Several typical electrophoretic patterns are presented with diseases in which they are most commonly found (Fig. 22-2). It must be strongly emphasized that no pattern is pathognomonic of any single disease and that there is considerable variation in the shape and height of the electrophoretic peaks in individual patients that may obscure a pattern. In addition, the patterns will not always appear when they should be expected and in some cases may be altered when two diseases are present together (e.g., acute infection in a patient with cirrhosis).

One electrophoretic configuration is called the acute reaction pattern. It consists of decreased albumin level and elevated alpha-2 globulin level and is found in acute infections in the early stages; some cases of myocardial infarct and tissue necrosis; some cases of severe burns, surgery, and other stress conditions; and in some of the rheumatoid diseases with acute onset. A second pattern consists of a slightly or moderately decreased albumin level, a slightly or moderately elevated gamma-globulin, and a slightly elevated or normal alpha-2 globulin level. This is the chronic inflammatory pattern and is found in chronic infections of various types, the granulomatous diseases, cirrhosis, and rheumatoid-collagen diseases. There may, of course, be various stages of transition between this chronic pattern and previously described acute one. A third pattern is typically found in the nephrotic syndrome. There is greatly decreased albumin level and a considerably increased alpha-2 level with or without an increase in the beta-globulin level. This differs from the acute stress pattern in that the alpha-2 elevation of the nephrotic syndrome is usually either slightly or moderately greater than that seen in acute reaction, whereas the albumin fraction in the nephrotic syndrome has a definitely greater decrease (sometimes to extremely low levels) than the albumin fraction of acute reaction.

A fourth pattern represents changes suggestive of far-advanced cirrhosis. It consists of a decreased albumin level with a moderately or considerably increased gamma-globulin level and variable degrees of incorporation of the beta peak into the gamma. The more pronounced the beta-gamma bridging becomes, the more suggestive the pattern is for cirrhosis. However, complete incorporation of the beta peak into the gamma region is actually uncommon, since it is found in only about 20% of well-established cases of cirrhosis. About 10% of cirrhotic patients have no gamma elevation at all, about 25% have mild to moderate gamma elevation without any beta-gamma bridging, about 8% have marked gamma elevation without any bridging, and about 33% have mild to moderate gamma elevation with mild to moderate beta-gamma bridging but without complete loss of the beta peak. Surprisingly, the electrophoretic pattern correlates poorly with degree of liver function abnormality. Correlation is not consistent even with microscopic findings at autopsy, although there is a tendency for more pronounced electrophoretic changes to be associated with more advanced microscopic abnormality.

A fifth pattern consists of a polyclonal gamma-globulin elevation, that is, a greatly increased gamma-globulin level that involves the entire gamma zone rather than a focal area and does not have a thin spikelike appearance. There may or may not be some degree of beta-gamma bridging, but the beta peak does not totally disappear. This pattern is most often seen in some cases of cirrhosis, in patients with chronic infection, in granulomatous diseases such as sarcoidosis or far-advanced pulmonary tuberculosis, in subacute bacterial endocarditis, and certain rheumatoid-collagen diseases such as rheumatoidarthritis systemic lupus or polyarteritis nodosa.

A sixth pattern consists of hypogammaglobulinemia, defined electrophoretically as decreased gamma-globulin level, usually without very marked changes in other globulin zones. This configuration is suggestive of the light chain variant of multiple myeloma (about 20% of myeloma cases) in which Bence Jones protein is excreted into the urine without a serum myeloma protein being evident with ordinary electrophoretic techniques. Patients with a substantial degree of hypogammaglobulinemia from other causes have the same electrophoretic picture.

Finally, there is the so-called monoclonal gammopathy spike (M protein and paraprotein are synonyms). This is located in the gamma area (much less frequently in the beta and rarely in the alpha-2) and consists of a high, relatively thin spike configuration that is more homogeneous and needle shaped than the other gamma or beta elevations discussed earlier. The majority of persons with the monoclonal spike on serum electrophoresis have myeloma. However, a sizable minority do not, and these cases are divided among Waldenstrцm’s macroglobulinemia, secondary monoclonal gammopathies, and idiopathic monoclonal gammopathy (discussed later).

Certain conditions may produce globulin peaks that simulate a small- or medium-sized monoclonal peak rather closely. A configuration of this sort in the alpha-2 area may occur in the nephrotic syndrome or in conditions that produce the acute reaction pattern (the alpha-2 elevation in both cases is due to elevated haptoglobin levels). A small monoclonal-type peak in the beta area may be seen in the third trimester of normal pregnancy or in some patients with chronic iron deficiency anemia (both due to increased transferrin levels). Similar beta region peaks may be caused by the presence of fibrinogen from incompletely clotted blood, by serum free hemoglobin, or by beta-2 microglobulin elevation. In the gamma area, somewhat similar peaks (but usually not as slender and needle like) may be found in rare patients with chronic disease, most often of the granulomatous type.