Type: L

Test 242

SuperUser Account — Tue, 16 Sep 2008 21:42:49 GMT

Test: Lactic Acid Dehydrogenase (LD)
Number: 001115
CPT: 83615
Synonyms: LD ; LDH
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.5 mL
Container: Red-top tube or gel-barrier tube
Collection: Separate serum from cells within 45 minutes of collection.
Storage Instructions: Maintain specimen at room temperature.
Causes for Rejection: Excessive hemolysis; improper labeling
Reference Interval: 100-250 IU/L
Use:

Causes of high LD: Neoplastic states* (especially with high alkaline phosphatase, very high total LD, and isomorphic pattern of LD isoenzymes); hypoxic cardiorespiratory diseases; hemolytic anemia*; megaloblastic anemias*, including pernicious anemia* (levels may be >2000 units/L and LD isoenzymes reveal LD₁:LD₂ flip); infectious mononucleosis*; inflammation; hypothyroidism (some cases*); myocardial infarct: LD begins to rise about 12 hours after infarct and usually returns to normal after CK (CPK) and AST (SGOT), isoenzymes usually most useful 48 hours from onset to reveal LD₁:LD₂ inversion*; pulmonary infarct (rarely, triad of LD, bilirubin, AST increases occurs); other lung diseases.

Diseases of liver*, including cirrhosis. Total LD in cirrhosis is usually not greatly increased. In acute viral hepatitis, LD is not greatly elevated and AST is usually three or more times higher (in relation to the upper limit of normal) than LD; chronic alcoholism is usually associated with some combination of high MCV (mean corpuscular volume), triglyceride, alkaline phosphatase, AST (SGOT), ALT (SGPT), GGT, bilirubin, and low folate*.

Renal infarct* - high LD, out of proportion to AST and alkaline phosphatase;¹ seizures, other CNS diseases; acute pancreatitis; collagen diseases; excessive destruction of cells*; fracture, other trauma, including head trauma, muscle damage; muscular dystrophy; focal necrosis; shock, hypotension; intestinal obstruction.

*LD isoenzymes may be useful.

Other causes of increased LD include specimen tube artifact, such as serum contact with clot or exposure to heat. Chemistry profile with very high LD and no glucose may relate to unseparated serum and cells in a tube at room temperature or higher. Since LD is found in virtually every tissue in the body, the diagnostic value of an elevated level is limited.

Limitations: Hemolysis elevates LD results; oxalate inhibits LD; ascorbic acid can decrease LD values.
Methodology: Kinetic
Additional Information: In infectious mononucleosis, LD is usually more elevated than AST, and there is usually an isomorphic pattern of LD isoenzymes. In viral hepatitis, by contrast, AST and ALT (the transaminases) are much more increased than is LD, about three or more times higher than total LD, and LD₅ is high. The differential diagnosis of acute infarct of myocardium includes pericarditis and angina, entities in which enzymes are usually not substantially increased. Bovine or porcine heparin therapy can cause increases of AST, ALT, and LD, with elevated LD hepatic fractions.²
Footnotes:

Winzelberg GG, Hull JD, Agar JW, et al, “Elevation of Serum Lactate Dehydrogenase Levels in Renal Infarction,” JAMA, 1979, 242(3):268-9.
Dukes GE Jr, Sanders SW, Russo J Jr, et al, “Transaminase Elevations in Patients Receiving Bovine or Porcine Heparin,” Ann Intern Med, 1984, 100(5):646-50

Test 301

SuperUser Account — Tue, 16 Sep 2008 21:43:34 GMT

Test: Lipase, Serum
Number: 001404
CPT: 83690
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.5 mL
Container: Red-top tube or gel-barrier tube
Collection: Separate serum from cells within 45 minutes of collection.
Storage Instructions: Refrigerate
Causes for Rejection: Improper labeling
Reference Interval: 0-59 units/L
Use: Diagnose pancreatitis, more specific for pancreatitis than is serum amylase; diagnose peritonitis, strangulated or infarcted bowel, pancreatic cyst
Methodology: Colorimetric
Contraindications: Urine specimens are inappropriate for lipase. Lipase activity is usually absent in urine, possibly from inactivation of the enzyme.
Additional Information: Serum lipase is usually normal in patients with elevated serum amylase, without pancreatitis, who have peptic ulcer, salivary adenitis, inflammatory bowel disease, intestinal obstruction, and macroamylasemia. Coexistence of increased serum amylase with normal lipase may be a helpful clue to the presence of macroamylasemia.¹ Lipase is elevated with amylase in acute pancreatitis, but the elevation of lipase is more prolonged.

In work-up of pancreatitis, in addition to serum lipase and amylase, the 2-hour urine amylase is of value. Electrolytes, serum calcium, glucose, and acetone are also often needed. Immunoreactive trypsin is technically more difficult than lipase and probably no better.² The serum lipase:amylase ratio may help distinguish alcoholic from nonalcoholic pancreatitis. Ratios >2 (expressed as multiples of the upper limits of normal) suggest an alcoholic etiology.³ Lipase isoform or isoenzymes have been studied.⁴

Footnotes:

Andrews PA and Thomas PA, “Macroamylasaemia as a Cause of Persistently Raised Serum Amylase,” Br J Surg, 1988, 75(10):1035.
Lott JA, Speicher CE, and Nemesánszky E, “Is Serum Amylase an Obsolete Test in the Diagnosis of Acute Pancreatitis?” Arch Pathol Lab Med, 1985, 109(4):314-5.
Gumaste VV, Dave PB, Weissman D, et al, “Lipase:Amylase Ratio. A New Index That Distinguishes Acute Episodes of Alcoholic From Nonalcoholic Acute Pancreatitis,” Gastroenterology, 1991, 101(6):1361-6.
Lott JA and Lu CJ, “Lipase Isoforms and Amylase Isoenzymes: Assays and Application in the Diagnosis of Acute Pancreatitis,” Clin Chem, 1991, 37(3):361-8

Test 410

SuperUser Account — Tue, 16 Sep 2008 21:45:20 GMT

Test: Lactate Dehydrogenase (LD) Isoenzymes
Number: 001842
CPT: 83625; 83615
Synonyms: Lactic Acid Dehydrogenase Isoenzymes ; LDH Isoenzymes ; LD Isoenzymes
Test Includes: Total serum LD and relative percentage of isoenzymes (LD_1-5)
Specimen: Serum
Volume: 3 mL
Minimum Volume: 1 mL
Container: Red-top tube
Collection: Separate serum from cells within 45 minutes of collection.
Storage Instructions: Maintain specimen at room temperature. Do not refrigerate or freeze. LD₅ is least stable with 13% lost at room temperature after 48 hours, 18% lost at refrigerated temperatures.
Patient Preparation: Cardiac enzymes and isoenzymes are best interpreted as a sequential series. Typically, a series of 3: 1 at admission (or initial event) and 2 more at 6- to 8-hour intervals.
Causes for Rejection: Hemolysis; prolonged contact of serum with red cells; specimen received frozen; specimen older than 48 hours after collection at time of testing
Reference Interval: Total: 100-250 IU/L; LD₁: 16% to 35%; LD₂: 24% to 41%; LD₃: 16% to 27%; LD₄: 5% to 14%; LD₅: 5% to 24%. See table.
LD Isoenzyme Interpretation

Abbrev¹	Total LDH	LD₁	LD₂	LD₃	LD₄	LD₅
Case 1	H	H	H	-	-	-
Case 2	H	H	H	-	-	-
Case 3	H	H>	H	-	-	-
Case 4	H	H>	H	-	-	H
Case 5	H	H	H	-	-	H
Case 6	H	-	-	-	H	H
Case 7	H	-	H	H	H	-
Case 8	H	H	H	H	H	H
Case 9	H	-	-	-	-	-
Case 10	N	-	-	-	-	-
Case 11	H	-	-	-	-	H
Case 12	Other patterns not shown

¹See following interpretation of abbreviations
H = high (increased)
- = within reference (normal) interval or decreased
N = within reference (normal) interval

Interpretations:

Case 1: Patient specimen was visibly hemolyzed which may have produced the elevations of LD₁ and LD₂ on the LD isoenzyme pattern.

Case 2: The LD isoenzyme pattern demonstrates elevations of LD₁and LD₂. These increases would be compatible with diagnostic considerations involving myocardial infarction, megaloblastic anemia, acute renal infarction, in vivo hemolytic process (eg, hemolytic anemia), or in the later stages of muscular dystrophy.

Case 3: The LD isoenzyme pattern demonstrates LD₁ greater than LD₂. In the appropriate clinical setting, this pattern is most compatible with postmyocardial infarction occurring at least 8-12 hours prior to venipuncture.

Case 4: The LD isoenzyme pattern demonstrates LD₁greater than LD₂ and an increase of LD₅. This pattern would be most compatible with passive hepatic congestion following an acute myocardial infarction or right-sided congestive heart failure associated with myocardial infarction.

Case 5: The LD isoenzyme pattern demonstrates elevations of LD₁ and LD₂and an increase of LD₅. This pattern would be compatible with diagnostic considerations involving passive hepatic congestion or right-sided congestive heart failure which may have followed acute myocardial damage.

Case 6: The LD isoenzyme pattern demonstrates elevations of LD₄and LD₅. These increases would be compatible with hepatic (cirrhosis, viral hepatitis, toxic hepatitis) or skeletal muscle injury. This pattern may also be associated with congestive heart failure.

Case 7: The LD isoenzyme pattern demonstrates elevations of LD₂, LD₃ and LD₄. Increases of these isoenzyme fractions are nonspecific but have been associated with septic shock, pulmonary emboli, and some neoplastic processes.

Case 8: The LD isoenzyme pattern demonstrates elevations of all isoenzymes without dominating fractions. This pattern is nonspecific but has been associated with septic shock, pulmonary emboli, and some neoplastic processes.

Case 9: The LD isoenzyme pattern appears normal despite elevation of the total LD.

Case 10: The LD isoenzyme pattern appears normal with a normal total LD.

Case 11: The LD isoenzyme pattern demonstrates an elevated LD₅ fraction which may be associated with hepatic anoxia due to congestive heart failure or the early stages of muscular dystrophy.

Case 12: The LD isoenzyme pattern is nonspecific. Recommend correlation with the clinical condition of the patient.
Use: Changes of LD isoenzymes periodically measured following onset of chest pain, studying the relationships of the anodic fractions, provide important information for the differential diagnosis of acute infarct of myocardium. The differential diagnosis of certain other diseases is enhanced as well with use of LD isoenzymes.

Useful in the differential diagnosis of acute myocardial infarction, megaloblastic anemia (folate deficiency, pernicious anemia), hemolytic anemia, and very occasionally renal infarct. These entities are characterized by LD₁ increases, often with LD₁: LD₂ inversion.

The isomorphic pattern (total LD significantly high with no increase in percentage, of any fraction) is seen with neoplasia, cardiorespiratory diseases, hypothyroidism, infectious mononucleosis, and other inflammatory states, uremia, and necrosis.

LD₅ increases are seen with striated muscle lesions (eg, trauma) and with liver diseases (eg, hepatic congestion, congestive heart failure, hepatitis, cirrhosis, alcoholism). LD₅ increase is probably more significant when the LD₅: LD₄ ratio is increased.

Although a modicum of controversy exists regarding the most suitable criteria for LD isoenzymes for the diagnosis of acute myocardial infarction, almost all laboratories recognize abnormality when LD₁ equals or is greater than LD₂. Alternatives to LD₁ greater than LD₂ have been proposed. Using an electrophoretic method (Helena), Rotenberg et al suggested the criterion of LD₁ >90 units/L.¹ A 1988 study examines application of LD₁: LD₄ and other ratios and finds that the LD₁: LD₄ ratio optimizes earlier and is the most powerful diagnostic ratio for acute myocardial infarction.²

A few percent of normal individuals may have LD₁: LD₂ ratios as high as 0.81. A ratio of 0.82-0.99 is suspicious of myocardial injury. A ratio >1.0 is diagnostic of myocardial injury, if other clinical criteria are met. In unstable angina, an increase of the LD₁: LD₂ ratio is described with normal total LD.³ However, progressively increasing LD₁: LD₂ ratio without complete inversion may have diagnostic significance for acute myocardial infarct.⁴

Persistent LD₁: LD₂ flip following acute myocardial infarct may represent a marker for reinfarction.⁵ Especially when acute myocardial infarction is complicated by shock, the isomorphic pattern may be found.⁶ LD₁: LD₂ inversion commonly appears subsequent to the isomorphic pattern in instances of acute myocardial infarction.⁷

The appearance of a LD ´´flip´´ (when LD₁ is greater than LD₂) is extremely helpful in diagnosis of MI. The presence of a LD ´´flip´´ a day following or with the detection of CK-MB is essentially diagnostic of MI, if baseline cardiac enzymes/isoenzymes are normal and if rises and falls are as anticipated for the diagnosis of acute MI. While CK-MB peaks 12-24 hours after onset of infarction, LD isoenzymes usually become diagnostic at about 36-55 hours after onset and return to normal between 3 and 14 days after onset.
Limitations: Timing is important in diagnosis of acute myocardial infarct (MI). In a small percentage of patients with acute myocardial infarction, the expected flip (reversal) of LD₁: LD₂ does not occur; in such patients, there is often simply an increase in LD₁.
Methodology: Electrophoresis
Additional Information: Patterns of LD isoenzymes in acute pulmonary edema include the isomorphic pattern and LD₅ increase.⁸ Serum LD increases also in patients with bacterial pneumonia, in whom LD isoenzyme patterns are described.⁹

Macroenzymes, high molecular weight complexes, occur with LD as well as with CK and other enzymes. LD isoenzymes may complex to IgA or IgG. Such LD macroenzymes are characterized by abnormal position of isoenzyme bands, broadening or abnormal motility of a band and otherwise unexplained increase of total serum LD. Some of these patients have abnormal ANA results and IgG complexes.¹⁰ Some have abnormalities of light chains.¹¹ Treatment with streptokinase was found to produce a LD-streptokinase complex which was seen as a band at the origin in electrophoresis.¹²

An isoenzyme band cathodal to LD₅ has been called LD₆. It is not an immunoglobulin complex. It has occurred in subjects with liver disease and is said to indicate a grave prognosis.^10,13,14

The association between LD₁ and testicular seminoma has been widely recognized. Its relationship to nonseminomatous testicular tumors as well are described.¹⁵ The ovarian equivalent of seminoma is dysgerminoma, which also may relate to LD₁ increases.^16,17 A variety of malignant tumors are characterized by total LD increases, sometimes with isomorphic patterns⁷ or with LD₅ increases.¹⁸ Increase LD₅: LD₁ ratio is suggestive of prostatic carcinoma or other cancers.¹⁹ Increases in LD₁: LD₄ ratio was found to be a good indicator of MI.²⁰

In a series of 220 patients with carcinoma of breast, LD was the most common enzyme elevated. The nonspecificity of single enzyme elevation was discussed, but enzymes provide an inexpensive baseline for postoperative follow-up. Enzyme elevation defines a subgroup of patients deserving further evaluation.²¹ In malignancy of various types, there is reported an abnormal isoenzyme of LD migrating between albumin and LD₁ on agarose gel electrophoresis.²²

An inverted LD₅: LD₄ ratio is not to be confused with LD₁: LD₂ ratio, used to evaluate acute MI. There is evidence that when LD₅ sufficiently exceeds LD₄, liver disease might exist. Such liver disease might be primary or secondary (eg, congestive heart failure). Additional tests which may be useful, if clinically indicated, to work up such possible liver disease or injury might include ALT (SGPT), GGT, serum protein electrophoresis, and prothrombin time. LD₅ is the striated muscle as well as the liver fraction. Although striated muscle problems are usually clinically obvious, occasionally the physician does not get a clinical history of the postictal state or of various withdrawal syndromes. In such situations, a CK may be helpful.
Footnotes: ????? 1. Rotenberg Z, Davidson E, Weinberger I, et al. The efficiency of lactate dehydrogenase isoenzyme determination for the diagnosis of acute myocardial infarction. Arch Pathol Lab Med. 1988; 112(9):895-897.
????? 2. Loughlin JF, Krijnen PM, Jablonsky G, et al. Diagnostic efficiency of four lactate dehydrogenase isoenzyme-1 ratios in serum after myocardial infarction. Clin Chem. 1988;34:1960-1965.
????? 3. Rotenberg Z, Weinberger I, Sagle A, et al. Lactate dehydrogenase isoenzymes in serum during unstable angina. Clin Chem. 1986; 32:1566-1567.
????? 4. Jablonsky G, Leung FY, Henderson AR. Changes in LD1/LD2 ratio during the first day after myocardial infarction. Clin Chem. 1985; 31:1621-1624.
????? 5. Rotenberg Z, Weinberger I, Sagie A, et al. Lactate dehydrogenase isoenzymes in serum during recent acute myocardial infarction. Clin Chem. 1987; 33:1419-1420.
????? 6. Rotenberg Z, Weinberger I, Davidson E, et al. Atypical patterns of lactate dehydrogenase isoenzymes in acute myocardial infarction. Clin Chem. 1988; 349(6):1096-1098.
????? 7. Jacobs DS, Robinson RA, Clark GM, et al. Clinical significance of the isomorphic pattern of the isoenzymes of serum lactate dehydrogenase. Ann Clin Lab Sci. 1977;7:411-421.
????? 8. Rotenberg Z, Weinberger I, Davidson E, et al. Patterns of lactate dehydrogenase isoenzymes in serum of patients with acute pulmonary edema. Clin Chem. 1988; 34(8)1882-1884.
????? 9. Rotenberg Z, Weinberger I, Davidson E, et al.Significance of isolated increases in total lactate dehydrogenase and its isoenzymes in serum of patients with bacterial Pneumonia. Clin Chem. 1988; 34(7):1503-1505.
????? 10. Gorus F, Aelbrecht W, Van Camp B. Circulating IgG-complex, dissociable by addition of NAD+. Clin Chem. 1982;28:236-239.
????? 11. Pesce MA. The CK and LD macroenzymes. Lab Management.1984; 22:29-41.
????? 12. Podlasek SJ, Dufour DR, McPherson RA. Alterations lactate dehydrogenase isoenzyme patterns after therapy with streptokinase of streptococcal infection. Clin Chem.1989; 35(8):1763-1766.
????? 13. Vladutiu AO. Cathodic lactate dehydrogenase (LDH 6): A sign of ominous prognosis? Arch Pathol Lab Med. 1983;107:612-613.
????? 14. Wolf PL. Lactate dehydrogenase-6: A biochemical sign of serious hepatic circulatory disturbance. Arch Intern Med. 1985; 145:1396-1397.
????? 15. Von Eyben FE, Blaabjerg O, Petersen PH, et al. Serum lactate dehydrogenase isoenzyme 1 as a marker of testicular germ cell tumor. J Urol. 1988; 140(5):989-990.
????? 16. Schwartz PE, Morris JM. Serum lactic dehydrogenase: A tumor marker for dysgerminoma. Obstet Gynecol. 1988;72(3 Pt 2):511-515.
????? 17. Yoshimura T, Takemori K, Okazaki T, et al, Serum lactate dehydrogenase and its isoenzymes in patients with ovarian dysgerminoma . Int J Gynaecol Obstet. 1988, 27:459-465.
?????18. Rotenberg Z, Weinberger I, Sagie A, et al, Total lactate dehydrogenase and its isoenzymes in serum of patients with non-small-cell lung cancer. Clin Chem. 1988,34:668-670.
?????19. Manzo V, Sun T, and Lien YY. Misdiagnosis of acute myocardial infarction. Ann Clin Lab Sci. 1980,20(5):324-328.
?????20. Galbraith LV, Leung FY, Jablonsky G, et al. Time-related changes in the diagnostic utility of total lactate dehydrogenase, lactate dehydrogenase isoenzyme-1, and two lactate dehydrogenase isoenzyme-1 ratios in serum after myocardial infarction. Clin Chem. 1990,36(7):1317-1322.
?????21. Clark CP 3d, Foreman ML, Peters GN, et al. Efficacy of preoperative liver function tests and ultrasound in detecting hepatic metastasis in carcinoma of the breast. Surg Gynecol Obstet. 1988,167(6):510-514.
?????22. Giannoulaki EE, Kalpaxis DL, Tentas C, et al. Lactate dehydrogenase isoenzyme pattern in sera of patients with malignant diseases. Clin Chem. 1989,35(3):396-399.

Test 431

SuperUser Account — Tue, 16 Sep 2008 21:45:46 GMT

Test: Leukocyte Alkaline Phosphatase (LAP) Score
Number: 001966
CPT: 85540
Synonyms: LAP Score
Test Includes: Blood films are stained and 100 neutrophilic leukocytes are scored from 0 to 4+ on the basis of the intensity of the precipitated dye in their cytoplasm. The values of the 100 cells are added and the total score reported.
Specimen: Smears made from fingerstick or Heparinized specimen; Heparin (green-top) tube - slides must be made within 24 hours of collection
Volume: Six properly labeled blood films (slides)
Minimum Volume: Two freshly made blood films
Container: Slides; Heparin (green-top) tube ? slides must be made within 24 hours of collection
Collection: Prepare smears on six (frosted end) slides from either fingerstick blood or immediately after drawing into heparin Vacutainer® and mixing. Air dry the slides and label with patient´s name. Submit all. Note: Do not use EDTA anticoagulant.
Storage Instructions: Smears are to be maintained at room temperature for up to 48 hours.
Causes for Rejection: Improper labeling; specimen more than 48 hours old
Reference Interval: 25-130
Use: Aids in the differential diagnosis of chronic myelocytic leukemia (CML) versus leukemoid reaction; aids in the evaluation of polycythemia vera, myelofibrosis with myeloid metaplasia, and paroxysmal nocturnal hemoglobinuria
Limitations: Pregnancy, increased number of immature forms of neutrophils, and postoperative or “stressful” states are associated with increased scores. The differential must have adequate numbers of mature neutrophilic granulocytes to perform the LAP.
Methodology: Enzyme reaction with leukocyte alkaline phosphatase liberating naphthol or a substituted naphthol compound which then couples with fast blue RR or other chromogen to form an insoluble precipitate. Color of the precipitate relates to the type of substituted naphthol substrate and diazonium dye used (color is reagent dependent). Cells are scored as to the degree of phosphatase activity present, 0 to 4+. One hundred cells are counted and the score totaled.
Additional Information: Low scores have been associated with CML, PNH, thrombocytopenic purpura, and hereditary hypophosphatasia. In CML regardless of the total white count, the score remains low. In CML, it has been demonstrated that the mRNA for leukocyte alkaline phosphatase by Northern blotting is undetectable.¹ This suggests either rapid degradation of the message or no transcription of the LAP gene. In nonleukemic neutrophilia, the LAP rises as the WBC rises. High scores have been seen in polycythemia vera, myelofibrosis, aplastic anemia, mongolism, hairy cell leukemia, leukemoid reactions, and neutrophilia either physiological or secondary to infection. It is also increased in Hodgkin disease. Serial LAP activity can be a useful adjunct in evaluating the activity of Hodgkin disease as well as its response to therapy. Increase in LAP does not occur in cases of sickle cell crisis, possibly due to zinc deficiency (leukocyte alkaline phosphatase is a zinc metalloenzyme) but more likely relating to a mild defect in the hypothalamic-pituitary-adrenal axis with decreased plasma cortisol response in patients in sickle cell crisis.²
Footnotes:

Rambaldi A, Terao M, Bettoni S, et al, “Differences in the Expression of Alkaline Phosphatase mRNA in Chronic Myelogenous Leukemia and Paroxysmal Nocturnal Hemoglobinuria Polymorphonuclear Leukocytes,” Blood, 1989, 73(5):1113-5.
Rosenbloom BE, Odell WD, and Tanaka KR, “Pituitary-Adrenal Axis Function in Sickle Cell Anemia and Its Relationship to Leukocyte Alkaline Phosphatase,” Am J Hematol, 1980, 9(4):373-9

References:

Miale JB, Laboratory Medicine, Hematology, 6th ed, St Louis, MO: CV Mosby Company, 1982, 207-9, 871.

Test 653

SuperUser Account — Tue, 16 Sep 2008 21:51:00 GMT

Test: Luteinizing Hormone (LH), Serum
Number: 004283
CPT: 83002 (per specimen)
Synonyms: ICSH ; Interstitial Cell Stimulating Hormone ; LH
Special Instructions: State patient´s age and sex on the request form.
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
Reference Interval: See table.^1,2

Age	Male (mIU/mL)	Female (mIU/mL)
0-23 mo	0.5-1.9	0.0-0.5
2-10 y	0.0-0.5	0.0-0.5
11-20 y	0.5-5.3	0.5-9.0
20-70 y	1.5-9.3	0.0-76.3
70-100 y	3.1-34.6	5.0-52.3
		Follicular: 1.9-12.5
		Midcycle: 8.7-76.3
		Luteal: 0.5-16.9
		Pregnant: 0.0-1.5
		Postmenopausal: 15.9-54.0
		Contraceptives: 0.7-5.6
Tanner Stage
I	0.0-3.6	0.0-0-3
II	0.3-4.8	0.1-4.1
III	0.6-6.3	0.2-9.1
IV & V	0.6-7.8	0.5-15

Use: The primary clinical use of LH measurement is in evaluating the normalcy of hypothalamic-pituitary-gonadal axis. Measurement of serum gonadotropin levels will allow for distinguishing between primary gonadal failure and deficient gonadal stimulation. LH measurement may also be of clinical importance because growth hormone and LH are frequently the first hormones to be affected by pituitary disease. The serum analysis of LH has also been found to be very useful in the diagnosis and treatment of infertility in women.
Limitations: Secretion of both LH and FSH is pulsatile, in response to the normal intermittent release of gonadotropin releasing hormone (GnRH). While both are pulsatile, LH exhibits a circadian rhythm while FSH does not.³ 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. Only 77% of patients with polycystic ovary syndrome have increase of LH.⁴ Increased LH with normal or low FSH may occur with obesity, hyperthyroidism, and in liver disease.⁵ Normal LH and FSH levels can occur in hypoestrogenic patients. FSH and LH within normal range can occur with CNS/pituitary failure.⁶
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 in males. 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. High concentrations of LH (during the follicular phase) in patients with polycystic ovary syndrome interfere with conception, and may contribute to early pregnancy loss in these patients. In males, LH has been called interstitial cell stimulating hormone (ICSH) because of its effect on testosterone production by Leydig cells. This is necessary for normal maturation of spermatozoa.
Footnotes:

Soldin SJ, Morales A, Albalos F, et al, “Pediatric Reference Ranges on the Abbott IMx for FSH, LH, Prolactin, TSH, T₄, T₃, Free T₄, Free T₃, T-Uptake, IgE, and Ferritin,” Clin Biochem, 1995, 28(6):603-6.
Tietz NW, ed, Clinical Guide to Laboratory Tests, 3rd ed, Philadelphia, PA: WB Saunders Co, 1995, 410.
Dunkel L, Alfthan H, Stenman UH, et al, “Developmental Changes in 24-Hour Profiles of Luteinizing Hormone and Follicle-Stimulating Hormone From Prepuberty to Midstages of Puberty in Boys,” J Clin Endocrinol Metab, 1992, 74(4):890-7.
Baker ER, “Diagnosis of Polycystic Ovary Syndrome,” JAMA, 1983, 250:671 (letter).
Plymate SR, “Diagnosis of Polycystic Ovary Syndrome,” JAMA, 1983, 250:671 (letter).
Speroff L, Glass RH, and Kase NG, Clinical Gynecologic Endocrinology and Infertility, 4th ed, Baltimore, MD: Williams & Wilkins, 1989

References:

Findling JW and Tyrrell JB, “Anterior Pituitary and Somatomedins: I. Anterior Pituitary,” Basic and Clinical Endocrinology, Greenspan FS and Forsham PH, eds, Los Altos, CA: Lange Medical Publications, 1983, 38-88.

Kossoy LR, Hill GA, Parker RA, et al, “Luteinizing Hormone and Ovulation Timing in a Therapeutic Donor Insemination Program Using Frozen Semen,” Am J Obstet Gynecol, 1989, 160(5 Pt 1):1169-72.

Nippoldt TB, Reame NE, Kelch RP, et al, “The Roles of Estradiol and Progesterone in Decreasing Luteinizing Hormone Pulse Frequency in the Luteal Phase of the Menstrual Cycle,” J Clin Endocrinol Metab, 1989, 69(1):67-76.

Test 719

SuperUser Account — Tue, 16 Sep 2008 21:52:57 GMT

Test: Lactic Acid, Plasma
Number: 004770
CPT: 83605
Synonyms: Lactate ; Plasma Lactate
Specimen: Plasma
Volume: 5 mL
Minimum Volume: 0.5 mL
Container: Gray-top (sodium fluoride/potassium oxalate) tube
Collection: Keep gray-top tube on ice. Draw blood in gray-top tube. Mix well by gentle inversion at least six times. Return to ice bath to cool. Avoid hand-clenching and, if possible, avoid use of a tourniquet. A tourniquet with patient clenching and unclenching hand will lead to buildup of high potassium and lactic acid from the hand muscles, and pH will decrease. It is best to avoid a tourniquet for electrolytes and lactic acid, or to release it after blood begins to flow into tube. If the tourniquet is released before blood is drawn, wait about a minute before drawing. Within 15 minutes from draw, separate the plasma from blood by centrifugation at 400xg for 10 minutes. Avoid excessive forces which contribute to hemolysis.
Storage Instructions: Refrigerate
Patient Preparation: Patient should not be on any intravenous infusion that would affect the acid-base balance. Patient should be in a fasting and resting state (should not exercise).
Causes for Rejection: Specimen not separated from cells within 15 minutes of draw; marked hemolysis; slight or moderate turbidity; perchloric acid supernatant; serum specimen
Reference Interval: 4.5-19.8 mg/dL
Use: Hypoperfusion is the most common cause of lactic acidosis and hyperlactacidemia may be the only marker of tissue hypoperfusion.¹ Suspect lactic acidosis when unexplained anion gap metabolic acidosis is encountered, especially if azotemia or ketoacidosis are not present. Evaluate metabolic acidosis, regional or diffuse tissue hypoperfusion, hypoxia, shock,² congestive heart failure, dehydration, complicated postoperative state, ketoacidosis or nonketotic acidosis in diabetes mellitus, patients with infections, inflammatory states, postictal state, certain myopathies, acute leukemia and other neoplasia, enzyme defects, glycogen storage disease (type I), thiamine deficiency, and hepatic failure. A spontaneous form of lactic acidosis occurs. It is a prognostic index in particular clinical settings, especially in critically ill patients in shock.³ A relationship to renal disease also exists. With skin rash, seizures, alopecia, ataxia, keratoconjunctivitis, and lactic acidosis in children, consider defective biotin metabolism.⁴ Phenformin, ethanol, methanol, and salicylate poisoning and ethylene glycol may cause lactic acidosis. Acetaminophen toxicity causes lactic acidosis, sometimes with hypoglycemia. Cyanide, isoniazid, and propylene glycol are among the causes of lactic acidosis.¹ Lactic acidosis may be due to inborn errors of metabolism.
Limitations: Gross hemolysis elevates plasma results. Intravenous injections, or infusions which modify acid-base balance, may cause alterations in lactate levels. Epinephrine and exercise elevate lactate, as may I.V. sodium bicarbonate, glucose, or hyperventilation. False-low values may be found with a high LD (LDH) value.
Methodology: Lactate - pyruvate; spectrophotometry
Additional Information: Phosphorus is sometimes significantly abnormal in lactic acidosis. Creatinine is higher in ketoacidosis than in lactic acidosis, by interference produced by acetoacetic acid on creatinine. Causes of lactic acidosis (usually <45 mg/dL) include carbohydrate infusions, exercise, diabetic ketosis, alcohol. Causes of lactic acidosis (>45 mg/dL) include shock (in which lactic acidosis may occur early, before fall in blood pressure, decrease in urine output), hypoxia (including congestive failure, severe anemia, hypotension) and malignancies. Severe lactic acidosis can develop in minutes. Lactic acidosis can accompany dehydration. Blood lactate concentration correlates negatively with survival in patients with acute myocardial infarction, with persistent elevation, >36 mg/dL for more than 12 hours, being associated with poor prognosis.⁵ At a given bicarbonate level, the average pCO₂ is lower in lactic acidosis than in diabetic ketoacidosis. Lactic acid determination is generally indicated if anion gap is <20 and if pH is >7.25 and the pCO₂ is not elevated. (Mizock uses pH 7.35 as a diagnostic criterion.¹) The measurement of lactate levels may be indicated in the clinical setting of metabolic acidosis. Serum salicylate, ethanol level, and osmolality may be helpful. Spontaneous lactic acidosis may be fatal. High CSF lactate levels suggest the meningitis is bacterial while low values suggest a viral cause.⁶
Footnotes:

Mizock BA, “Lactic Acidosis,” Dis Mon, 1989, 35(4):233-300.
Anderson CT Jr, Westgard JO, Schlimgen K, et al, “Contribution of Arterial Blood Lactate Measurement to the Care of Critically Ill Patients,” Am J Clin Pathol, 1977, 68(1):63-7.
Schuster HP, “Prognostic Value of Blood Lactate in Critically Ill Patients,” Resuscitation, 1984, 11(3-4):141-6 (review).
Thoene J, Baker H, Yoshino M, et al, “Biotin-Responsive Carboxylase Deficiency Associated With Subnormal Plasma and Urinary Biotin,” N Engl J Med, 1981, 304(14):817-20.
Henning RJ, Weil MH, and Weiner F, “Blood Lactate as a Prognostic Indicator of Survival in Patients With Acute Myocardial Infarction,” Circ Shock, 1982, 9(3):307-15.
Bailey EM, Domenico P, and Cunha BA, “Bacterial or Viral Meningitis? Measuring Lactate in CSF Can Help You Know Quickly,” Postgrad Med, 1990, 88(5):217-9, 223 (review)

References:

Bishop PA, May M, Smith, JF, et al, “Influence of Blood Handling Techniques on Lactic Acid Concentrations,” Int J Sport Med, 1991, 13(1):56-9.

Test 964

SuperUser Account — Tue, 16 Sep 2008 22:00:48 GMT

Test: Lidocaine (Xylocaine®), Serum
Number: 007013
CPT: 80176
Synonyms: Lidocaine, Serum ; Xylocaine®
Specimen: Serum or plasma
Volume: 1 mL
Minimum Volume: 0.3 mL
Container: Red-top tube or green-top (heparin) tube
Collection: Transfer separated serum or plasma to a plastic transport tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage time, the decrease in drug level due to absorption may be clinically significant.

Draw specimens 12 hours after initiating therapy for arrhythmia prophylaxis, then every 24 hours thereafter. Obtain specimens every 12 hours when cardiac or hepatic insufficiency exists.

Storage Instructions: Refrigerate
Causes for Rejection: Gel-barrier tube; hemolysis; gross lipemia; icteric specimen
Reference Interval: Therapeutic: 1.5-6.0 μg/mL
Use: This class 1B agent depresses automaticity and reduces refractory period duration in the HIS-Purkinje system and ventricles but has little effect on atrial tissue. Therapeutic doses do not slow AB nodal or intraventricular conduction velocity except in the ischemic myocardium. Lidocaine can cause hyperpolarization and significant increases in conduction velocity in tissues depolarized by stretch or low extracellular potassium concentrations.

Because it acts rapidly and moderate doses usually do not depress myocardial contractility or AV conduction; intravenous lidocaine has been used for immediate suppression of ventricular ectopy and hemodynamically stable ventricular tachycardia during acute myocardial infarction. However, prophylactic use is no longer recommended, because it does not improve the survival rate. Lidocaine may control ventricular arrhythmias caused by digitalis toxicity and those that develop during cardiac surgery, cardiac catheterization, or cardioversion. It usually does not correct supraventricular arrhythmias and may increase the ventricular rate.

Methodology: Immunoassay
Additional Information: This drug is used in therapy of ventricular but not supraventricular arrhythmias. Following initial parenteral administration of a bolus, lidocaine is rapidly cleared with a short half-life of approximately 10 minutes (first-pass effect). After approximately 30 minutes, there is a slower elimination phase about 90 minutes long. With continuous intravenous administration, a half-life of about 1.5-2 hours may be achieved, hence, prolonged administration by the I.V. route is often necessary to achieve the desired therapeutic result. Time to reach steady-state by I.V. is 6-12 hours. In most cases, a relatively constant plasma level may be maintained by slow intravenous infusion administered over a period of 6-10 hours. Blood levels are also elevated by impaired cardiac or hepatic function. The drug is metabolized by the liver to two active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX). Both accumulate and MEGX most likely contributes to toxicity. Toxic symptoms may include confusion, respiratory depression, seizures, dizziness, drowsiness, paresthesias, hypotension, bradycardia, and double vision. Convulsions, cardiac and respiratory arrest may occur. Barbiturates and phenytoin seem to enhance drug metabolism and lower serum levels, whereas propranolol, cimetidine, and norepinephrine increase levels.

Lidocaine is approximately 70% bound to plasma proteins, especially alpha₁ acid glycoprotein (the concentration of which is variable) and to albumin.

References:

AMA, Division of Drugs and Toxicology, Drug Evaluations Subscription, Chicago, IL: American Medical Association, Winter 1993.

Blanke RV and Decker WJ, “Analysis of Toxic Substances,” Fundamentals of Clinical Chemistry, 3rd ed, Tietz NW, ed, Philadelphia, PA: WB Saunders Co, 1987, 869-905.

Test 1055

SuperUser Account — Tue, 16 Sep 2008 22:04:27 GMT

Test: Lead, Blood (Adult)
Number: 007625
CPT: 83655
Synonyms: Pb, Blood
Specimen: Whole blood
Volume: 7 mL
Minimum Volume: 0.5 mL
Container: Royal blue-top (EDTA) tube, lavender-top (EDTA) tube or brown-top (sodium heparin) tube. Submit original tube.
Collection: Sampling time is not critical for industrial exposure monitoring. Metals with timing “not critical” have very long elimination half-lives and accumulate in the body over years, some for a lifetime. After a couple of weeks of exposure, specimens can be collected at any time.
Storage Instructions: Maintain specimen at room temperature.
Causes for Rejection: Clotted specimen
Reference Interval:

Environmental exposure (WHO): 0-19 μg/dL
Occupational exposure: BEI® (sampling time is not critical): 30 μg/dL;¹ OSHA Lead Standard: 40 μg/dL

Use: Monitor exposure to lead
Methodology: Atomic absorption spectrometry (AAS)
Additional Information: Hematologic consequences ascribed to lead toxicity may be basophilic stippling, mild anemia, and reticulocytosis. Other characteristics of toxicity may include increased urine Δ-aminolevulinic acid, increased erythrocyte protoporphyrins, and decreased aminolevulinic acid dehydrase. Lead lines on gums or at the metaphyses of long bones in children may also be present.² Early symptoms of lead poisoning include anorexia, apathy or irritability, fatigue, and anemia.³ Toxic effects include GI distress, joint pain, colic, headache, stupor, convulsions, and coma. Another test that may be used to evaluate lead intoxication is free erythrocyte protoporphyrin (FEP); however, a blood lead assay is the definitive test.⁴

Lead and organic lead compounds have numerous commercial and industrial applications, including paints, plastics, storage batteries, bearing alloys, insecticides, and ceramics. Exposure may also occur through the inhalation of dust containing lead emitted by automobile exhaust. A common source of lead exposure among children is through the mouthing of inanimate objects, specifically objects with paint and paint chips that contain lead. Acute lead exposure is rare; however, toxicity may occur through acute ingestion of a lead salt or acetate. Blood is the preferred specimen by which the extent of an acute or recent exposure to lead may be measured.

BEI® are reference values intended as guidelines for evaluation of occupational exposure. BEI® represent biological levels of chemicals that correspond to workers with inhalation exposure equivalent to the threshold limit value (TLV®) of the chemicals. TLV®s refer to the airborne concentrations of substances and represent conditions under which it is believed that nearly all workers may be repeatedly exposed, day after day, without adverse health effects.¹

Footnotes:

TLV®s and BEI®s, Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices 2004, American Conference of Governmental Industrial Hygienists (ACGIH).
Tsalev DL and Zaprianov ZK, Atomic Absorption Spectrometry in Occupational and Environmental Health Practice, Boca Raton, FL: CRC Press, 1983-4.
Baselt RC, Biological Monitoring Methods for Industrial Chemicals, 2nd ed, Littleton, MA: PSG Publishing Co, 1988.
Carson BL, Ellis HV III, and McCann JL, Toxicology and Biological Monitoring of Metals in Humans: Including Feasibility and Need, Chelsea, MI: Lewis Publishers, 1986

Test 1057

SuperUser Account — Tue, 16 Sep 2008 22:04:32 GMT

Test: Lead, Urine
Number: 007633
CPT: 82570; 83655
Synonyms: Pb, Urine
Test Includes: Lead, urine; creatinine, urine; lead:creatinine ratio; lead, urine (24-hour)
Special Instructions: Request form must state total volume collected in 24-hour, if applicable. Do not use preservative. Preservatives used for routine analysis may contain mercuric oxide (ie, Stabilur), which interferes with all metal testing. If both urinalysis and metal testing are ordered, please submit a separate urine specimen (containing no additive) for the metal testing.
Specimen: Urine (random or 24-hour)
Volume: 5 mL
Minimum Volume: 2.5 mL
Container: Plastic urine container, no preservative
Collection: Sampling time is not critical for industrial exposure monitoring. Metals with timing “not critical” have very long elimination half-lives and accumulate in the body over years, some for a lifetime. After a couple of weeks of exposure, specimens can be collected at any time.

Optional protocol: If the specimen is a 24-hour collection, instruct the patient to void at 8 AM and discard the specimen. Then collect all urine including the final specimen voided at the end of the 24-hour collection period (ie, 8 AM the next morning). Screw the lid on securely. Collect without preservatives. Mix well. Sampling time is not critical for industrial monitoring.

Storage Instructions: Maintain specimen at room temperature.
Reference Interval:

Environmental exposure: <50 μg/L, <80 μg/24 hours
Occupation exposure: BEI® (sampling time is not critical): 150 μg/g creatinine;¹ chelation therapy: <600 μg/24 hours (after 1 g EDTA I.V. or 2 g DMSA P.O.)

Use: Monitor exposure to lead or lead chelation therapy
Methodology: Atomic absorption spectrometry (AAS); inductively-coupled plasma-mass spectrometry (ICP-MS)
Additional Information: Lead poisoning through chronic exposure is characterized by gastrointestinal disturbance, anemia, insomnia, weight loss, motor weakness, muscle paralysis, and neuropathy. Ingestion of large quantities may produce death.²

Increased urinary lead excretion indicates excessive lead exposure, regardless of clinical presentation. Erythrocyte protoporphyrin and whole blood lead levels are probably more sensitive indicators of excessive lead exposure. In cases of borderline blood levels, an EDTA lead mobilization test may be considered. Chelation therapy monitoring may be indicated. Lead and organic lead compounds have numerous commercial and industrial applications, use in paints, plastics, storage batteries, bearing alloys, insecticides, and ceramics. Exposure may also occur through the inhalation of dust containing lead emitted by automobile exhausts. A common source of lead exposure among children is derived through the mouthing of inanimate objects, specifically objects with paint and paint chips that contain lead. Acute lead exposure is rare; however, toxicity may occur through acute ingestion of a lead salt or acetate. Urine is suggested specimen in which chronic lead poisoning may be monitored.

Footnotes:

BEI® (Biological Exposure Indices) based on 1994-1995 Recommendations of the American Conference of Governmental Industrial Hygienists (ACGIH).
Baselt RC and Cravey RH, Disposition of Toxic Drugs and Chemicals in Man, 4th ed, Chemical Toxicology Institute, 1995.
TLV®s and BEI®s, Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices 2004, American Conference of Governmental Industrial Hygienists (ACGIH)

Test 1066

SuperUser Account — Tue, 16 Sep 2008 22:04:53 GMT

Test: Lithium (Eskalith®), Serum
Number: 007708
CPT: 80178
Synonyms: Eskalith® ; Li, Blood ; LiCO₃
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.3 mL
Container: Red-top tube or gel-barrier tube; if a red-top tube is used, transfer separated serum to a plastic transport tube.
Collection: Collect trough level (just prior to next dose); at least 6-12 hours after the last dose.
Storage Instructions: Refrigerate
Causes for Rejection: Hemolysis; specimen collected in tube containing lithium heparin
Reference Interval: Therapeutic: 0.6-1.4 mEq/L
Use: Lithium as lithium carbonate is used as a psychoactive agent in the treatment of manic depressive disorders. Lithium therapy demands daily monitoring of serum lithium levels until the proper dose schedule is determined. Serum elimination half-life ranges from 20-60 hours. Insomnia in a low-range group is described. Tremor, gastrointestinal symptoms, urinary frequency, and weight gain were less frequent at lower levels.¹ Intoxication never occurs suddenly. Several days to a week before full-blown symptoms develop, a patient will experience lethargy, drowsiness, tremor, muscle twitching, dysarthria, anorexia and vomiting or diarrhea. A fully developed case of intoxication shows coma to semicoma, rigidity, hyperactive reflexes and seizures at times. There is a high incidence of pulmonary complications. It is advisable to perform periodic plasma sodium determinations. Low plasma sodium levels are associated with lithium retention; high levels with lithium elimination. Varying degrees of nephrogenic diabetes insipidus have been reported to occur in 33% of lithium treated patients. Lithium significantly inhibits antidiuretic hormone induced water transport in kidney. Lithium interferes with solute and water absorption from the gastrointestinal system producing nausea, vomiting, diarrhea, and abdominal pain. These symptoms may occur at any time, at any serum level. They most commonly occur during early treatment stages and usually clear spontaneously or by adjustment of dosage. Chronic lithium administration has a goitrogenic effect on 4% of lithium treated patients, with or without hypothyroidism. In general, lithium administration results in slightly decreased serum T₄ levels and transiently elevated levels of TSH in nearly 33% of these patients.

Lithium affects the cardiac conduction system by incomplete substitution for other cations, especially sodium and potassium. These electrolyte changes account for the usually unimportant and reversible T-wave depressions observed in 10% to 20% of patients on lithium therapy.

Methodology: Ion-selective electrode (ISE)
Additional Information: Lithium is completely absorbed 6-8 hours after oral administration. Since the onset of action is slow (5-10 days), parenteral administration is of no advantage. The plasma half-life is 17-36 hours, and this drug is eliminated almost entirely by the kidneys. Lithium clearance averages approximately 20% of creatinine clearance, but significant variability exists among patients.

Lithium ion is not protein bound, is distributed in total body water, and is concentrated in various tissues to different degrees. After a steady-state has been achieved, the lithium level in cerebrospinal fluid is about 40% of that in serum, and renal clearance for an individual remains relatively constant.

In general, a good correlation exists between the serum concentration of lithium ion and therapeutic efficacy and toxicity. However, some patients who show no therapeutic benefit have adequate serum concentrations of lithium but low erythrocyte concentrations. Since lithium works intracellularly, the erythrocyte concentration of the drug may be more relevant than levels in serum. Therefore, in unresponsive patients, doses that produce higher than usual serum concentrations can be used if erythrocyte concentrations are lower.

Footnotes:

Gelenberg AJ, Kane JM, Keller MB, et al, “Comparison of Standard and Low Serum Levels of Lithium for Maintenance Treatment of Bipolar Disorder,” N Engl J Med, 1989, 321(22):1489-93

References:

AMA, Division of Drugs and Toxicology, Drug Evaluations Subscription, Chicago, IL: American Medical Association, Spring 1992.

Test 1456

SuperUser Account — Tue, 16 Sep 2008 22:23:34 GMT

Test: Lyme Disease Antibodies, Total Immunoglobulins
Number: 015271
CPT: 86618
Synonyms: Borrelia burgdorferi Antibodies ; Ixodes Tick Bite Agent
Test Includes: Index result for the presence of either IgG or IgM antibodies
Specimen: Serum
Volume: 1 mL
Minimum Volume: 0.5 mL
Container: Red-top tube or gel-barrier tube
Storage Instructions: Maintain specimen at room temperature.
Causes for Rejection: Hemolysis; lipemia; gross bacterial contamination
Reference Interval:

Negative: <0.90 index
Equivocal: 0.90-1.09 index
Positive: >1.09 index

Use: Aid in the diagnosis of acute and later stages of infection by B. burgdorferi, the spirochete associated with Lyme disease
Limitations: Clinical evidence for lyme disease helps to ensure that antibody levels are not due to cross-reactive responses from spirochetal or other antibodies.
Methodology: Enzyme immunoassay (EIA)
Additional Information: Lyme disease is a common vector-borne disease in the U.S. caused by Borrelia burgdorferi which is transmitted through the bite of infected ticks. It may become a chronic disease involving the skin (rash), joints (arthritis), central nervous system, and heart. The disease responds to antibiotic therapy. In early disease, a negative result does not exclude the diagnosis and response may be blunted by antibiotics.

Test 1601

SuperUser Account — Tue, 16 Sep 2008 22:30:51 GMT

Test: Luteinizing Hormone (LH), Serum, 4 Specimens
Number: 026955
CPT: 83002 (x4)
Special Instructions: Please refer to the directions for Sequential Sampling.

Test 1602

SuperUser Account — Tue, 16 Sep 2008 22:30:52 GMT

Test: Luteinizing Hormone (LH), Serum, 2 Specimens
Number: 026971
CPT: 83002 (x2)
Special Instructions: Please refer to the directions for Sequential Sampling.

Test 1626

SuperUser Account — Tue, 16 Sep 2008 22:31:58 GMT

Test: Lead Standard Profile, Blood
Number: 038158
CPT: 83655; 84202
Synonyms: Lead and Protoporphyrin (FEP/ZPP)
Test Includes: Lead, blood; protoporphyrin, free erythrocyte; zinc protoporphyrin
Specimen: Whole blood
Volume: 7 mL
Minimum Volume: 0.5 mL
Container: Royal blue-top (EDTA) tube or lavender-top (EDTA) tube. Submit original tube.
Collection: Mix tube thoroughly to avoid clotting. Hemolysis will not affect the tests. Recollect if clots are present.
Storage Instructions: Refrigerate
Causes for Rejection: Clotted specimen
Reference Interval: See individual tests.
Use: Monitor exposure to lead
Methodology: Lead by atomic absorption spectrometry (AAS); ZPP by fluorometry
Additional Information: See individual tests.

Test 1642

SuperUser Account — Tue, 16 Sep 2008 22:32:29 GMT

Test: Luteinizing Hormone (LH), Serum, 3 Specimens
Number: 039230
CPT: 83002 (x3)
Special Instructions: Please refer to the directions for Sequential Sampling.

Test 1643

SuperUser Account — Tue, 16 Sep 2008 22:32:30 GMT

Test: Luteinizing Hormone (LH), Serum, 5 Specimens
Number: 039248
CPT: 83002 (x5)
Special Instructions: Please refer to the directions for Sequential Sampling.

Test 1654

SuperUser Account — Tue, 16 Sep 2008 22:32:58 GMT

Test: Lactose Tolerance Test
Number: 046300
CPT: 82951; 82952 (x3)
Synonyms: Lactose Consumption Test
Test Includes: Fasting, 15, 30, 60, 90, and 120 minutes glucose measurements
Special Instructions: Lactose load: Infants: 0.6-1.3 g/kg body weight; children up to 12 years: 1.7 g/kg body weight with a minimum of 10 g and a maximum of 50 g, in as small a quantity of water as possible. Adults: 100 g in 300 mL water. If severe lactase deficiency is suspected, the dose should be lowered. Label each tube with patient´s name and time interval.
Specimen: Plasma
Volume: Full tube for each sample
Minimum Volume: 1 mL
Container: Gray-top (sodium fluoride/potassium oxalate) tube
Collection: Draw fasting sample prior to lactose administration. Then collect blood specimen at 15, 30, 60, 90, and 120 minutes following administration.
Storage Instructions: Maintain specimen at room temperature.
Patient Preparation: Patient should fast for 8 hours before testing. No smoking or gum chewing allowed during test. Patient is encouraged to drink a moderate amount, 1-2 glasses of water during test. Patient should remain seated or in bed during test.
Causes for Rejection: Gross elevation of fasting blood glucose; improper labeling
Use: Evaluate lactose intolerance, malabsorption syndromes. May be abnormal with Crohn disease, small bowel resections, jejunitis, Giardia lamblia infestation, Whipple disease, and cystic fibrosis.
Methodology: Enzymatic
Additional Information: Lactose is a disaccharide digested by lactase. It yields glucose and galactose. The latter is converted to glucose by the liver after its absorption. Glucose is measured and it is the increase or lack of increase over the fasting specimen that is used for interpretation. A normal response will show a glucose increase >20 mg/dL over the baseline sample. Those with lactase deficiency will demonstrate bloating, cramps, and diarrhea, and will show a glucose increase <10 mg/dL. Diabetic patients may have abnormal lactose tolerance curves due to abnormal carbohydrate metabolism and not necessarily due to lactose intolerance. Since 25% of normal individuals have flat glucose tolerance tests, it has been suggested that patients with flat lactose tolerance tests should also have a glucose tolerance test. Ethanol can prevent conversion of galactose to glucose by the liver; thus, blood or urine galactose can be measured.

Test 1738

SuperUser Account — Tue, 16 Sep 2008 22:37:22 GMT

Test: Lidocaine
Number: 060016
CPT: 86003
Specimen: Serum
Volume: 1.0 mL
Container: One 8.5 mL red-top tube or one 8.5 mL gel-barrier tube
Storage Instructions: Refrigerate
Methodology: Quantitative allergen-specific IgE test

Test 1784

SuperUser Account — Tue, 16 Sep 2008 22:39:15 GMT

Test: Lenscale
Number: 060100
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 1805

SuperUser Account — Tue, 16 Sep 2008 22:40:07 GMT

Test: Lime
Number: 060293
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 1871

SuperUser Account — Tue, 16 Sep 2008 22:43:24 GMT

Test: Lepidoglyphus Destructor
Number: 064444
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 1889

SuperUser Account — Tue, 16 Sep 2008 22:44:09 GMT

Test: Lilac Tree
Number: 066548
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 1890

SuperUser Account — Tue, 16 Sep 2008 22:44:12 GMT

Test: Locust Tree
Number: 066555
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 1926

SuperUser Account — Tue, 16 Sep 2008 22:45:43 GMT

Test: Lentil
Number: 067298
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 1937

SuperUser Account — Tue, 16 Sep 2008 22:46:11 GMT

Test: Lettuce
Number: 067553
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