates iron deficiency. High serum ferritin levels may be associated with inflammation, liver disease, megaloblastic anemia, hemolytic anemia, sideroblastic anemia, thalassemia, iron overload (hemochromatosis, hemosiderosis), malignant diseases including leukemia and malignant lymphoma and are described with CEA elevations in patients with breast cancer. Very high levels indicate iron overload. Oral and injected iron increase ferritin levels. Increased serum ferritin may be a risk factor in primary hepatocellular carcinoma.²

Primary hemochromatosis is inherited in an autosomal recessive manner with preliminary evidence that the involved gene is linked to the A locus of the histocompatibility complex on chromosome 6. Inappropriate increase in iron absorption and parenchymal tissue deposition eventuates in hepatic cirrhosis, diabetes, testicular atrophy, and fine, soft, bronze to slate gray skin and very high serum ferritin levels (usually >1000 ng/mL).

Red cell ferritin in conjunction with serum ferritin may be useful in distinguishing iron deficiency from iron overload in patients who have β-thalassemia.³

The decline in serum ferritin occurring during adolescence has been shown to be due to the onset of menarche rather than as a result of the accompanying growth spurt.⁴

Elevated serum ferritin levels in patients with cancer is associated with a poor prognosis which may be due in part to deleterious biological effects of tumor ferritins on lymphocyte and granulocyte function.⁵ Extensive data is accumulating on the nature of isoferritins and their association with and possible utilization in the evaluation of malignant neoplasia.⁶

Footnotes:

Sheehan RG, Newton MJ, and Frenkel EP, “Evaluation of a Packaged Kit Assay of Serum Ferritin and Application to Clinical Diagnosis of Selected Anemias,” Am J Clin Pathol, 1978, 70(1):79-84.
Hann HW, Kim CY, London WT, et al, “Increased Serum Ferritin in Chronic Liver Disease: A Risk Factor for Primary Hepatocellular Carcinoma,” Int J Cancer, 1989, 43(3):376-9.
Van Der Weyden MB, Fong H, Hallam LJ, et al, “Red Cell Ferritin and Iron Overload in Heterozygous Beta-Thalassemia,” Am J Hematol, 1989, 30(4):201-5.
Kagamimori S, Fujita T, Naruse Y, et al, “A Longitudinal Study of Serum Ferritin Concentration During the Female Adolescent Growth Spurt,” Ann Hum Biol, 1988, 15(6):413-9.
Hann HW, Stahlhut MW, Lee S, et al, “Effects of Isoferritins on Human Granulocytes,” Cancer, 1989, 63(12):2492-6.
Albertini A, Arosio P, Chiancone E, et al, “Ferritins and Isoferritins as Biochemical Markers,” Proceeds of Advanced Course on Ferritins and Isoferritins as Biochemical Markers, Amsterdam, Holland: Elsevier/North Holland Biomedical Press, 1984

References:

Bothwell TH, Charlton RW, and Motulsky AG, “Hemochromatosis,” The Metabolic Basis of Inherited Disease, Scriver CR, Beaudet AL, Sly WS, et al, eds, 6th ed, New York, NY: McGraw-Hill Information Services Co, 1989, 1433-62.

Grail A, Hancock BW, and Harrison PM, “Serum Ferritin in Normal Individuals and in Patients With Malignant Lymphoma and Chronic Renal Failure Measured With Seven Different Commercial Immunoassay Techniques,” J Clin Pathol, 1982, 35(11):1204-12.

Halliday CE, Halliday JW, and Powell LW, “The Clinical Manifestations of Chronic Iron Overload,” Baillieres Clin Haematol, 1989, 2(2):403-21 (review).

Hann HW, Lange B, Stahlhut MW, et al, “Prognostic Importance of Serum Transferrin and Ferritin in Childhood Hodgkin´s Disease,” Cancer, 1990, 66(2):313-6.

Lustbader ED, Hann HW, and Blumberg BS, “Serum Ferritin as a Predictor of Host Response to Hepatitis B Virus Infection,” Science, 1983, 220(4595):423-5.

Test 1127

SuperUser Account — Tue, 16 Sep 2008 22:07:36 GMT

Test: Fungus Stain
Number: 008136
CPT: 87206
Synonyms: Calcofluor ; KOH
Specimen: Aspirate, biopsy, body fluid, bronchoalveolar lavage, hair, nails, skin, sinus, sputum, stool, swab of conjunctiva, throat, tissue, urine, or vaginal
Volume: 50 mL bronchoalveolar lavage, 5 mL fluids, 2 mL tissue
Container: Sterile leakproof container or swab
Collection:

Biopsy: Surgical specimen in sterile container. A small amount of sterile nonbacteriostatic water should be used to prevent drying.

Body fluid, aspirates: Aspirated material in sterile container.

Skin and nails: Cleanse the area with 70% alcohol prior to specimen collection. Nail scraping should be from a subsurface portion of the infected nail. Skin should be taken from the active border of the lesion.

Hair: Epilate 10-12 hairs and place them in a sterile container.

Stool: Random sample in sterile container.

Swabs of throat, nose, nasopharynx, ear, vagina: Swab affected area or visible lesion.

Urine: Clean catch midstream sample in sterile container.

Wound: Purulent material, fluid, scraping of lesion border, or swab (least preferred) in sterile transport container. Swabs cannot be split for other tests.

Avoid contamination of the specimen with commensal organism as much as possible. Specify the source of the specimen and include any pertinent clinical information.

Storage Instructions: Maintain specimen at room temperature.
Patient Preparation: Usual sterile preparation (see Blood Culture, Routine [008300] ).
Causes for Rejection: Swab without evidence of specimen present; leaking specimen; inappropriate specimen transport device including syringe with needle; unlabeled specimen or name discrepancy between specimen and request label; specimen received after prolonged delay (usually more than 72 hours); specimen received in expired transport
Use: Determine the presence or absence of fungal forms in clinical specimens submitted for direct microscopic exam
Additional Information: KOH/calcofluor: Microscopic examination of nails does not have the sensitivity of culture. KOH alone can be difficult to read and time-consuming. KOH plus the whitener calcofluor increases the sensitivity of the smear. The KOH/calcofluor requires a fluorescence microscope for reading but is superior to KOH alone and replaces the PAS stain for detection capabilities. Positive smears using KOH/calcofluor can be expected in about 60% of positive cultures. If the smear is positive then the likelihood that the culture will grow a dermatophyte is greater than if the smear is negative. See table for retrospective recovery data.

Fungi Grown From Smear-Positive Nails	Fungi Grown From Smear-Negative Nails
T. rubrum (54%)	Various “saprophytes” (50%)
Various “saprophytes” (23%)	Yeasts (19%)
Yeasts (12%)	T. rubrum (12%)
T. mentagrophytes (6%)	T. mentagrophytes (6%)
Fusarium sp (2%)	Fusarium sp (5%)
Scopulariopsis sp (2%)	T. tonsurans (2%)
	Aspergillus sp (2%)
	Chrysosporium sp (2%)
	Paecilomyces sp (2%)

Test 1176

SuperUser Account — Tue, 16 Sep 2008 22:09:47 GMT

Test: Fungus (Mycology) Culture
Number: 008482
CPT: 87101
Synonyms: Blood Culture, Fungus ; Culture, Fungus (Mycology) ; Fungus Blood Culture ; Fungus Culture, Blood ; Mold Culture ; Yeast Culture
Test Includes: Culture for fungi. Isolation and identification (additional charges/CPT code[s] may apply) if culture results warrant. CPT coding for microbiology and virology procedures often cannot be determined before the culture is performed.
Specimen: Aspirate, biopsy, blood, body fluid, bronchoalveolar lavage, hair, nails, skin, sputum, stool, swab of conjunctiva, throat, tissue, urine, or vaginal
Volume: 2 mL or 1 cm³ tissue, 10 mL blood, whole nails, 50 mL body fluid (5 mL CSF), 5 mL aspirates or sputum; skin scrapings may be submitted on Mycosel® media (not supplied by LabCorp)
Container: Sterile container for fluid or tissue or green-top (heparin) tube, blood culture bottle
Collection:

Biopsy: Surgical specimen in sterile container. A small amount of sterile nonbacteriostatic water should be added to prevent drying.

Body fluid, aspirates: Aspirated material in sterile container.

Eye: For keratitis, scrapings with a Kimura spatula directly inoculated using “C” streaks are best.

Skin: Cleanse the area with 70% alcohol and collect a portion from the active border of the lesion.

Nails: For all types of onychomycosis, clean the nail area well with 70% alcohol, then, depending on type of nail disease, collect the following:

Distal subungual: Clip the abnormal nail as close to the proximal edge as possible. Scrape the nail bed and underside of nail plate with a curet. Discard the outermost debris, which likely contains contaminants. Nail clippings are less desirable for culture.
Proximal subungual: Pare down the normal surface of nail plate in the area of the lunula. Collect white material from the deeper portion of plate.
White superficial: Scrape the white spots, discarding the outermost surface, which likely contains contaminants. Collect the white areas directly underneath.
Candida infection: Collect material closest to the proximal and lateral nail edges.

Hair: Epilate 10-12 hairs and place them in a sterile container.

Stool: Random sample in sterile container.

Swabs: Throat, nose, nasopharynx, and ear swabs are acceptable; material from the ear is better than a swab.

Urine: Clean catch midstream sample in sterile container.

Wound: Aspirate of purulent material or fluid, scraping of lesion border, or swab (least preferred) in sterile container. Swabs cannot be split for other tests.

Avoid contamination of the specimen with commensal organisms as much as possible. Specify the source of the specimen and include any pertinent clinical information. Cultures are incubated 1-4 weeks (depending on source) before a final negative report is issued.

Storage Instructions: Refrigerate nonsterile respiratory specimens; all others should be maintained at room temperature.
Patient Preparation: Usual sterile preparation (see Blood Culture, Routine [008300] ).
Causes for Rejection: Unlabeled specimen or name discrepancy between specimen and request label; specimen received after prolonged transport (usually more than 72 hours); swab without evidence of specimen present; specimen received after leaking transport container into specimen bag; inappropriate transport device, including syringe with needle. Trach-suction devices will often leak if the cap with tubing is not removed and replaced by a solid cap. This may need to be done by personnel collecting the specimen as the solid cap is usually in with the device. If there is not solid cap, the specimen should be transferred to a leakproof sterile cup with metal cap.
Use: Isolate and identify fungi. Blood: establish the diagnosis of fungal infections including fungemia, fungal endocarditis, and disseminated mycosis in patients at risk for fungal infections.
Limitations: Blood: A single (or even multiple) negative fungal blood culture does not exclude disseminated fungal infection. If disseminated or deep fungal infection is strongly suspected despite repeatedly negative blood cultures, biopsy of the appropriate tissue and/or bone marrow aspiration for sections and fungus culture should be considered.

Stool: Use of this test is generally limited to detection of Candida. Stool cultures have a low yield and are not recommended for the isolation of systemic fungi; however, Histoplasma capsulatum is recovered from the stool of AIDS patients with disseminated infection.

Methodology: Culture
Additional Information:

Blood: Fungemia can be a complication of venous or arterial catheterization, hyperalimentation, the acquired immunodeficiency syndrome (AIDS), and therapy with steroids, antineoplastic drugs, radiation, or broad spectrum antimicrobial agents. Intravenous drug abusers are prone to Candida endocarditis. Although many fungal species including Histoplasma capsulatum, Coccidioides immitis, and Cryptococcus neoformans are recoverable from blood cultures, the most common cause of fungemia is Candida albicans followed by other Candida sp, including Candida glabrata. Fungemia represents a failure of the host defense system. Fungemia may be precipitated by contamination of an indwelling catheter or, in the critically ill and immunocompromised patient, contamination of the gastrointestinal and less frequently the urinary tract.¹ In a review of 356 patients with neoplastic disease, Candida sp was recovered in 7% of neutropenic patients.

In the potentially immunocompromised host, a temperature of 38.5°C (101°F) for more than 2 hours, which is not associated with the administration of a pyrogenic drug (chemotherapy), indicates the presence of infection until proven otherwise. In these patients, characteristic signs and symptoms are frequently absent. A careful physical examination including mouth, anus, and genitalia may reveal the site of infection. Therapy must be instituted as soon as appropriate specimens are collected. Most infections in these patients are caused by gram-negative organisms (eg, E. coli, Pseudomonas sp, Klebsiella sp) and by S. aureus; however, fungi and other usually nonpathogenic organisms must be considered significant.²

Rarely blastospores (budding yeast structures) and pseudohyphae can be seen by examination of Wright stained venous peripheral blood smears. This technique may allow early diagnosis and therapy before culture results are available.³

Eye: The more common causes of keratomycosis include Fusarium solani, Candida albicans, Aspergillus fumigatus, Curvularia sp, Aspergillus flavus, other species of Aspergillus, Penicillium, Paecilomyces, Fusarium, and many other species.⁴ A keratomycosis-like clinical presentation may also be encountered caused by Nocardia asteroides and Mycobacterium fortuitum. Keratomycosis is a rare complication of contact lens use.⁵

Sinus: Fungal sinusitis has been increasingly recognized in otherwise healthy teenagers who often present with a history of recurrent sinusitis, asthma, and/or polyps. At surgery, material is consistently described as thick peanut butter-like or pistachio pudding-like. Dematiaceous fungi are the most common cause.

Skin: Candida sp may colonize skin. Clinical diagnosis of Candida infection involves consideration of predisposing factors such as occlusion, maceration altered cutaneous barrier function. Signs of Candida infection include bright erythema, fragile papulopustules, and satellite lesions.⁶ Patients with defects in T-lymphocyte responses, such as AIDS patients or individuals being treated with antineoplastic drugs, are especially susceptible to many fungal infections including superficial mycoses.^7,8 See table.

Selection of Specimens for the Diagnosis
of Superficial Mycosis and Dermatomycosis

Diagnosis	Specimen of Choice
Superficial mycoses
Piedra	Hair
Tinea nigra	Skin scraping
Pityriasis versicolor	Skin scraping
Dermatomycoses (cutaneous mycoses)
Onychomycosis	Nail scraping
Tinea capitis	Hair (black dot)
Tinea corporis	Skin scraping
Tinea pedis	Skin scraping
Tinea cruris	Skin scraping
Candidiasis
Thrush	Scraping of oral white patches
Diaper dermatitis	Scraping of pustules at margin
Paronychia	Scraping skin around nail
Cutaneous candidiasis	Scraping of pustules at margin
Erosio interdigitalis blastomycetia (coinfection with gram-negative rods)	Scrapings of interdigital space (routine culture also)
Congenital candidiasis	Scraping of scales, pustules and cutaneous debris, cultures of umbilical stump, mouth, urine, and stool
Mucocutaneous candidiasis	Scraping of affected area

Selection of Specimens for the Diagnosis
of Systemic and Subcutaneous Mycosis

Diagnosis	Specimen of Choice in Order of Usefulness
Systemic Mycoses
Aspergillosis	Sputum Bronchial aspirate Biopsy (lung)
Blastomycosis	Skin scrapings Abscess drainage (pus) Urine Sputum Bronchial aspirate
Candidiasis	Sputum Bronchial aspirate Blood Cerebrospinal fluid Urine Stool
Coccidioidomycosis	Sputum Bronchial aspirate Cerebrospinal fluid Urine Skin scrapings Abscess drainage (pus)
Cryptococcosis	Cerebrospinal fluid Sputum Abscess drainage (pus) Skin scraping Urine
Mycomycosis / phycomycosis / zygomycosis	Sputum Bronchial aspirate Biopsy (lung)
Paracoccidioidomycosis (South American blastomycosis)	Skin scrapings Mucosal scrapings Biopsy (lymph nodes) Sputum Bronchial aspirate
Subcutaneous Mycoses
Chromomycosis	Footnotes: Dyess DL, Garrison RN, and Fry DE, “Candida Sepsis. Implications of Polymicrobial Blood-Borne Infection,” Arch Surg, 1985, 120(3):345-8. Whimbey E, Kiehn TE, Brannon P, et al, “Bacteremia and Fungemia in Patients With Neoplastic Disease,” Am J Med, 1987, 82(4):723-30. Kates MM, Phair JB, Yungbluth M, et al, “Demonstration of Candida in Blood Smears,” Lab Med, 1988, 19:25. Rebell GC and Foster RK, “Fungi of Keratomycosis,” Manual of Clinical Microbiology, 3rd ed, Lennette EH, Balows AL, Hausler WJ, et al, eds, Washington, DC: ASM Press, 1980. White GL Jr, Thiese SM, and Lundergan MK, “Contact Lens Care and Complications,” Am Fam Physician, 1988, 37(4):187-92. McKay M, “Cutaneous Manifestations of Candidiasis,” Am J Obstet Gynecol, 1988, 158(4):991-3. Herrod HG, “Chronic Mucocutaneous Candidiasis in Childhood and Complications of Non-Candida Infection: A Report of the Pediatric Immunodeficiency Collaborative Group,” J Pediatr, 1990, 116(3):377-82. Diamond RD, “The Growing Problem of Mycoses in Patients Infected With the Human Immunodeficiency Virus,” Rev Infect Dis, 1991, 13(3):480-6. Hector RF, “Compounds Active Against Cell Walls of Medically Important Fungi,” Clin Microbiol Rev, 1993, 6(1):1-21. Boyars MC, Zwischenberger JB, and Cox CS Jr, “Clinical Manifestations of Pulmonary Fungal Infections,” J Thorac Imaging, 1992, 7(4):12-22. Fraser RS, “Pulmonary Aspergillosis: Pathologic and Pathogenetic Features,” Pathol Annu, 1993, 28(Pt 1):231-77. Clarke A, Skelton J, and Fraser RS, “Fungal Tracheobronchitis. Report of 9 Cases and Review of the Literature,” Medicine (Baltimore), 1991, 70(1):1-14. Cohen R, Roth FJ, Delgado E, et al, “Fungal Flora of Normal Human Small and Large Intestine,” N Engl J Med, 1969, 280(12):638-41. Chretien JH and Garagusi VF, “Current Management of Fungal Enteritis,” Med Clin North Am, 1982, 66(3):675-87. Gupta TP and Ehrinpreis MN, “Candida-Associated Diarrhea in Hospitalized Patients,” Gastroenterology, 1990, 98(3):780-5. Sanderson PJ and Bukhari SS, “Candida spp and Clostridium difficile Toxin-Negative Antibiotic-Associated Diarrhoea,” J Hosp Infect, 1991, 19(2):142-3. Wong-Beringer A, Jacobs RA, and Guglielmo BJ, “Treatment of Funguria,” JAMA, 1992, 267(20):2780-5. Kunin CM and Lipsky BA, “Treatment of Candiduria,” JAMA, 1989, 262:691-2 (question and answer). Frangos DN and Nyberg LM Jr, “Genitourinary Fungal Infections,” South Med J, 1986, 79(4):455-9 References: Anaissie EJ, Bodey GP, and Kantarjian H, “A New Spectrum of Fungal Infections in Patients With Cancer,” Rev Infect Dis, 1989, 11(3):369-78. Batra P, “Pulmonary Coccidioidomycosis,” J Thorac Imaging, 1992, 7(4):29-38. Cohn MS, “Superficial Fungal Infections. Topical and Oral Treatment of Common Types,” Postgrad Med, 1992, 91(2):239-44, 249-52. Danna PL, Urban C, Bellin E, et al, “Role of Candida in Pathogenesis of Antibiotic-Associated Diarrhoea in Elderly Inpatients,” Lancet, 1991, 337(8740):511-4. Elewski BE, Rinaldi MG, and Weitzman I, Diagnosis and Treatment of Onychomycosis: A Clinician´s Handbook, Calfon, NJ: SynerMed, 1995. Ginsburg CM, “Tinea capitis,” Pediatr Infect Dis J, 1991, 10(1):48-9. Gray LD and Roberts GD, “Laboratory Diagnosis of Systemic Fungal Diseases,” Infect Dis Clin North Am, 1988, 2(4):779-803. Guerra-Romero L, Telenti A, Thompson RL, et al, “Polymicrobial Fungemia: Microbiology, Clinical Features, and Significance,” Rev Infect Dis, 1989, 11(2):208-12. Hay RJ, “Fungal Skin Infections,” Arch Dis Child, 1992, 67(9):1065-7. Meyer RD, “Cutaneous and Mucosal Manifestations of the Deep Mycotic Infections,” Acta Derm Venereol Suppl (Stockh), 1986, 121:57-72 (review). Rasmussen JE, “Cutaneous Fungus Infections in Children,” Pediatr Rev, 1992, 13(4):152-6. Rezabek GH and Friedman AD, “Superficial Fungal Infections of the Skin Diagnosis and Current Treatment Recommendations,” Drugs, 1992, 43(5):674-82. Roy JB, Geyer JR, and Mohr JA, “Urinary Tract Candidiasis: An Update,” Urology, 1984, 23(6):533-7. Saral R, “Candida and Aspergillus Infections in Immunocompromised Patients: An Overview,” Rev Infect Dis, 1991, 13(3):487-92. Schuyler MR, “Allergic Bronchopulmonary Aspergillosis,” Clin Chest Med, 1983, 4(1):15-22. Tang CM and Cohen J, “Diagnosing Fungal Infections in Immunocompromised Hosts,” J Clin Pathol, 1992, 45(1):1-5. Telenti A, Steckelberg JM, Stockman L, et al, “Quantitative Blood Cultures in Candidemia,” Mayo Clin Proc, 1991, 66(11):1120-3. Ullrich R, Heise W, Bergs C, et al, “Gastrointestinal Symptoms in Patients Infected With Human Immunodeficiency Virus: Relevance of Infective Agents Isolated From Gastrointestinal Tract,” Gut, 1992, 33(8):1080-4. “Urinary Tract Candidosis,” Lancet, 1988, 2(8618):1000-2 (review). Wey SS, Mori M, Pfaller MA, et al, “Risk Factors for Hospital-Acquired Candidemia: A Matched Case-Controlled Study,” Arch Intern Med, 1989, 149(10):2349-53. Wheat LJ, “Systemic Fungal Infections: Diagnosis and Treatment. I. Histoplasmosis,” Infect Dis Clin North Am, 1988, 2(4):841-59 (review). Test 1250 SuperUser Account — Tue, 16 Sep 2008 22:13:29 GMT Test: Fine Needle Aspiration Cytology Number: 009001 CPT: 88173 Synonyms: Breast ; Breast Cyst Fluids ; Lymph Nodes ; Salivary Gland ; Thyroid ; Thyroid Cysts Test Includes: Cytologic evaluation of specimens obtained by fine needle aspiration from lesions of all body sites Special Instructions: Include patient´s name, date or birth, Social Security number, source, previous malignancy, drug therapy, radiation therapy, and all other pertinent clinical information on the request form. It is recommended to do an aspirate only on a palpable mass (“blind” sticks are discouraged except for those under radiologic guidance). A minimum of two separate passes should be done, preferably more (inadequate specimens result in false-negative diagnosis). It is very important to specify the source of the specimen along with clinical history and clinical impression. If a cyst is aspirated, indicate this fact on the request form; it will most likely be hypocellular but will not be a false-negative. If the patient has a known diagnosis of malignancy, please include that information on the request form. Whatever the specimen source, please include your clinical impression and reason for doing the aspiration (eg, “fine-needle aspiration on lymph node: suspect lymphoma vs metastatic carcinoma vs infectious process”). If an infectious process is in the differential, please submit a portion of the specimen to microbiology in an appropriate sterile medium or transport container. Once the specimen is smeared and/or put in an alcohol container, it is unsuitable for culture. Specimen: Aspirated material Container: Slide(s); Coplin jar(s) Collection: Use a small gauge (eg, 25-g or 22-g) needle to avoid dilution with blood. Immobilize the palpable mass with your nondominant hand. Using a syringe holder will allow you to keep your nondominant hand on the mass. Insert the needle into the mass and pull back on the syringe plunger, creating negative pressure, using it as a cutting tool. Make short 5 mm “in-and-out” motions until you see material coming into the hub of the needle. When you start to see material in the hub, stop, release negative pressure on the syringe, and pull out to make the slides. Do not aspirate material into the syringe or dilute with blood or saline. This interferes with making good direct smears. (See preparation of slides below.) If you do not see any material at all in the hub or syringe, continue the short 5 mm strokes until you have done 15-20 strokes. Pull out and attempt to express material on slides (see below). Repeat the above procedure again using a clean needle for a second pass (and more passes if needed). Many physicians use no local anesthesia. If you decide to give a local, please avoid aspirating the local anesthetic into the needle. It will dilute as well as distort the specimen. Making direct smears (preferred method): Using a graphite pencil, label 8-10 slides with the patient´s name before starting the procedure. After aspiration, make sure to have positive pressure in the syringe (if need be, remove the needle, pull back the plunger, then reattach the needle to gain positive pressure). Avoid aspirating the material from the needle into the syringe. Touch the end of the needle to the end of the glass slide and express one to two drops of material. (If too much material is expressed, the slides will be too thick for optimal interpretation. A thin monolayer of cells is desired.) Place a second slide on top of the first, allowing the drop to spread, then gently pull slides apart toward opposite end. Fix immediately in 95% ethyl alcohol. Note: It is imperative to fix the slides immediately to avoid air drying. Continue making more slides in this fashion until all the material in the needle is used. Do not discard the needle yet. Rinse the needle in a labeled container of balanced salt solution and an equal volume of 50% ethanol. Send all material to the lab. Alternative to making direct smears (less desirable, but acceptable): Express the specimen directly into a balanced salt solution and an equal volume of either 50% ethyl alcohol or Saccomanno fixative. Send to the laboratory for slide preparation. If a cyst is aspirated, use the alternative method outlined above. The laboratory will spin the specimen for concentration. Storage Instructions: Refrigerate Causes for Rejection: Improper labeling; improper fixation; air-drying artifact; specimen was submitted in a vial that expired according to the manufacturer´s label Use: Diagnose primary or metastatic malignant neoplasms; differential diagnosis of benign versus malignant processes Methodology: The fluid will be centrifuged, supernatant poured off, and diagnostic cells aspirated from the remaining material. Filters, thin preps, and/or cytospins will be made along with a cell block, if applicable. Microscopic examination is performed. Test 1312 SuperUser Account — Tue, 16 Sep 2008 22:16:10 GMT Test: Fine Needle Aspiration Cytology With Immediate Assessment Number: 009365 CPT: 88172; 88173 Synonyms: Adrenals ; Breast ; Liver ; Lung ; Lymph Node ; Pancreas ; Salivary Gland ; Soft Tissues ; Thyroid Test Includes: Rapid Pap stain or Diff-Quick® on collected specimen for evaluation of adequacy of specimen. Determination of adequacy is done while the patient is undergoing the procedure. Allows clinician/radiologist to determine accuracy of sampling as well as determining if continued samplings are necessary. Special Instructions: Include patient´s name, date of birth, sex, Social Security number, previous malignancy, drug therapy, radiation therapy, and all other pertinent clinical information, including history of alcohol abuse, on the request form. Laboratory personnel must be present for needle aspiration procedures under radiologic guidance if rendering of initial interpretation of quality of the specimen is desired. Call the cytology department manager for time arrangement. Twenty-four hour notification is preferred. Specify body site. Include pertinent clinical data on the request form (ie, age, history of carcinoma or infection, history of smoking, exposure to carcinogenic agents). A minimum of two samplings of the site is suggested. Specimen: Aspirated material Container: Slides Collection: Smears will be prepared by the cytotechnologist when present. Radiologist collects specimen. If technologist is not present follow this procedure for preparing slides. Fill Pap jar with 95% ethyl alcohol Using a graphite pencil, label slides with patient´s last name and first initial. Localize mass. Disinfect area. Apply local anesthesia on/in area to be needled. Introduce needle into mass. Create negative pressure and maintain. Sample area vigorously on several planes, maintaining the negative pressure. Note: Sample may be only in barrel of needle not in syringe. If no specimen is seen in syringe it does not mean an adequate sample has not been obtained! Release the plunger of the syringe to equalize pressure. Withdraw the needle from the mass. Place bevel of needle directly on one of the glass slides (in approximately the center of the slide). Express one to two drops of material onto this glass slide. Visible material expressed? Place the other glass slide on top of the first, and gently pull the slides apart - dispensing the material on the slides evenly. Important!! Place the slides back to back, in the jar of fixative immediately! No material expressed? Make a second attempt to express material on slide by first removing the needle from syringe. Pull back on syringe plunger, then place needle back onto syringe. Express one to two drops of material on the slide. If no material is expressed on the slide, rinse the barrel of the needle by aspirating saline into the barrel of the needle by aspirating saline into the syringe and expressing the saline wash into a clean container. Add an equal volume of Saccomanno fixative to this fluid. Attach the request form and transport the specimen to the laboratory. Storage Instructions: Slides in 95% ethyl alcohol will maintain well at room temperature. Saline wash of needle with Saccomanno fixative added in equal volume will maintain well at room temperature. Saline wash without fixative must be refrigerated and transported to cytology as soon as possible. Patient Preparation: To be determined by attending physician(s) Causes for Rejection: Improper labeling; improper fixation; air-drying artifact; specimen was submitted in a vial that expired according to the manufacturer´s label Use: Diagnose primary or metastatic malignant neoplasms; differential diagnosis of benign versus malignant processes Methodology: The fluid will be centrifuged, supernatant poured off, and diagnostic cells aspirated from the remaining material. Filters, monolayers, and/or cytospins will be made along with a cell block, if applicable. Microscopic examination is performed. Test 1489 SuperUser Account — Tue, 16 Sep 2008 22:25:02 GMT Test: Fecal Reducing Substances Number: 016766 CPT: 84377 Synonyms: Reducing Substances, Stool Test Includes: Total reducing substances Specimen: Stool (fresh random) Volume: 1 g Minimum Volume: 0.5 g Container: Screw-cap plastic vial Collection: Deliver specimen to laboratory as soon as possible; delay may cause falsely low results. Storage Instructions: Refrigerate at 2°C to 8°C. Causes for Rejection: Specimen collected in a diaper or other absorbent surface; specimen on outside of container Reference Interval: Normal: <0.25 g/dL; trace: 0.25-0.50 g/dL; increased: >0.50 g/dL Use: Detect deficiency of intestinal border enzymes, primarily sucrase and lactase (disaccharidases) due to congenital deficiency or nonspecific mucosal injury Methodology: Copper sulfate reduction (Clinitest®) Additional Information: Sugars should be rapidly absorbed in the upper small intestine. If not, however, they remain in the intestine and cause osmotic diarrhea by the osmotic pressure of the unabsorbed sugar in the intestine, drawing fluid and electrolytes into the gut. Carbohydrate malabsorption is a major cause of the watery diarrhea and electrolyte imbalance seen in patients with the short bowel syndrome. As a result of bacterial fermentation, the stools become acid with a high concentration of lactic acid. The pH measurement reflects this process. The unabsorbed sugars are measured as reducing substances. Although sucrose is not a reducing sugar, it is subjected to acid hydrolysis in the gut, and thus, is also measured as a reducing substance. Idiopathic lactase deficiency is common, occurring in 70% to 75% of Southern European Greeks and Italians, 70% of Black adults, >90% of Oriental adults, and 5% to 20% of white American adults. Lactase activity declines with age in humans and is controlled genetically. It is influenced in its phenotypic expression as lactase malabsorption by several nongenetic factors, eg, adaption to nutritional intake of dairy products, biological (circadian) rhythm of enzyme activity, hormones and hormonal changes of the body and the brain, gastrointestinal functions such as motility and the nutritional components of digested food.¹ There is considerable variation in lactose tolerance between lactase deficient subjects. A 50 g lactose load has been reported to cause symptoms in 75% of lactase deficient adults whereas 10 g cause symptoms in only 50%.² A glass of milk has approximately 12 g of lactose. Classically, stools from patients with disaccharidase deficiency are liquid, acid, and frothy in appearance. The use of mucosal disaccharidase enzyme activity as an isolated diagnostic criterion may have limited value.³ Footnotes: Enck P and Whitehead WE, “Lactase Deficiency and Lactose Malabsorption. A Review,” Z Gastroenterol, 1986, 24(3):125-34. Cooper BT, “Lactase Deficiency and Lactose Malabsorption,” Dig Dis, 1986, 4(2):72-82 (review). Calvin RT, Klish WJ, and Nichols BL, “Disaccharidase Activities, Jejunal Morphology, and Carbohydrate Tolerance in Children With Chronic Diarrhea,” J Pediatr Gastroenterol Nutr, 1985, 4(6):949-53 Test 1528 SuperUser Account — Tue, 16 Sep 2008 22:27:11 GMT Test: First Trimester Screen with Nuchal Translucency Number: 017500 CPT: 84163; 84702; 86336 Synonyms: First Trimester Screening, Combined Test Test Includes: hCG; pregnancy-associated plasma protein A (PAPP-A) Special Instructions: For test inquiries, call CMBP Genetic Services at 800-345-GENE. Client must provide a fetal nuchal translucency (NT) measurement and crown rump length measurement. The NT measurement must be performed by a sonographer credentialed by the Nuchal Translucency Quality Review Program, the Fetal Medicine Foundation, or other equivalent entity. The sonographer´s credential/certification number must be provided. The following information must also be provided: patient´s weight, patient´s date of birth, and the number of fetuses. Also indicate relevant patient history (ie, prior Down syndrome pregnancy, ultrasound anomalies). Complete information is necessary to interpret the test. Patient information may be provided to the laboratory using the Maternal Prenatal Screening requisition form 0900. Testing is provided from 10.0-13.9 weeks gestation. Specimen: Serum Volume: 3 mL Minimum Volume: 1 mL Container: Gel-barrier tube, no thrombin additive Collection: Avoid hemolysis. Send complete specimen in the original tube. Do not pour off. Storage Instructions: Refrigerate Causes for Rejection: Gross hemolysis; gross lipemia; quantity not sufficient for analysis; improper specimen type Use: Screening test in the first trimester of pregnancy for fetal Down syndrome and trisomy 18 Methodology: PAPP-A: enzyme immunoassay (EIA); hCG: immunochemiluminometric assay (ICMA) References: Wald NJ, Rodeck C, Hackshaw AK, et al, “First and Second Trimester Antenatal Screening for Down´s Syndrome: The Result of the Serum, Urine and Ultrasound Screening Study (SURUSS),” J Med Screening, 2003, 10(2):56-104. Test 1610 SuperUser Account — Tue, 16 Sep 2008 22:31:13 GMT Test: Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) Number: 028480 CPT: 83001; 83002 Synonyms: FSH and LH ; LH and FSH ; Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) Test Includes: Follicle-stimulating hormone (FSH); luteinizing hormone (LH) Specimen: Serum Volume: 1.5 mL Minimum Volume: 0.6 mL (Note: This volume does not allow for repeat testing.) Container: Red-top tube or gel-barrier tube Collection: If a red-top tube is used, transfer separated serum to a plastic transport tube. Storage Instructions: Refrigerate Causes for Rejection: Plasma specimen Methodology: Immunochemiluminometric assay (ICMA) Test 1638 SuperUser Account — Tue, 16 Sep 2008 22:32:22 GMT Test: Follicle-Stimulating Hormone (FSH), Serum, 3 Specimens Number: 038935 CPT: 83001 (x3) Special Instructions: Please refer to the directions for Sequential Sampling. Test 1639 SuperUser Account — Tue, 16 Sep 2008 22:32:24 GMT Test: Follicle-Stimulating Hormone (FSH), Serum, 5 Specimens Number: 038943 CPT: 83001 (x5) Special Instructions: Please refer to the directions for Sequential Sampling. Test 1667 SuperUser Account — Tue, 16 Sep 2008 22:33:36 GMT Test: Fecal Fat and Muscle Fibers, Qualitative Number: 049684 CPT: 82705; 89160 Synonyms: Muscle Fiber, Stool ; Stool Meat Fibers ; Stool Muscle Fiber Test Includes: Qualitative fat (total and neutral) and muscle fibers Specimen: Stool (random) Volume: 3 g Minimum Volume: 1 g Container: Plastic screw-cap vial Collection: Do not contaminate outside of container; do not overfill container. Storage Instructions: Refrigerate at 2°C to 8°C. Do not freeze. Patient Preparation: Patient is required to eat adequate amounts of red meat for 24-72 hours before testing. Specimens obtained with a warm saline enema or Fleet® Phospho-Soda® are acceptable. Specimens obtained with mineral oil, bismuth, or magnesium compounds are unsatisfactory. Barium procedures or laxatives should be avoided for 1 week prior to collection of the specimen. Causes for Rejection: Purgatives other than saline or Fleet®; specimen contaminated with urine; specimen obtained with mineral oil, bismuth, or magnesium compounds; specimen on outside of container Reference Interval: Total fats (neutral fats, soaps, and fatty acids): normal (<100 droplets/hpf) Neutral fats: normal (<60 droplets/hpf) Muscle fibers: normal (<10 fibers/hpf) Use: Evaluate malabsorption syndromes, pancreatic exocrine dysfunction, or gastrocolic fistula Methodology: Microscopic examination following staining with Sudan IV. Only fibers with identifiable cross striations are counted. Test 1752 SuperUser Account — Tue, 16 Sep 2008 22:37:56 GMT Test: Feathers, Finch Number: 060042 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: 10 mL red-top tube or 10 mL gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 1770 SuperUser Account — Tue, 16 Sep 2008 22:38:40 GMT Test: Fly, House (Fly Common) Number: 060075 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: 10 mL red-top tube or 10 mL gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 1811 SuperUser Account — Tue, 16 Sep 2008 22:40:21 GMT Test: Fennel, Fresh Number: 060369 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: Red-stopper tube or gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 1869 SuperUser Account — Tue, 16 Sep 2008 22:43:19 GMT Test: Foxtail, Meadow Number: 063834 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: Red-stopper tube or gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 1898 SuperUser Account — Tue, 16 Sep 2008 22:44:32 GMT Test: Fir, Douglas Number: 066852 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: Red-stopper tube or gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 1900 SuperUser Account — Tue, 16 Sep 2008 22:44:37 GMT Test: Fennel,Dog Number: 066902 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: Red-stopper or gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 1935 SuperUser Account — Tue, 16 Sep 2008 22:46:06 GMT Test: Flounder Number: 067496 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: Red-stopper tube or gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test Test 2018 SuperUser Account — Tue, 16 Sep 2008 22:49:42 GMT Test: Fescue, Meadow Number: 068833 CPT: 86003 Specimen: Serum Volume: 0.2 mL Container: Red-stopper tube or gel-barrier tube Storage Instructions: Refrigerate Methodology: Quantitative allergen-specific IgE test

Type: F

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