Active hepatitis B vaccination of dialysis patients and medical staff

Abstract

One hundred six patients with terminal renal insufficiency and 29 medical personnel were given three doses of hepatitis B vaccine at an interval of 0, 1, and 6 months (Merck, Sharp and Dohme, West Point, Pennsylvania, part of a joint study no. 649). Chronic hemodialysis patients (N = 99) received 40 micrograms vaccine (V) i.m. Uremic patients, who were just about to start chronic dialysis treatment (N = 7), were given 40 micrograms V, and at the first vaccination 3 ml hyperimmune globulin (HBIG) in addition. The medical personnel was alternately vaccinated with 20 micrograms V (N = 8), 40 micrograms (N = 11), 40 micrograms V, and 3 ml HBIG at the first vaccination (N = 10). After 12 months, 50% of the male dialysis patients, 66% of the female dialysis patients, and 95% of the medical staff developed anti-HBs antibodies. The anti-HBs titer of the dialysis patients was ten times lower than in the medical staff. The simultaneous passive immunization did not lead to any impairment of the anti-HBs titer in the dialysis patients and staff. The type of renal disease, length of time on dialysis, hematocrit, and immunoglobulin concentration did not influence the rate of immunization. After 12 months, 43 patients without antibody response were vaccinated a fourth time. Sixteen of these patients then developed anti-HBs, improving the immunization rate from 56.5 to 71.7%. A fifth vaccination only led to seroconversion, when brief or borderline anti-HBs could already be demonstrated previously. In dialysis patients who fail to develop anti-HBs after three doses of vaccine, a fourth vaccination is recommended after 12 months.

Differentiation of Monocyte Derived Dendritic Cells in End Stage Renal Disease is Skewed Towards Accelerated Maturation

“…The immune defect in ESRD patients is associated with a reduced T-cell stimulation, leading to a high susceptibility for infectious complications [2][3][4][5]22]. This impaired T-cell activation is related to an impaired co-stimulation by APC.…”

“…a secondary immune defect [2] that is frequently observed as non-responsiveness to standard vaccinations [3][4][5]. On the cellular level, this immune defect is at least partly related to an impaired activation of T-lymphocytes and reduced secretion of the T-cell growth factor interleukin-2 (IL-2) [6].…”

Altered CD46-mediated T cell co-stimulation in haemodialysis patients

“…Furthermore, immune dysfunction is reflected by a poor vaccination response against T helper dependent antigens, e.g. hepatitis B or influenza, while the response against T helper independent antigens, such as pneumococci, seems to be unaffected [7][8][9]. Although the cause of immune dysfunction in CRF patients thus far has not completely been delineated, uraemia per se seems to play a pivotal role.…”

“…Paradoxically, although the role of activated complement components as endogenous adjuvants in vaccination responses has been recognized widely [25], in HD patients impairment of these responses occurs despite complement activation during dialysis sessions [8]. Therefore involvement of complement activation in immune dysfunction needs to be elucidated in more detail.…”

Selective blockade of the antigen-receptor-mediated pathway of T cell activation in patients with impaired primary immune responses.

“…Immunodeficiency in these patients is secondary to chronic renal failure (1 1-19) and can be quantitated by means of the individual capacity to mount a primary immune response to hepatitis B vaccine. In this regard, controlled efficacy studies in the United States and Europe recently demonstrated that a high proportion of uremic patients fail to respond to otherwise highly immunogenic vaccines (20)(21)(22)(23)(24)(25)(26)(27).…”