large enough to affix complement but still small enough to remain soluble and to circulate freely. Once the situation of antibody excess occurs, the antigen-antibody complexes become large and insoluble, are rapidly phagocytized, and are of minimal pathogenicity. Presumably, the immune complex formation during the period of antigen excess is responsible for the transient arthritis observed in patients in the course of acute hepatitis B virus infection.

In addition to the serum sickness-like syndrome associated with hepatitis B infection, arthropathies are among the most common manifestations during the prodromal period of acute hepatitis B virus infection. The arthritis associated with acute hepatitis B virus infection typically resolves over a period of days or, at most, several weeks; it does not appear to result in long-term joint abnormalities.

Joint symptoms related to hepatitis B virus infection in cases of known time of exposure (e.g., following the transfusion of contaminated blood) usually begin within 1 to 4 weeks after the infection. All joints may be involved, usually symmetrically. The joints involved, in decreasing order of frequency, are the small joints of the hands, the wrists, and the knees (Gocke, 1975). Symptoms are often of sudden onset and may consist simply of prominent stiffness and pain or of warmth, redness, and painful joint effusions. The latter are especially prominent in the knees. The arthralgia or arthritis that occurs following acute hepatitis B virus infection is presumed to be caused by antigen-antibody-mediated vascular responses (Coombs and Gell type III).

Polyarteritis following hepatitis B virus infection has clearly been observed in humans (McMahon et al., 1989). Furthermore, 30-50 percent of patients with biopsy-proven polyarteritis nodosa have persistent hepatitis B virus infection (Gocke, 1977). Such patients have low serum complement levels and circulating HBsAg-antibody complexes. Immune complexes and complement components have been detected, albeit rarely, in diseased vessels by immunofluorescence staining. The association of polyarteritis nodosa with hepatitis B infection (McMahon et al., 1989) is thought to be related to a situation of continued antigenic stimulation in individuals who develop antibodies to hepatitis B virus.

VAERS contains a large number of cases (submitted between November 1990 and July 1992) in which there was a possible association between arthritis and hepatitis B vaccination. There are 57 reasonably well documented cases of individuals who developed arthritis within 2 months after receiving recombinant hepatitis B vaccine. Of the 57 vaccinated individuals, 52 were health care workers; 79 percent were women.