Put us to the test by mikeholy


									 Lab Updates
                                                                                   November 2008
An archive of Lab Updates is posted on Our Net or external web site: http://www.ummlabs.org/ClientNews.asp

                                                                               Inside this issue:
                                                                                    Lab Evaluation for
                                                                                  the Jaundiced Patient

                                                                            Quantitative Urine Chemistry Tests:
                                                                                24 Hr vs. Random Urine

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                                                                             Lab Updates | March 2008
                  Lab Evaluation for the Jaundiced Patient

UMass Memorial
Medical Center Laboratories
One Biotech Park, Suite 200
365 Plantation Street
Worcester, MA 01605-2376
800-476-4431 or 508-334-2863
                                             JAUNDICE IS A YELLOWISH STAINING OF THE INTEGUMENT, sclerae,
                                             deeper tissues, and excretions with bile pigments, which are increased in the
                                             I. Overview
                                             A. Physiology
FAX: 508-334-4210                              1. Serum bilirubin accumulated when its production from heme exceeds its
Email: LabsCS@ummhc.org                           metabolism and excretion.

L. Michael Snyder, M.D.                        2. An imbalance between the production and clearance of serum bilirubin
Chairman, Dept. of Hospital Laboratories          results either from excess release of bilirubin precursors into the blood-
Professor of Medicine and Pathology               stream, or from physiologic processes that impair the hepatic uptake,
University of Massachusetts Medical School        metabolism, or excretion of this metabolite.

Guy M. Vallaro, Ph.D.                          3. Jaundice is clinically detectable when the serum bilirubin exceeds 2.0-2.5
Vice President, Lab Operations                    mg/d1. Because elastin has a high affinity for bilirubin, and scleral tissue is
Medical Center customer liaison                   rich in elastin, scleral icterus is usually a more sensitive sign than
                                                  generalized jaundice.
Betsy Harder
Sr. Director, Lab Outreach Program
Non-Medical Center customer liaison

    2 Lab Updates | November 2008
                                                                    A. Extrahepatic biliary obstruction
                                                                      1. The history, physical examination, and initial laboratory
                                                                         assessment have a sensitivity of 90%-95%. The specificity,
                                                                         however, is only 76%. When radiologic imaging is
                                                                         factored in, the specificity rises to 98%.
                                                                      2. Approximately 40% of patients with this diagnosis
                                                                         present with jaundice.
                                                                      3. In the setting of complete obstruction, acholic stools are
                                                                         seen and no urobilinogen is detected in the urine (given
                                                                         the dependence upon enterohepatic circulation).
                                                                      4. In patients with extrahepatic biliary obstruction,
                                                                         alkaline phosphatase would be expected to rise to levels
B. Bilirubin metabolism                                                  2 to 3 times normal. A normal level would be uncom-
                                                                         mon. Serum transaminases would generally be less
  1. Unconjugated bilirubin. More than 90% of serum
                                                                         than 300 U/L.
     bilirubin in normal individuals is in an unconjugated
     form, circulating as an albumin-bound complex. This            B. Intrahepatic cholestasis. Consider intrahepatic etiologies
     is not filtered by the kidneys.                                   in the differential diagnosis because high levels may be
                                                                       seen in patients with primary biliary cirrhosis and granu-
  2. Conjugated bilirubin. The remainder is conjugated
                                                                       lomatous hepatitis.
     (primarily as a glucuronide), rendering it water soluble,
     and thus capable of being filtered and excreted by the           1. This group of disorders is defined by the lack of
     kidney.                                                             evidence of mechanical obstruction and cannot be
                                                                         explained on the basis of hepatocellular injury alone.
  3. Hepatic phase. Hepatic metabolism has three phases:
                                                                         Among these disorders are those characterized by
     uptake, conjugation, and excretion.
                                                                         disordered enzyme function (intrinsic/acquired),
     a. Uptake phase: Unconjugated bilirubin is bound to                 infiltrative disorders, and drugs.
        albumin and is presented to the hepatocyte, where
                                                                      2. A diagnosis of intrahepatic cholestasis made by
        the complex dissociates and bilirubin enters the cell
                                                                         clinical assessment and supported by negative find-
        either by diffusion or transport across the membrane.
                                                                         ings from ultrasound or computed tomography (CT)
     b. Conjugation phase: Bilirubin is then conjugated in               scan offers 95% specificity. In a patient in whom
        a two-step process. This occurs in the endoplasmic               extrahepatic obstruction is not strongly suspected,
        reticulum and is catalyzed by glucuronyl transferase.            no further investigation of the extrahepatic biliary tree
        Bilirubin glucuronide is generated.                              is indicated.
     c. Excretion phase: In an energy-dependent process             IV. Clinical Approach. The combination of history and physical
        occurring in the biliary canaliculi, conjugated bilirubin       examination is useful in directing the initial evaluation.
        is excreted into the bile. It is important to remember
                                                                    A. History
        that this is the rate-limiting step. When this phase is
        impaired, either through obstruction or excretory             1. Seek risk factors for hepatitis and cirrhosis
        defects, the conjugated bilirubin is presumed to reflux          a. Drug use [i.e., prescribed or over-the-counter (OTC)]
        through the hepatic sinusoids into the bloodstream.              b. Toxin exposures (alcohol, androgens)
  4. Intestinal phase. After excretion into the bile, conjugated         c. Viral exposures (intravenous drug abuse, tattoos,
     bile is transported into the duodenum. It is not re-                   sexual promiscuity, transfusion, travel from
     absorbed by intestinal mucosa. In the intestine, it is                 endemic areas)
     either excreted in the feces unchanged or metabolized
                                                                      2. Inquire about changes in stool and urine characteristics
     by intestinal bacteria to urobilinogen. Urobilinogen is
     then reabsorbed where a small portion is metabolized in             a. Stool changes include:
     the liver, and the remainder bypasses the liver and is                (1) Acholic (clay-colored) if there is complete biliary
     excreted by the kidney.                                                   obstruction (no conjugated bilirubin entering
II. Differential Diagnosis (Table 20-1)                                        the intestine)
III. Notes on the Differential Diagnosis                                   (2) Silver stools (hemoccult-positive and biliary
                                                                               obstruction at the ampulla of Vater)

                                                                                            Lab Updates | November 2008 3
b. Urinary pigment changes include:
      (1) No change, suggesting no reflux into serum of
                                                                        Differential Diagnosis of Jaundice
          conjugated bilirubin (hemolysis, advanced hepato-
                                                                          1. Unconjugated hyperbilirubinemia
          cellular disease)
                                                                             • Hemolysis
     (2) Darkening of color suggests reflux of conjugated                    • Gilbert’s syndrome
         bilirubin (compatible with, but not diagnostic of                   • Ineffective erythropoiesis
         obstnictive causes)                                                 • Hematoma resorption
   3. Other clinical clues are sought, which are related to               2. Conjugated hyperbilirubinemia
      stigmata of liver disease, the presence of hyperbiliru-                A. Extrahepatic biliary obstruction
      binemia, and associated with the underlying etiologies.                   • Choledocholithiasis
      These clues include:                                                      • Ascending cholangitis
     a. Pruritus (in primary biliary cirrhosis, bile salt deposition)           • Pancreatitis
     b. Pain (obstruction)                                                      • Sclerosing cholangitis
     c. Fever (cholangitis, abscess)                                            • HIV cholangiopathy
     d. Weight loss (malignancy)                                                • Biliary stricture or cyst
     e. Prior biliary surgery (recurrent stone, stricture)                      • Malignancy
B. Physical examination                                                           • Pancreas
    1. Identify stigmata of chronic liver disease by looking                      • Ampuiiary carcinoma
       for signs of                                                               • Cholangiocarcinoma
       a. Spider angiotnata                                                       • Metastatic
       b. Palmar erythema                                                    B. Intrahepatic cholestasis
       c. Gynecomastia                                                          • Abscess
       d. Testicular atrophy                                                    • Tumor
                                                                                • Primary biliary cirrhosis
   2. Seek evidence of portal hypertension (venous conges-                      • Cholestatic jaundice of pregnancy
      tion, splenomegaly) and coagulopathy (bruising,                           • Dubin-Johnson syndrome
      bleeding, petechiae), and note characteristics of the                     • Rotors syndrome
      liver examination (e.g., the size, texture, bruit/rub,                    • Benign recurrent intrahepatic cholestasis
      nodalarity).                                                              • Sepsis
   3. Suspect an obstructive or infectious process when                         • Infiltrative disease
      pain and fever are present.                                                 • Sarcoid
   4. Identify a primary or metastatic source in patients                         • Amyloid
      with asymptomatic jaundice (as neoplasm is a                              C. Hepatocellular jaundice
      common etiology).                                                            • Hepatitis virus
      a. Hemoccult-positive stool suggests a primary                               • Toxin or drugs (alcohol)
         gastrointestinal tract tumor.                                             • Cirrhosis
      b. A palpable, nontender gallbladder suggests the                            • Ischemia
         presence of a tumor (e.g., cholangiocarcinoma                                                                  Table 20-1
         or adenocardnoma of the ampulla of Vater or
         pancreatic head).                                              1. The first step is to determine the total bilirubin
   5. Look for the presence of scleral icterus, as this is a               and the bilirubiun fractions. This allows the clinician
      key point in distinguishing jaundice from hypercaroten-              to determine whether the problem is due to excess
      emia. Carotene does not deposit in the sclera.                       production or impaired conjugation (indirect/
V. Diagnostic Evaluation (see-Appendix A for Jaundice                      unconjugated predominant) versus impaired excretion
   algorithim)                                                             (direct/conjugated predominant).

A. Laboratory evaluation. These studies are of proven benefit           2. Alkaline phosphatase elevations out of proportion
   in determining the proximate etiologies in the patient                  to the hepatic transarninses would favor extra- or
   presenting with jaundice. With this approach, the clinician             intrahepatic cholestasis.
   can confidently assign probabilities to the major categories         3. Hepatic transaminase elevations out of proportion to
   that most frequently account for jaundice.                              the alkaline phosphatase favor hepatocellular etiologies.

4 Lab Updates | November 2008
   4. The complete blood count (CBC) can be extremely               c. Ultrasonography may be preferable, given its lower
      useful. The most important points include the                    cost and radiation exposure.
      interpretation of or for:                                   2. CT scanning is slightly more sensitive (74%-96%) and
      a. Anemia (hemolysis, bleeding)                                specific (90%-94%) than ultrasound in detecting the
      b. Mean, corpuscular volume (microcytosis suggests             presence of biliary obstruction.
         iron deficiency; round rnacrocytosis suggests               a. CT scan is more likely to show the site and cause of
         chronic liver disease or ineffective erythropoiesis;           obstruction when compared to ultrasound.
         gastrointestinal malignancy)                                b. CT also gives information in instances where staging
      c. Thrombocytopenia [sequestration in portal hyperten-            a suspected neoplasm has clinical significance.
         sion, sepsis, autoimmune disease, bone marrow               c. In patients where mass lesions (i.e., malignancy,
         suppression (alcohol)]                                         abscess) are suspected or where technical limitations
      d. Reticulocytosis (hemolysis)                                    make ultrasound difficult to interpret, CT is preferred.
   5. Urinalysis provides information about bilirubinuria         3. Percutaneous transhepatic cholangiography (PTC):
      and urobilinogen. In reality, data from urinalysis adds        The technical success rate of this procedure is approxi-
      little incremental benefit to the decision-making              mately 90%-99%. Its use is limited by a major compli-
      process.                                                       cation rate of 3%-5% and has been largely supplanted
     a. The presence of urobilinogen eliminates the possi-           by endoscopic retrograde cholangiopancreatography
        bility of complete biliary tract obstruction. That is,       (ERCP).
        bile has entered the intestine, where it undergoes        4. ERCP offers a lower complication rate than PTC and
        enterohepatic metabolism.                                    provides a greater number of therapeutic options
     b. The presence of bilirubinuria, on the other hand,            (stone extraction, stent placement).
        suggests that conjugation is taking place.                   a. This test could reasonably be used in patients with
   6. Coagulation studies are useful in two areas.                      a high likelihood of extrahepatic obstruction (e.g.,
                                                                        those who have had recent biliary surgery; symptoms
     a. If an invasive intervention is considered, coagulation
                                                                        of cholangitis, palpable gallbladder, pain or fever,
        studies can be used to assess bleeding risk.
     b. If the prothrombin time is prolonged and other
                                                                     b. When palliation is the primary intent, ERCP is an
        causes of coagulopathy are unlikely, chronic liver
                                                                        appropriate initial procedure.
        disease or hepatocellular etiologies become
        increasingly likely.                                      5. Magnetic resonance cholangiopancreatography
                                                                     (MRCP) is a radiologic technique that produces images
   7. Serum amylase would be obtained in cases where
                                                                     of the pancreaticobiliary tree, which are similar in
      extrahepatic obstruction is suspected on the basis of
                                                                     appearance to those obtained by invasive methods.
      history and physical examination.
                                                                     It appears to have similar diagnostic accuracy to ERCP.
B. Diagnostic imaging. It is estimated that 25%=40% of
                                                                     a. MRCP is indicated for patients with allergies to iodi-
   common bile duct obstructions are missed by both ultra-
                                                                        nated contrast media, patients who have undergone
   sound and CT scanning However, when intrahepatic
                                                                        unsuccessful ERCP (3%-10%), and patients with
   cholestasis or hepatocellulat etiologies are suspected,
                                                                        altered anatomy (i.e., secondary to surgical
   then either of these noninvasive strategies is acceptable.
                                                                        procedures or congenital abnormalities).
   1. Ultrasound: This is the least invasive and lowest cost
                                                                     b. ERCP has advantages over MRCP, which include the
      of the imaging procedures available to assess obstruc-
                                                                        ability to perform therapeutic interventions, perform
      tive jaundice. Ultrasound determines the presence of
                                                                        manometry or endoscopic ultrasound, directly
      obstructive jaundice by detecting dilated bile ducts.
                                                                        visnalize the ampulla, and biopsy lesions.
     a. The sensitivity is 55%-93%, and the specificity is
                                                                 Reference: Sachs, Howard J., “Jaundice”. Guide to Diagnostic
                                                                            Testing. pp 130-135.
     b. False negatives are generally due to two factors:
       (1) Inability to visualize the biliary tee (often         If you have questions, comments or suggestions, please contact:
           secondary to interposed bowel gas)                    Dr. L. Michael Snyder Chairman, Department Hospital of Laboratories
       (2) Absence of biliary dilatation in the presence
           of obstruction.
                                                                 at 508-334-0280

                                                                                         Lab Updates | November 2008 5
                                                  Jaundice: Diagnostic Evaluation Algorithm

                                     Jaundice                                              Conjugated hyperbilirubemia

  History:                          CBC,                    Physical Exam:
                                    Reticulocytes                                      Alkaline phosphatase             Transaminase                     Refer to
  • Stool characteristics                                   • Assess for stigmata of   predominant pattern              predominant pattern              hepatocellular
  • Urine characteristics                                     chronic liver disease
                                    Total and direct                                                                                                     jaundice
  • Pain, fever, weight loss,                                 (see text)
    pruritis, travel, IVDU                                  • Scleral inspection
  • Sexual promiscuity,                                     • Hepatic exam (size,      Extrahepatic biliary          Intrahepatic cholestasis
    blood transfusions,                                       texture, auscultatory    obstruction suspected         suspected
                                    ALT, AST                  findings, tenderness),
                                    Amylase                   splenomegaly,
  • Prior biliary surgery
                                    PT                        palpable mass
                                    Urinalysis              • Stool guaiac
                                                                                       Acute abdominal        Painless/insidious           Diagnostic imaging
                                                                                       pain/fever             onset                        CT/US

                                                                                       Diagnostic imaging       Diagnostic imaging
  Direct: total bilirubin > 50%               Indirect total bilirubin ratio > 80%     • Ultrasound             • CT Scan                   Diagnostic       Nondiagnostic
                                                                                       • CT Scan                • Ultrasound

  Refer to conjugated                         Unconjugated hyperbilirubinemia
                                                                                       Diagnostic     Nondiagnostic          Diagnostic
                                                                                                                                                      ANA        HCG
                                              Hemolysis                                                                                               ASMA
                                              CBC with:
                                              • Reticulocytosis
                                              • Peripheral smear with schistocytes
                                              Serum with:                                       Diagnostic     Nondiagnostic                           PBC   Cholestatic
                                              • LDH elevated                                                                                                 jaundice of
                                                AST elevated                                                                                                 pregnancy
                                              Haptoglobin decreased                    Choledocolithiasis          See
                                                                                       Ascending                   intrahepatic
                                                                                       cholangitis                 chlolestasis
           NO                                                       YES                Pancreatitis
                                                                                                                                          Mass         See
                                                                                                                                          lesion       extrahepatic
  Abnormal transaminases                                 Review smear
                                                                                                                                          • Tumor      biliary
                                                                                                                                          • Abscess    obstruction
                                                         PT, aPTT
  NO                                    YES              FDP
                                                         Creatinine                                 Sclerosing                Malignancy
  *Gilbert’s Syndrome           Diffuse                                                             cholangitis               • Pancreas
  Ineffective                   hepatocellular                                                      HIV cholangiopathy        • Ampulla
  erythropoiesis                disease                    Refer to                                 Stricture                 • Cholangiocarcinoma
  Hematoma                                                 hemolytic                                Choledocolithiasis        • Metastatic
  resorption                                               anemia in                                                          Stricture
  *Common cause for                                        Chapter 41                                                         Choledocholal cyst
  but an uncommon               Refer to                                                                                                                     Dubin-Johnson
  cause for jaundice            hepatocellular                                                                                                               Rotor
                                jaundice                                                                                                                     BRIC
                                                                                                                                                             • Sarcoid
                                                                                                                                                             • Amyloid

                                                                                                                                                          Appendix A

6 Lab Updates | November 2008
                   Jaundice: Diagnostic Evaluation Algorithm

                                  Transaminase predominant pattern


                             Diagnostic imaging                 Re-assess history for toxins/drug
                             CT/US                              Hepatitis serologies; HAV, HBSAg,
                                                                HBSAb, HCV

      Diagnostic                          Nondiagnostic Studies                          Diagnostic

lesion                                              Cirrhosis                          Toxin/drug
• Tumor                                             Ischemia                           Viral Infection
• Abscess                                           Alcohol

            See extrahepatic
            biliary obstruction

                                                                                                          Appendix A

                                                                                          Lab Updates | November 2008 7
   Quantitative Urine Chemistry Tests: 24 Hr vs. Random Urine
Urine is an ultra filtrate of plasma with selected solutes          Potassium (K):
reabsorbed, other solutes secreted, and the final water             Urinary K levels are helpful in the evaluation of patients with
volume determined by the state of hydration of the body.            unexplained hypokalemia, electrolyte and acid-base balance.
Therefore when an individual is healthy, the final urine            In the presence of such hypokalemia, urine excretion is help-
contains essentially those solutes the body does not need.          ful to separate renal from non-renal losses. Excretion <20
The volume and solute composition of urine can vary greatly         mmol/24 hours is evidence that hypokalemia is not from
depending on the individuals’ diet, physical activity and health.   renal loss. Renal loss >50 mmol/L in a hypokalemic, hyper-
Because of these variables, normal urine values for each            tensive patient not on a diuretic may indicate primary or
organic and inorganic component are difficult to establish.         secondary aldosteronism. Urinary K may be elevated with
Quantitative urine assays often require a timed (24 Hr)             dietary (food and/or medicinal) increase, hyperaldosteronism,
collection because of diurnal variations in excretion of many       RTA, onset of alkalosis, and with other disorders. Time
substances and the effect of exercise, hydration and body           relationships are important in interpretation. K will decrease
metabolism on excretion rates. Random urine collection is           in Addison disease and in renal disease with decreased urine
convenient and minimizes the subject compliance concerns,           flow (nephrosclerosis, pyelonephritis, glomerulonephritis).
however, has drawbacks, mostly due to the variability of
                                                                    Chloride (Cl):
urinary output. Much of this variability can be compensated
                                                                    Cl is reabsorbed with Na throughout the nephron. Because
for by adjustment of the concentration of the measured
                                                                    of its relationship with other electrolytes, urinary Cl results
analyte based on the level of creatinine in the urine.
                                                                    can be used to help assess volume status, salt intake,
Sodium (Na):                                                        causes of hypokalemia, and to aid in the diagnosis of renal
Urinary Na determinations are usually performed to detect           tubular acidosis (RTA). Approximately 30% of the hypo-
or confirm the presence of conditions that affect body fluids       volemic patients have more than 15 mmol/l difference
(for example, dehydration, vomiting, and diarrhea) or disorders     between urine Na and Cl concentrations. This is due to the
of the kidneys or adrenal glands. It is diagnostically useful       excretion of Na with another anion (such as HCO3-) or to
in 3 clinical settings:                                             the excretion of Cl with another cation (such as NH4+). It
                                                                    is helpful to measure urine Cl concentration in a patient
  1. Volume depletion: To determine the route of Na
                                                                    who seems to be volume depleted, but has somewhat
     loss. Low urinary Na indicated extra renal loss and
                                                                    elevated urine Na concentration. It is also helpful in patients
     high value indicates renal salt wasting or adrenal
                                                                    with a normal anion gap metabolic acidosis. In the absence
                                                                    of renal failure, this may be due to diarrhea or one of the
  2. Differential Diagnosis of Acute Renal Failure: High            forms of RTA. The normal response to acidemia is to increase
     values are consistent with acute tubular necrosis.             urinary acid excretion, primarily NH4+. When urine NH4+
  3. In hyponatremia, low urinary Na indicates avid renal           levels are high, the urine anion gap [(Na + K)-Cl] will have a
     Na retention, which may be attributable to either              negative value, since Cl levels will exceed that of Na and K
     severe volume depletion or Na retaining states seen            by the approximate amount of NH4+ in the urine. Thus, the
     in cirrhosis, the nephrotic syndrome and CHF. When             urine Cl concentration may be inappropriately high in diarrhea
     hyponatremia is associated with urinary Na excretion,          induced hypovolemia because of the need to maintain the
     that equals or exceeds the dietary Na intake, it is            electro neutrality as NH4+ excretion is enhanced.
     likely SIADH present.

8 Lab Updates | November 2008
Phosphorus (P):
Urinary P levels are used to evaluate calcium/phosphorus
balance. High urinary P (i.e., increased renal losses) occurs
in primary hyperparathyroidism, vitamin D deficiency, RTA,
diuretic use. Phosphates are among the substances which
may be lost in the Fanconi syndrome. Renal loss of phosphate
may itself lead to rickets or osteomalacia. Low levels are
observed in hypoparathyroidism, pseudohypoparathyroid-
ism, vitamin D intoxication.
They are also useful in the evaluation of nephrolithiasis,
hypophosphatemia with normal serum calcium, high
alkaline phosphatase, and hypercalciuria. Low urinary P
occurs with osteomalacia from excessive antacid ingestion.
Children with thalassemia may have normal P absorption,
but high renal phosphaturia, leading to a deficiency of P.
Increasing dietary intake of K has been reported to increase
serum phosphate concentrations apparently by decreasing
renal excretion of phosphate. During the last trimester of
pregnancy there is a six fold increase in calcium and P
accumulation as the fetus triples its weight. Plasma P
concentrations and increased urinary phosphate may               Uric Acid:
provide a useful means to assess response to phosphate           Uric acid is produced in the liver from the degradation of
supplements in the premature infants.                            dietary and endogenously synthesized purine compounds.
                                                                 The normal adult male has a total body urate pool of
Glucose:                                                         approximately 1200 mg, twice that of the adult female.
Detection of glucose on a semi quantitative urine dipstick       This gender difference may be explained by an enhancement
or Clinitest tablets is an insensitive means of screening        of renal urate excretion due to the effects of estrogenic
for type 2 diabetes. The high rate of false-negative results     compounds in premenopausal women. Under normal steady
suggests that the urine dipstick is not adequate as a            state conditions, daily turnover of 60 percent of the urate
screening test. Additionally, not all patients with glucosuria   pool is achieved by balanced production and elimination
have diabetes. Glucosuria can occur with defects in renal        of uric acid. Human tissues do not have the ability to meta-
tubular function, as seen in Type 2 (proximal) RTA and in        bolize urate. Thus, in order to maintain homeostasis, urate
familial renal glucosuria, a genetic disorder associated with    must be eliminated by the gut and the kidney. The entry of
salt-wasting, polyuria, and volume depletion. Quantitative       urate into the intestine is most likely a passive process that
urine glucose tests aid in the evaluation of glucosuria, renal   varies with serum urate concentration. Intestinal tract bacteria
tubular defects, and in the management of diabetes mellitus.     are able to degrade uric acid. This breakdown process is
Calcium (Ca):                                                    responsible for approximately 1/3rd of total urate turnover,
Urinary Ca levels reflects intake rates of intestinal Ca         and accounts for nearly all urate disposed of by extra
absorption, bone resorption and renal loss. Its evaluation       renal routes. Under normal conditions, uric acid is almost
is useful in the patients with disorders of bone disease, Ca     completely degraded by colonic bacteria with little being
metabolism, renal stones and follow-up of patients on Ca         found in the stool. Urinary uric acid excretion accounts for
therapy for osteopenia. Hypercalcemia of any cause raises        the remaining 2/3rd of the uric acid turned over daily.
urinary Ca excretion and its measurement adds little to the      Urine uric acid testing may be done to diagnose kidney
differential diagnosis of hypercalcemia. Fasting Ca excretion    stones. It may also be used to monitor people with gout,
is useful when assessing the contribution of abnormal renal      since many of these patients develop uric acid kidney stones.
tubular handling of Ca to disorders of Ca homeostasis and        Hyperuricosuria is present in patients with renal calculus for-
may be the best test of Ca excretion in the investigation of     mation. Even mild renal failure decreases uric acid excretion.
possible familial benign hypocalciuric hypercalcemia.            Uric acid excretion is decreased with hypertension.

                                                                                         Lab Updates | November 2008 9
Urea Nitrogen (UN):                                                  Creatinine:
Urine UN is a measure of protein breakdown in the body.              Creatine is synthesized from amino acids in the kidney, liver
This test is mainly used to determine a person’s protein bal-        and pancreas. The creatine is then transported in the blood
ance and the amount of dietary protein needed by severely            to other organs where it is synthesized into creatinine. In the
ill patients. It is also used to determine how much protein a        absence of kidney disease, the urinary creatinine is excreted
person takes in. Urea is excreted by the kidneys, so excretion       in rather constant amounts and represents glomerular filtra-
of urea can reflect kidney function. Low levels usually indi-        tion and active tubular excretion of the kidney. Because the
cate malnutrition, kidney problems and high levels usually           creatinine is excreted from the body at a constant rate, there
indicate too much protein intake and/or increased protein            are expected values for creatinine in normal human urine.
breakdown in the body.                                               Specimen validity testing is the evaluation of the specimen
                                                                     to determine if it is consistent with normal human urine
Magnesium (Mg):
                                                                     (creatinine values greater than 20 mg/dL). Creatinine is made
Mg is an important but commonly neglected electrolyte.
                                                                     at a steady rate and is not affected by diet or by normal
Mg depletion could be a common condition found in 26%
                                                                     physical activities. Urine creatinine is not ordered alone.
of hospitalized patients. It usually results from insufficient
                                                                     Creatinine clearance, which requires a serum creatinine,
Mg intake and excessive renal loss; although renal wastage
                                                                     offers useful renal function data. Serum creatinine alone is
associated with a renal tubular defect or diuretic treatment
                                                                     not an adequate index of glomerular filtration rate.
also occurs. Both insufficient Mg intake and extra renal loss
result in a low urine Mg excretion. Measurement of urine             Effective November 18, 2008, UMass Memorial laboratories
Mg excretion is an essential investigation in these patients.        will be introducing new random urine chemistry tests with
Mg urinary excretion is enhanced by increasing blood alcohol         results standardized with creatinine levels and will be making
levels, diuretics, Bartter syndrome, corticosteroids, cis-platinum   reference range changes to the following 24 hr urine tests.
therapy and aldosterone. Renal Mg wasting occurs in renal
transplant recipients who are on cyclosporine and prednisone.
                                                                      If you have questions, comments or suggestions, please contact:
Renal conservation of Mg is diminished by hypercalciuria,
                                                                      Dr. L.V. Rao, Director at 508-334-7593 or

salt-losing conditions, and the syndrome of inappropriate
                                                                      via email at RaoL@ummhc.org
secretion of antidiuretic hormone. Mg deficiency is often
inadequately documented by serum Mg levels. Urinary Mg                Ms. Judy Rennell, Manager at 508-334-3803 or
                                                                      via email at Rennellj@ummhc.org
analyses have been advocated before and after therapeutic
Mg administration to further investigate the significance
of an apparent low serum Mg.

10 Lab Updates | November 2008
The reference range changes are:

  Test       Specimen       Mnemonic       Test          Test           Current             New
  Type         Type                       Name           Units      Reference Range   Reference Range
 Change        24 Hr          NAEX        Sodium       mmol/day         80-180             Males:
               Urine                    Urine 24 Hr                                    <10 Yr: 41-115
                                                                                      10-14 Yr: 63-177
                                                                                       >14 Yr: 40-120
                                                                                       <10 yr: 20-69
                                                                                      10-14 Yr: 48-168
                                                                                       >14 Yr: 27-287
  New         Random          NACR         Sodium      mmol/gm                             Males:
               Urine                   Urine, Random   Creatinine                         23-229
 Change        24 Hr           KEX       Potassium     mmol/day         40-80             Males:
               Urine                    Urine 24 Hr                                    <10 Yr: 17-54
                                                                                      10-14 Yr: 22-57
                                                                                      >14 Yr: 25-125
                                                                                       6-10 Yr: 8-37
                                                                                      10-14 Yr: 18-58
                                                                                      >14 Yr: 25-125
  New         Random           KCR       Potassium     mmol/gm                             Males:
               Urine                   Urine, Random   Creatinine                         13-116
 Change        24 Hr           CLEX      Chloride      mmol/day        100-250             Males:
               Urine                    Urine 24 Hr                                    <10 Yr: 36-110
                                                                                      10-14 Yr: 64-176
                                                                                      >14 Yr: 110-250
                                                                                       >60 Yr: 95-195
                                                                                        <10 Yr: 18-74
                                                                                      10-14 Yr: 36-173
                                                                                      >14 Yr: 110-250
                                                                                       >60 Yr: 95-195
  New         Random           CLCR       Chloride     mmol/gm                             Males:
               Urine                   Urine, Random   Creatinine                         25-253
 Current       24 Hr          PHEX     Phosphorous      gm/day          0.4-1.3
               Urine                   Urine, 24 Hr
  New         Random          PHCR      Phosphorous     mg/gm                              Males:
               Urine                   Urine, Random   Creatinine                     <40 Yr: 36-1770
                                                                                       >40 Yr: 54-860
                                                                                      >40 Yr: 111-927
                                                                                      >40 Yr: 105-1081

                                                                                          (continues on page 12

                                                                        Lab Updates | November 2008 11
The reference range changes are: (continued from page 11

  Test         Specimen        Mnemonic           Test         Test           Current             New
  Type           Type                            Name          Units      Reference Range   Reference Range
 Change          24 Hr            GLEX          Glucose       gm/day        0.04-0.21            <0.5
                 Urine                        Urine, 24 Hr
   New          Random            GLCR          Glucose       mg/gm                             Males:
                 Urine                       Urine, Random   Creatinine                     <40 Yr: 3-181
                                                                                            >40 Yr: 19-339
                                                                                            <40 Yr: 5-203
                                                                                            >40 Yr: 8-331

 Change          24 Hr            CAEX          Calcium       mg/day         100-250           100-300
                 Urine                        Urine, 24 Hr
   New          Random            CACR          Calcium       mg/gm                             Males:
                 Urine                       Urine, Random   Creatinine                        12-244
 Change          24 Hr            UREX         Uric Acid      mg/day         300-1000          250-750
                 Urine                        Urine 24 Hr
   New          Random            URCR          Uric Acid     mg/gm                             Males:
                 Urine                       Urine, Random   Creatinine                        104-593
 Change          24 Hr            CREX         Creatinine     mg/day         800-1800           Males:
                 Urine                        Urine, 24 Hr                                    800-2000
 Change         Random            RUCR         Creatinine     mg/dL                             Males:
                 Urine                       Urine, Random                                  <40 Yr: 24-392
                                                                                            >40 Yr: 22-328
                                                                                            <40 Yr: 16-327
                                                                                            >40 Yr: 15-278
 Change          24 Hr            UNEX       Urea Nitrogen    gm/day          2.5-27            12-20
                 Urine                        Urine 24 Hr
   New          Random           UNCR        Urea Nitrogen    gm/gm                             Males:
                 Urine                       Urine, Random   Creatinine                        2.8-9.8
 Current         24 Hr           MGEX         Magnesium       mg/day          72-120
                 Urine                        Urine, 24 Hr
   New          Random           MGCR         Magnesium        mg/g                             Males:
                 Urine                       Urine, Random   Creatinine                        18-110

12 Lab Updates | November 2008
                        UMass Memorial Laboratories
                          Patient Service Centers
Worcester PSC Locations
Belmont Street PSC                  Medical Office Building                  UMass Memorial-Hahnemann Campus
67 Belmont Street                   25 Oak Avenue                            281 Lincoln Street
Worcester, MA 01605                 Worcester, MA 01605                      Worcester, MA 01605
Mon–Fri 8:00am - 5:00pm             Mon–Fri 8:00am - 5:00pm                  Mon–Fri 7:00am - 5:30pm
Closed 12:15pm - 1:15pm             508-792-3656                             508-334-8100
                                    Medical Office Building PSC              UMass Memorial-Memorial Campus
City Hospital Campus PSC            116 Belmont Street                       119 Belmont Street
26 Queen Street, 1st Floor          Worcester, MA 01605                      Worcester, MA 01605
Worcester, MA 01610                 Mon–Fri 8:00am - 5:00pm                  Mon–Fri 7:00am - 6:00pm
Mon–Fri 8:00am - 5:00pm             Closed 12:15pm - 1:15pm                  Sat & Sun 8:00am - 1:00pm
Closed 12:00pm - 1:00pm             508-753-6854                             508-334-6486
                                    Park Avenue PSC                          UMass Memorial-University Campus
Grove Medical PSC                   255 Park Avenue                          55 Lake Avenue North
26 Queen Street, 6th Floor          Suite 210                                Worcester, MA 01655
Worcester, MA 01610                 Worcester, MA 01609                      Mon–Fri 7:30am - 5:30pm
Mon–Fri 8:00am - 5:00pm             Mon–Fri 8:00am - 5:00pm                  508-856-7797
Closed 12:15pm - 1:15pm             Closed 12:15pm - 1:15pm
                                                                             Vernon Medical Center PSC
508-334-0275                        508-798-5127
                                                                             10 Winthrop Street
Hahnemann Professional PSC                                                   Building #2, 1st Floor
291 Lincoln Street                                                           Worcester, MA 01604
Worcester, MA 01605                                                          Mon–Fri 8:00am - 5:00pm
Mon–Fri 8:00am - 5:00pm                                                      508-831-0624

Central Massachusetts Locations
Clinton PSC                         Fitchburg PSC                            Marlborough/Bolton Street PSC
Clinton Hospital                    HealthAlliance/Burbank Hospital Campus   320 Bolton Street, Suite G1
201 Highland Street                 275 Nichols Street, 4th Floor            Marlborough, MA 01752
2nd Floor, Suite 1                  Fitchburg, MA 01420                      Mon–Fri 8:00am - 5:00pm
Mon & Wed 8:00am - 5:30pm           Tues, Wed, & Thurs 8:30am - 9:00pm       Closed 11:15am - 12:15pm
Tues, Thurs & Fri 8:00am - 5:00pm   Mon & Fri 8:30am - 5:30pm                508-229-0574
Closed 1:00pm - 1:30pm              978-878-8352
                                                                             Marlborough/Lakeview PSC
Clinton, MA 01510
                                    Holden PSC                               640 Bolton Street
                                    52 Boyden Street                         Marlborough, MA 01752
Douglas PSC                         Holden, MA 01520                         Mon–Fri 8:00am - 5:00pm
15 West Street                      Mon–Fri 7:00am - 4:30pm                  Closed 12:15pm - 1:15pm
Douglas, MA 01516                   Closed 12:30pm - 1:00pm                  508-303-1990
Mon–Fri 8:00am - 12:00pm            508-829-8262
                                                                             Marlborough/Maple Street PSC
                                    Lancaster PSC                            340 Maple Street
                                    136 High Street Ext                      Marlborough, MA 01752
                                    Lancaster, MA 01523                      Mon–Fri 8:00am - 5:00pm
                                    Mon–Fri 8:00am - 5:00pm                  Closed 12:15pm - 1:15pm
                                    Closed 12:00pm - 1:00pm                  508-229-7847

                                                                             Lab Updates | November 2008 13
                         UMass Memorial Laboratories
                           Patient Service Centers
Central Massachusetts Locations
Milford PSC                         Shrewsbury/Julio Drive PSC         Sterling PSC
91 Water Street                     26 Julio Drive                     104 Leominster Road
Milford, MA 01757                   Shrewsbury, MA 01545               Sterling, MA 01564
Mon–Fri 8:00am - 5:00pm             Mon–Fri 8:00am - 5:00pm            Mon–Fri 8:00am - 5:00pm
Closed 12:15pm - 1:15pm             Closed 12:00pm - 1:00pm            978-422-5109
508-482-9210                        508-845-3615
                                                                       Westborough PSC
Northborough PSC                    Shrewsbury/Main Street PSC         154 Main Street
112 Main Street                     604 Main Street                    Westborough, MA 01581
Northborough, MA 01532              Shrewsbury, MA 01545               Mon 7:30am - 4:30pm
Mon–Fri 8:00am - 5:00pm             Mon–Fri 8:00am - 5:00pm            Tues–Thurs 8:30am - 5:30pm
Closed 12:15pm - 1:15pm             Closed 12:15pm - 1:15pm            Fri 7:00am - 4:00pm
508-393-3704                        508-845-6521                       Closed 12:30pm - 1:30pm

Eastern Massachusetts Locations
Brockton PSC and Laboratory         Hyannis PSC                        Raynham PSC
1073 Pleasant Street                700 Attucks Lane, Suite 1D         675 Paramount Drive, Suite 102
Brockton, MA 02301                  Hyannis, MA 02601                  Raynham, MA 02767
Mon–Fri 8:00am - 5:00pm             Mon–Fri 8:00am - 5:00pm            Mon–Fri 8:00am - 5:00pm
508-559-2158                        Closed 12:15pm - 1:15pm            Closed 12:15pm - 1:15pm
                                    508-790-5723                       Sat 8:00am - 1:00pm
Framingham PSC
61 Lincoln Street, 2nd Floor        North Andover/Chestnut Green
                                                                       Waltham/Hope Avenue PSC
Framingham, MA 01702                565 Turnpike Street PSC
                                                                       20 Hope Avenue, Suite G03
Mon–Fri 8:00am - 5:00pm             565 Turnpike Street, Suite 83
                                                                       Waltham, MA 02453
Closed 12:15pm - 1:15pm             North Andover, MA 01845
                                                                       Mon–Fri 8:00am - 5:00pm
508-370-7259                        Mon–Fri 8:30am - 5:30pm
                                                                       Closed 12:15pm - 1:15pm
                                    Closed 12:15pm - 1:15pm
Dartmouth PSC                                                          781-899-2586
72 State Road
                                                                       Waltham/Lexington Street PSC
Dartmouth, MA 02301                 North Andover/Andover Street PSC
                                                                       6 Lexington Street, 2nd Floor
Mon–Fri 7:00am - 4:00pm             451 Andover Street, Suite 206
                                                                       Waltham, MA 02453
Closed 12:00pm - 1:00pm             North Andover, MA 01845
                                                                       Mon–Fri 8:00am - 4:30pm
Sat 7:00am - 11:00am                Mon–Thurs 7:30am - 4:30pm
                                                                       Closed 12:00pm - 12:30pm
508-997-4132                        Fri 7:00am - 4:00pm
                                    Closed 12:15pm - 1:15pm
Harvard Street PSC                  978-989-9238                       Wilmington PSC
632 Blue Hill Avenue
                                                                       64 Concord Street, Suite D
Dorchester, MA 02121
                                                                       Wilmington, MA 01887
Mon & Wed 8:30am - 8:30pm
                                                                       Mon–Fri 8:30am - 5:00pm
Tues, Thurs & Fri 8:30am - 5:30pm
                                                                       Closed 12:15pm - 12:45pm

Western Massachusetts Locations
Springfield PSC
(Opening soon)

14 Lab Updates | November 2008
                        UMass Memorial Laboratories
                          Patient Service Centers
Connecticut Locations
Avon PSC                                East Hartford PSC         Plainville PSC
44 Dale Road                            580 Burnside Avenue       7 North Washington Street
Suite 301                               Suite 1                   Suite 107
Avon, CT 06001                          East Hartford, CT 06108   Plainville, CT 06062
Mon–Fri 8:00am - 5:00pm                 Mon–Fri 8:00am - 5:00pm   Mon–Fri 7:00am - 5:30pm
Closed 12:15pm - 1:15pm                 Closed 12:15pm - 1:15pm   860-410-1892
860-679-0471                            860-610-0386
Enfield PSC                             Hartford PSC
139A Hazard Avenue                      21 Woodland Street
Building #4, Suite 15                   Suite 210
Enfield, CT 06082                       Hartford, CT 06105
Mon–Fri 7:30am - 4:30pm                 Mon–Fri 7:00am - 4:00pm
Closed 12:15pm - 1:15pm                 Closed 12:15pm - 1:15pm
860-763-0136                            860-247-0085

New Hampshire Locations
Exeter PSC
19 Hampton Road, Unit 10-B
Exeter, New Hampshire 03833
Mon–Fri 7:00am - 4:00pm
Closed 12:15pm - 1:15pm

Rhode Island Locations
Cumberland PSC                          Westerly PSC              Westerly Urgent Care PSC
106 Nate Whipple Highway                27 Crestview Drive        77 Franklin Street, Suite A
Suite 103                               Westerly, RI              Westerly, RI
Cumberland, RI                          Mon–Fri 8:00am - 5:00pm   Mon–Fri 7:00am - 4:00pm
Mon–Fri 7:00am - 3:30pm                 Closed 1:00pm - 2:00pm    Closed 12:15pm - 1:15pm
Closed 12:00pm - 12:30pm                401-596-8095              401-596-8075
North Providence PSC
1830 Mineral Springs Avenue
North Providence, RI
(Opening soon)

Please note that hours are subject to change

                                                                  Lab Updates | November 2008 15
                                  New Patient Service Center
We are one of the largest
laboratory providers in New England
UMass Memorial Laboratories has opened a
Patient Service Center (phlebotomy draw station)
at 632 Blue Hill Avenue, Dorchester, MA

The vision of UMass
Memorial Laboratories is:
• To be a leading provider of laboratory services
  throughout New England, meeting the needs
  of patients and providers in the region, and
• To be one of the top ten academic medical
                                                        Street PSC
  center-based laboratories in the United States
                                                      Franklin Park Zoo

                                                    Harvard Street PSC
                                                    632 Blue Hill Avenue, Dorchester, MA
                                                    Harvard Street PSC is located at 632 Blue Hill Avenue, Dorchester, MA.
                                                    The hours are Monday and Wednesday 8:30am-8:30pm,
                                                    Tuesday, Thursday and Friday 8:30am-5:30pm.
                                                    The phone number at Harvard Street PSC is 617-822-5523.

     Providing a higher level of service. If you don’t believe it, put us to the test!™

                                                                                                           NONPROFIT ORG.
                                                                                                           WORCESTER, MA
                                                                                                            PERMIT NO. 51
 UMass Memorial
 Medical Center Laboratories
 One Biotech Park, Suite 200
 365 Plantation Street
 Worcester, MA 01605-2376

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