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A retrospective survey of the occurrence of pneumococcal septicaemia and meningitis in splenectomized adults was performed at a regional haematological centre after the introduction of pneumococcal vaccination in 1978. During this period 4 episodes of pneumococcal septicaemia were observed in 3 vaccinated, splenectomized patients. In all episodes the pathogenic strain was of an unusual serotype not included in the vaccine lending indirect evidence for the clinical efficacy of the pneumococcal vaccine, even in immunocompromised patients.

16 splenectomized adults, all vaccinated with a 14-valent pneumococcal vaccine (Pneumovax) 1978-79 had their pneumococcal antibody concentrations measured before and up to 10 years after vaccination. The antibody concentrations after vaccination declined to 71% in 2 years and remained at this level during the 10-year study period. Further studies are needed to see whether this applies to all vaccinated splenectomized adults.

Total haemolytic complement activity, C2, C5, total alternative pathway activity, factor B, and C3d were measured in 85 splenectomized patients from 1 month to 32 years after splenectomy. Furthermore the patients were investigated for circulating immune complexes. No major deficiencies of the complement factors were detected. In a few patients a reduced C2 level was caused by genetically determined defects or was due to complement consumption in conjunction with circulating immune complexes. The complement levels were normal in 2 patients who had survived overwhelming infections after splenectomy. C5 was elevated in a major proportion of the patients, and it is suggested that this might be caused by post-splenectomy monocytosis. Circulating immune complexes were found in 20% of all cases, irrespective of the presence of residual splenic tissue. Thus the commonly cited impairment of the complement system after splenectomy does not seem to be substantiated, and the deficient resistance against bacterial infections in splenectomized patients does not seem to include abnormalities of the complement system.

In normals without impairment of the splenic function, less than 1% of the circulating erythrocytes are vacuolated. Autotransplantation of splenic tissue (splenosis) or growth of accessory spleens may occur after splectomy. 39 patients splenectomized after traumatic rupture of the spleen were investigated by spleen Tc-scanning, employing heat-damaged autologous erythrocytes, and the splenic filter function was studied by counting the % of vacuolated erythrocytes using interference-phase-contrast microscopy. Residual splenic tissue was detected in 18 patients and in these the median % of vacuolated erythrocytes was found to be significantly lower than in patients without ectopic splenic tissue (21.0% versus 44.8%, P less than 0.01). There was, however, a marked overlap between the 2 groups. The reason for this might be that very small splenic implants are not detected by Tc-scanning.

The IgG-, IgM- and IgA- anti-pneumococcal antibody response to pneumococcal vaccination in 29 splenectomized adults and adolescents with hereditary spherocytosis or previous traumatic splenic rupture was determined by an enzyme-linked immunosorbent assay. It was not significantly different from that of 12 healthy controls except for a lower IgM class antibody increase in the splenectomized against one of four antigens studied. The antibody response was predominantly of IgG class, but significant increases in IgM and IgA class antibodies against all four antigens (polysaccharide types 2, 6A, 12F and 14) studied were observed. In 1/29 splenectomized and 2/12 healthy individuals (7%) the IgG antibody class did not predominate. In 36 adults and adolescents splenectomized due to traumatic rupture or during surgery for gastric ulcer, 77% of the peak geometric mean total antibody concentration four weeks after vaccination was still present after 21 months (16-26 months).

In 42 patients splenectomized after injury of the spleen or for non-malignant diseases residual splenic tissue was detected by 99mTc scanning in 19 (Group I) and not detected in 23 (Group II). Autoantibodies detected by the indirect immunofluorescent method occurred in 16 (38%) of the splenectomized patients and in 6 (14%) of 42 age- and sex-matched controls (P less than 0.02). In patients with residual splenic tissue the incidence of autoantibodies did not differ significantly form that in the controls, whereas autoantibodies occurred significantly more often in patients without residual splenic tissue (39%) than inthe corresponding control groups (9%) (P = 0.016). Antibodies to nuclear antigens (ANA), smooth muscle (SMA), reticulin (RetA) and cytoplasm of gastric parietal cells (PA) were detected, and the antibody titres tended to be higher in the patients than in the controls. None of the patients showed any clinical signs of autoimmune disease. These findings indicate that splenectomy disturbs the regulation of autoantibody function, and it is possible that this might be caused by a reduction of the number of T suppressor cells for which the spleen is a major pool. It is suggested that residual tissue may prevent an increased occurrence of autoantibodies in splenectomized patients.

Antibody-dependent cell-mediated cytotoxicity (ADCC) by monocytes was determined in 45 adults approximately 4 years after splenectomy for either abdominal trauma or accidental injury during operation for benign gastroduodenal ulcer. Compared to controls, both groups of splenectomized persons showed increased numbers of monocytes and decreased monocyte ADCC. The decrease of monocyte ADCC was only significant in those splenectomized persons in whom accessory splenic tissue was not detectable by isotope scanning. Addition of the spleen-dependent peptide tuftsin to monocytes in vitro did not augment their ADCC. An increase serum concentration of immune complexes was neither related to the presence of splenic tissue nor to the monocyte cytotoxicity. Vaccination with pneumococcal polysaccharide had no effect on monocyte ADCC. It is suggested that the defective monocyte cytotoxicity observed in splenectomized persons without detectable splenic tissue might be relevant to post splenectomy infectious susceptibility.

In 45 splenectomized individuals without malignancies, residual splenic tissue was detected by 99mTc-scanning using reinjection of labelled heat-damaged and autologous erythrocytes. The angiotensin-converting enzyme in serum (SACE) and the blood monocyte count were measured in order to demonstrate an eventual association between these parameters as well as the influence of residual splenic tissue. In 20 patients with detectable spleen tissue SACE was normal (26.2 +/- 4.4 U/ml), but in 25 patients without residual spleen tissue SACE was slightly elevated (28.7 +/- 6.4 U/ml; p less than 0.02) as compared with healthy controls (24.4 +/- 6.2 U/ml). In both groups of patients blood monocytes were markedly increased. However, no correlation could be demonstrated between SACE and the monocyte count in any group. In 2 patients SACE was above the upper limit of the normal range (greater than 36.8 U/ml) as found in sarcoidosis but no signs of this disease could be demonstrated. It is concluded that splenectomy must be taken into account when the significance of raised SACE is evaluated. It may be suggested that the spleen exerts an effect on the metabolism of SACE or on the ACE-producing cells in the organism.

The in vitro immunoglobulin (Ig) secretion of pokeweed mitogen (PWM)-activated peripheral blood lymphocytes (PBL) from individuals splenectomized post-trauma was monitored with a protein A plaque-forming cell (PFC) assay. Cultures of unfractionated as well as reconstituted cultures of isolated erythrocyte rosette-forming (E-RFC)-positive (T lymphocytes) and E-RFC-negative (B lymphocytes) cells were established. Using unfractionated cells, the response was substantially reduced or absent, whereas cultures of autologous untreated B and 2000 rads irradiated T cells restored the response to normal levels. Normal T cells were not able to stimulate patients' B cells to Ig-secretion and patients' untreated T cells did not induce plaque formation in normal B cells, whereas irradiated patients' T cells induced development of approximately 50% of the response induced by normal irradiated T cells. These results indicate that the immunological defect in splenectomized individuals is not merely restricted to a high level of radiosensitive T cell suppression but also involves an impaired B cell function and T/B cell cooperation.

Splenosis or ectopic spleens were detected in 22 of 45 patients splenectomized after either abdominal trauma or accidental lesions of the spleen during operation. The incidence of ectopic spleen tissue in various groups of splenectomized patients has been investigated by a sensitive scanning method employing reinjection of 99mTc-labelled heat damaged autologous erythrocytes. In comparison 7 cases were found among 45 patients who underwent splenectomy for haematological reasons. The time span between the operation and a positive scan varied between 3 months and 11 years. None of the patients in the haematological group with reoccurrence of spleen tissue presented any signs of relapse of their primary disorder. The only patient with overwhelming infection was a girl in whom splenectomy was performed for hereditary spherocytosis. She recovered from the sepsis and her scan was negative. It is concluded that recurrence of spleen tissue is frequent after traumatic lesions of the spleen but rare after selective splenectomy for haematological reasons. This may account for the lesser tendency to overwhelming sepsis after post-traumatic splenectomy.

The antibody response of 67 splenectomized adults and adolescents with benign underlying diseases to a 14-valent pneumococcal capsular polysaccharide vaccine was determined by an enzyme-linked immunosorbent assay. It was not significantly different from that of 12 healthy non-splenectomized adult volunteers for 13 of the 14 polysaccharide antigens studied. Residual splenic tissue as detected by Tc-scintigraphy was without any influence on the vaccination response. In comparison 5 untreated splenectomized adults with malignant diseases and 11 splenectomized adults receiving immunosuppressive therapy exhibited a significantly reduced combined geometric mean of their postvaccination antibody concentrations (all 14 antigens added) and of their combined geometric mean antibody fold increase as compared to the healthy non-splenectomized adults. The reduction in antibody response was most pronounced in the group of immunosuppressed patients. Immunogenicity of each of the 14 vaccine antigens varied considerably as judged by the geometric means of the postvaccination arbitrary antibody concentrations. Also individual variation in postvaccination antibody concentration against each antigen was large.