Volume 11, Number 01

SERUM DIGOXIN When should specimens be drawn? As with other drugs, serum levels of digoxin rise rapidly after a single dose. There is then a period during which the drug passes into the tissue phase and an equilibrium is reached with the serum phase. Following this, the drug is slowly excreted in the urine. Since the therapeutic level of digoxin is very close to the level at which toxic signs and symptoms appear, it is very important to monitor this drug. The ideal time to do this is during the time of equilibrium which has been shown to be 8-24 hours after a single daily oral dose. The following graph illustrates this point.

It should be noted that it takes 1-2 weeks before a stable state is reached and testing should not begin until after that time. Acute renal failure and uremia are known to cause an increase in serum digoxin values. Hypokalemia, hypercalcemia and hypomagnesemia may precipitate digitalis toxicity. Quinidine, administered at the same time, causes increased serum digoxin values. Although the half-life of digoxin is 1.6 days, it may be markedly prolonged in renal or liver disease. Specimens for serum digoxin should be drawn into a red top tube 8-24 hours after the last dose. Therapeutic range is 1.2-2.6 nmol/L. Levels above 2.0 nmol/L with symptoms of toxicity would suggest decreasing the dose. Levels above 3.2 nmol/L are often accompanied by serious toxic effects

HIGH HEMOGLOBIN/HEMATOCRIT What does it indicate? Physicians are occasionally confronted with a hematology report containing a hemoglobin or hematocrit that is abnormally high with very few other findings. Sometimes the report is part of a routine exam, or it may be part of a pre-operative work-up. The question becomes: what does it mean? The usual causes may be listed: Polycythemia, vera Polycythemia, secondary (cardio-pulmonary, shunts) Polycythemia, familial (rare) Dehydration (including fever, diuretic use) Shock (physiologic reaction) High altitude adaptation Lab error (eliminated by repeats) Carbon monoxide (includes smoking > 1 pkg/day) Anabolic steroids Renal disease, e.g. hypernephroma. Most of the above conditions, other than polycythemia, can be distinguished by the history. Let us focus on the findings indicative of polycythemia, vera: Determining the patient's red cell mass is essential to distinguishing polycythemia vera from other forms of polycythemia. Normal is 28-30 ml/kg body weight. An elevated platelet count (sometimes markedly) helps to distinguish polycythemia vera. This occurs because more than one cell line may be involved in the proliferative disorder. An elevated leukocyte alkaline phosphatase is found in polycythemia vera and helps distinguish it from secondary polycythemia. Other tests may include: Arterial oxygen saturation to exclude secondary polycythemia. Carboxyhemoglobin level, especially heavy smokers. Scan of Liver and spleen: about 2/3 of patients with polycythemia vera have spenomegaly. Bone marrow exam. Usually shows hypercellularity with increased megakaryocytes and decreased iron stores. RBC count is increased. WBC is variable. Coagulation tests may be elevated in polycythemia vera, and these patients are at risk of hemorrhage and thrombosis (because of platelet excess) at surgery.

SERUM PROTEIN ELECTROPHORESIS Indications and interpretation Protein electrophoresis is valuable tool in the evaluation of the following diseases: Chronic liver disease Multiple myeloma Hypoglobulinemia Collagen diseases Nephrotic syndrome Malnutrition and Macroglobulinema The patterns produced are diagnostic with some of these diseases and in others, very suggestive. Particularly with myeloma and other paraproteinemias, further investigation is warranted, such as immunoglobulin studies of the serum and protein analysis with electrophoresis of the urine. These tests will be the subject of a newsletter in the near future. A specimen for serum protein electrophoresis should be collected in a red top tube. Use of plasma and hemolysed specimens should be avoided since they both add extra bands to the pattern.

Increased in: Dehydration Decreased in: Nephrotic syndrome Liver disease Malabsorption Malnutrition GI loss Burns Severe dermatitis of the weeping or serous type Chronic disease

Increased in: Acute and chronic infections Fever Decreased in: Nephrosis Alpha-1 anti- trypsin deficiency

Increased in: Biliary cirrhosis Obst. jaundice Nephrosis Myeloma (rare) Ulcerative colitis Decreased in: Acute hemolytic anemias

Increased in: Obstructive jaundice Biliary cirrhosis Myeloma (occas.) Decreased in: Nephrosis

Increased in: Autoimmune disease Cancers Chronic infections Collagen diseases Leukemias Liver disease Paraproteinemias e.g. Multiple myeloma Waldenstrom's macroglobulinemia Benign Franklin's disease Cryoglobulinemia Decreased in: Agamma and hypoglobulinemia Nephrotic syndrome

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