Group Of Healthy Blood Donors Research Articles

Infection with hepatitis B and C viruses and human retroviruses (HTLV-I and HIV) among high-risk Lebanese patients.

Three groups of Lebanese patients (haemophiliacs, patients on cycled cancer chemotherapy who were regularly receiving blood transfusions, and intravenous drug users) and a control group of healthy blood donors were checked for markers of infection with hepatitis viruses (B and C) and human retroviruses (HIV and HTLV-I). Compared with the controls, all three groups of patients were more likely to be seropositive for antibody to hepatitis C virus (anti-HCV), and the haemophiliacs and cancer patients (but not the relatively young drug users) were more likely to be seropositive for hepatitis B virus (HBV). All the haemophiliacs and cancer patients found to be carrying the surface antigen of HBV (HBsAg) and/or to be seropositive for anti-HCV had given the same result when tested before the screening of blood and blood products for HBsAg and anti-HCV became routine practice in Lebanon (a decade before the present study). The four intravenous drug users (IVDU) found seropositive for HBV (two cases) or anti-HCV (two cases) had seroconverted in the 2 years prior to the present study. In addition to highlighting the problem of HCV infection among IVDU, the present results emphasise the need for the careful screening of donated blood for all blood-borne viruses, and for the exclusive use of disposable equipment in the management of cancer patients. The anti-HBV vaccination of IVDU is recommended but only the results of further clinical evaluation will show whether the similar vaccination of patients on cycled cancer chemotherapy is of value. Although none of the patients or controls was found positive for anti-HIV-1, anti-HIV-2 or anti-HTLV-I, the routine screening of blood and blood products for these viruses (particularly for HIV) should remain mandatory.

Health Risk of Occupational Exposure in Welding Processes II. Immunological Effects

Many of epidemiological studies have certified the relationship between welding and various forms of health damages. In our study we performed an immunological research within a group of twenty men, working in the risky environment of manufacturing of stainless steel constructions (11 welders and 9 grinders, average age was 31 years, 55% of smokers, average time period in welding occupational exposure was 8 years). The exposed group of men was compared with a group of healthy blood donors, marked as the control group (people with various types of employment, living in same locality as a people from exposed group). People within the control group were not occupationally exposed to harmful chemical compounds (from 30 to 100 men were chosen for the individual immune parameters, average age of the whole group was 38 years, 40% of smokers). When compared with the control group, the exposed group of welders and grinders showed higher level of C3 complement (p < 0.001), orosomucoid (p < 0.05), beta-2-microglobulin (p < 0.001), neopterin (p < 0.001) and all fagocytic cells (p < 0.001). On the contrary, in the group of exposed people decreased values of IgA (p < 0.001), IgG (p < 0.001), IgM (p < 0.001), transferin (p < 0.001), alpha-1-antitrypsin (p < 0.001), alpha-2-macroglobulin (p < 0.001), haptoglobulin (p < 0.001) and ceruloplasmin (p < 0.05) were found. Some of these changes were characteristic for the exposed group. They could be considered as precursors of biological markers of effect for given type of exposure.

The -260 C-->T promoter polymorphism of the lipopolysaccharide receptor CD14 and severe sepsis in trauma patients.

CD14, expressed on the cell surface of monocytes and hepatic Kupffer cells, interacts with Gram-positive and Gram-negative bacteria. Upon CD14 stimulation, these cells respond with the enhanced release of cytokines involved in the pathophysiology of sepsis. The purpose of this study was to evaluate whether the genotype distribution of the -260 C-->T promoter polymorphism of the CD14 gene is associated with the development of severe sepsis in trauma patients. Fifty-eight severely injured blunt trauma patients with an injury severity score of 16 or more and without pre-existing chronic diseases. Genotyping for the single nucleotide exchange polymorphism of the CD14 gene was performed by means of a real-time polymerase chain reaction with fluorescence-labeled hybridization probes. Diagnosis of severe sepsis was based on the criteria of the ACCP/SCCM criteria. Fourteen out of the 58 patients (24.6%) developed a trauma-related severe sepsis. The overall allele frequency was 0.58 for the C allele and 0.42 for the T allele. The genotype distribution (TT 0.19, CT 0.47 and CC 0.35) did not differ significantly from a previously reported control group of healthy blood donors. There was no significant difference of the genotype distribution or allele frequency between trauma patients with severe sepsis and patients with an uncomplicated clinical course. This pilot study suggests that the CD14 -260 polymorphism is not associated with an increased risk of severe sepsis in trauma patients.

Seroprevalence of Babesia infections in humans exposed to ticks in midwestern Germany.

Babesiosis is considered to be an emerging tick-borne disease in humans worldwide. However, most studies on the epidemiology of human babesiosis to date have been carried out in North America, and there is little knowledge on the prevalence of infection and frequency of disease in other areas. The aim of this study was to investigate the prevalence of Babesia infections in a human population in Germany. A total of 467 sera collected between May and October 1999 from individuals living in the Rhein-Main area were tested for the presence of immunoglobulin G (IgG) and IgM antibodies to antigens of Babesia microti and Babesia divergens by indirect fluorescent-antibody (IFA) tests. These sera were derived from 84 Lyme borreliosis patients suffering from erythema migrans, 60 asymptomatic individuals with positive borreliosis serology, and 81 individuals with a history of tick bite. Cutoff values for discrimination between seronegative and seropositive results in the IFA tests were determined using sera from 120 healthy blood donors and 122 patients suffering from conditions other than tick-borne diseases (malaria, n = 40; toxoplasmosis, n = 22; syphilis, n = 20; Epstein-Barr virus infection, n = 20; and presence of antinuclear antibodies, n = 20). The overall specificities of the IFA tests for B. microti and B. divergens were estimated to be >or=97.5%. Positive IgG reactivity against B. microti antigen (titer, >or=1:64) or B. divergens antigen (titer, >or=1:128) was detected significantly more often (P < 0.05) in the group of patients exposed to ticks (26 of 225 individuals; 11.5%) than in the group of healthy blood donors (2 of 120 individuals; 1.7%). IgG antibody titers of >or=1:256 against at least one of the babesial antigens were found significantly more often (P < 0.05) in patients exposed to ticks (9 of 225) than in the control groups (1 of 242). In the human population investigated here, the overall seroprevalences for B. microti and B. divergens were 5.4% (25 of 467) and 3.6% (17 of 467), respectively. The results obtained here provide evidence for concurrent infections with Borrelia burgdorferi and Babesia species in humans exposed to ticks in midwestern Germany. They also suggest that infections with Babesia species in the German human population are more frequent than believed previously and should be considered in the differential diagnosis of febrile illness occurring after exposure to ticks or blood transfusions, in particular in immunocompromised patients.

CD14 gene −159C/T polymorphism is not associated with coronary artery disease and myocardial infarction

Background Monocyte differentiation antigen CD14 is considered an important cell-activating mediator of inflammatory responses that may result in atherosclerosis, coronary artery disease (CAD), thrombus formation, and myocardial infarction (MI). We assessed the possibility that a C → T nucleotide substitution polymorphism in the promoter (position −159) of the gene encoding CD14 constitutes a risk factor for CAD and MI. Methods Consecutive patients with significant, angiographically documented coronary stenoses but without symptoms or signs of old or acute MI constituted the group with CAD (n = 998). Consecutive patients with angiographic examination with old or acute MI constituted the group with MI (n = 793). Subjects matched with patients for age and gender but without angiographic evidence of CAD and without symptoms or signs of MI (n = 340) and a group of healthy blood donors (n = 104) served as controls. Results Genotype distributions of the −159C/T polymorphism were similar across the groups; CC:CT:TT was 26.9%:51.0%:22.1% in blood donors, 25.9%:52.0%:22.1% in matched control subjects, 27.4%:49.9%:22.7% in patients with CAD, and 29.2%:49.2%:21.6% in patients with MI. The lack of association persisted also after adjustment for the presence of conventional cardiovascular risk factors. In addition, no significant differences were found between genotype distributions of control subjects and selected subgroups of patients with CAD or MI. Conclusion These findings indicate that, in the sample of patients examined in this study, the −159C/T polymorphism of the CD14 gene is not related to CAD or MI. (Am Heart J 2002;143:971-6.)

A survey of infectious agents as risk factors for primary sclerosing cholangitis: are Chlamydia species involved?

The aetiology of primary sclerosing cholangitis (PSC) is unknown, and the role of micro-organisms has been studied only to a limited extent. We tested the hypothesis that past or persisting infection with common viruses or atypical bacteria might play a role in genetically susceptible hosts. Case-control study. Serological screening for antibodies against 22 viruses as well as Chlamydia spp. and Mycoplasma pneumoniae was carried out in 41 well-established PSC patients. All 5110 sera tested in 1997 for these micro-organisms at our laboratory served as a background reference group. Subsequently, Chlamydia anti-lipopolysaccharide (LPS) antibodies were determined by enzyme-linked immunosorbent assay (ELISA) in the PSC group and in three race-matched control groups (inflammatory bowel disease (IBD) group, n = 35; non-IBD patients group, n = 39; healthy blood donor group, n = 40). Subtyping in Chlamydia trachomatis and C. pneumoniae serotypes by specific anti-major outer membrane protein (MOMP) assays was carried out in the four groups. Immunohistochemical staining using specific markers for chlamydiae was carried out on liver biopsies of 14 PSC patients. There was a markedly elevated seroprevalence of Chlamydia-LPS antibodies compared with the 1997 reference group. The odds ratios (ORs) for the presence of immunoglobulin G, immunoglobulin M and immunoglobulin A antibodies for the PSC patients versus the control group were 2.4 (95% confidence interval (CI) 1.1 to 5.4), 1.9 (95% CI 0.9 to 4.0) and 6.7 (95% CI 3.0 to 17.0), respectively. All other micro-organisms tested showed normal antibody profiles that did not differ from the 1997 reference group. The seroprevalence of Chlamydia-anti-LPS antibodies was elevated markedly in the PSC patients compared with the IBD, non-IBD and blood donor groups. The outcomes in the C. trachomatis and C. pneumoniae anti-MOMP assays did not correlate with the anti-LPS-positive PSC sera. The actual presence of Chlamydia bodies in liver tissue could not be demonstrated. Our findings suggest an association between PSC and (previous) infection with Chlamydia.

Prothrombin gene G20210-->A transition is a risk factor for cerebral venous thrombosis.

It has been recently reported that a G-->A transition at nucleotide position 20210 in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increased risk of deep venous thrombosis. To date, it is unknown whether this polymorphism also represents a risk factor for cerebral venous thrombosis (CVT). Venous blood samples were collected from 45 patients with CVT and from 354 healthy blood donors as controls. A second control group consisted of 131 subjects with acute ischemic stroke or transient ischemic attack (TIA). Genomic DNA was isolated from peripheral blood leukocytes. Amplification of DNA was performed by polymerase chain reaction (PCR). The G-->A transition at nucleotide position 20210 of the prothrombin gene was detected by allele-specific restriction digestion. The G20210-->A transition in the prothrombin gene was found in a heterozygous form in 4 of 45 patients with CVT (8.9%) and in 8 of 354 healthy control subjects (2.3%). This difference was statistically significant (P=0.010). The G20210-->A transition increased the relative risk for CVT approximately 5-fold (age-adjusted odds ratio 5.7; 95% CI 1.5 to 21.5). In contrast, in the group of patients with acute cerebral ischemia, only 3 of 131 subjects (2.3%) were heterozygous for the G20210-->A transition, which corresponded to the prevalence in the group of healthy blood donors. The recently described G20210-->A transition in the 3'-untranslated region of the prothrombin gene is an inherited risk factor for CVT but obviously not for acute ischemic stroke or TIA.

Distribution of hepatitis G viremia and antibody response to recombinant proteins with special regard to risk factors in 709 patients.

A new virus named hepatitis G virus (HGV) has been detected recently. Until now, no assays for the detection of antibodies against different HGV proteins have been commercially available. Therefore, a strip immunoblot assay has been established to investigate seroreactivity against recombinant structural (core) and nonstructural proteins (NS3 and NS4) of HGV produced in Escherichia coli. Seropositivity for HGV was evaluated and concordanced with HGV polymerase chain reaction (PCR) results in 709 subjects. These individuals were classified into a nonrisk or a risk group, on the basis of infection with human immunodeficiency virus (HIV) or hepatitis C virus (HCV) or frequent parenteral exposure, including hemophilia, intravenous drug addiction, receipt of blood transfusion, or hemodialysis. The nonrisk group consisted of 257 healthy blood donors with normal alanine transaminase (ALT) levels (ALT < 30 U/L) and 154 patients with suspected non-A-E hepatitis (ALT > 45 U/L). In the group of healthy blood donors, 1.9% (5 of 257) had detectable HGV viremia and 15.9% (41 of 257) showed antibody response to HGV. In the collective of patients with suspected non-A-E hepatitis, results from 1.9% of patients (3 of 154) were positive by HGV PCR, and 15.6% of patients (24 of 154) showed seropositivity against the recombinant HGV proteins. In six groups of patients (n = 298) with different risk factors, the prevalence of both HGV viremia (V) and serological reactivity (SR) was higher compared with that of the nonrisk group: V, 6.80%-35.2%; serological reactivity (SR), 25.4%-52.9%. The following conclusions can be derived from our data. HGV infection is widespread in the general population. The prevalence of antibodies against HGV or detectable HGV viremia is higher in patients with risk factors for parenteral viral transmission than in those without risk factors. The majority of HGV infections (70.2%) is self-limiting and not persistent in our collective of patients. We found no correlation between HGV viremia and clinical or biochemical signs of hepatitis in individuals without risk factors for acquiring parenterally transmitted agents.

Patients with psoriasis have elevated levels of serum eosinophil cationic protein and increased numbers of EG2 positive eosinophils in the duodenal stroma

The occurrence of EG2-positive (EG2+) eosinophils and IgE in biopsy specimens of duodenal mucosa and skin from 39 psoriasis patients was studied, with emphasis on the relation to serum eosinophil cationic protein (ECP), serum IgE and the presence or absence of serum IgA and IgG antigliadin antibodies. Psoriasis patients had significantly elevated serum levels of ECP even after exclusion of five of 37 sera which were Phadiatop positive. The elevated serum ECP was not associated with the presence of IgA or IgG antibodies to gliadin. After exclusion of Phadiatop positive sera the serum IgE values did not differ from those of a group of healthy blood donors. Patients with psoriasis had a pronounced increase of EG2+ cells in their duodenal stroma. Patients without antibodies to gliadin tended to have even more EG2+ cells than those with such antibodies and those with increased duodenal intraepithelial lymphocytes. IgE+ cells were present in most duodenal specimens, and in some specimens there were > 100 IgE+ cells/section. The number of EG2+ cells was increased in lesional skin and, in some patients, also in non-involved skin, but there was a more pronounced increase in EG2 reactivity in the duodenal than in the skin specimens. IgE reactivity was increased both in non-involved and involved skin and was significantly related to the number of IgE-positive cells in the duodenal stroma. The results of this study indicate that the gastrointestinal tract and the eosinophil granulocyte might be involved in psoriasis in a hitherto unknown way.

Angiotensin converting enzyme gene deletion allele is independently and strongly associated with coronary atherosclerosis and myocardial infarction.

To investigate the association of the three angiotensin converting enzyme (ACE) genotypes, DD, ID, and II, with the occurrence or absence of coronary atherosclerosis and with myocardial infarction and hypertension. Cohort analysis study. North-Italy reference centre. 388 white Italian patients (281 males; mean age 60.7 (SD 12.5) years) with proven coronary atherosclerosis (n = 255) or with angiographically normal coronary arteries (n = 133). A further group of 290 healthy blood donors was tested for allele frequency comparison. ACE/ID polymorphism was analysed with polymerase chain reaction on DNA from white blood cells. Coronary atherosclerosis, myocardial infarction, hypertension. The D and I allele frequencies were respectively 0.63 and 0.37 in the overall healthy blood donor group and 0.66 and 0.34 in the overall study group. In the latter, univariate analysis showed (1) that coronary atherosclerosis (255 patients) was associated with the deletion allele, with an odds ratio (OR) of 5.78 for DD/II, P < 0.001, and 2.39 for ID/II, P = 0.006; and (2) that myocardial infarction (154 patients) was associated with the DD genotype (OR DD/II = 2.56, P = 0.007), but not with the ID genotype (OR DD/II = 1.96, P = 0.056). Finally, hypertension proved to be unrelated with the ACE genotype. The distribution between the three genotypes of known risk factors for coronary artery disease was similar. Logistic regression modelling, performed to test the association of the selected risk factors simultaneously with coronary atherosclerosis and myocardial infarction, showed that the deletion allele (whether DD or ID) was the strongest risk factor for atherosclerosis, and that the D allele was significantly associated with the risk of infarction (although to a lesser extent than with coronary atherosclerosis). ACE deletion polymorphism is strongly and independently associated with coronary atherosclerosis and, to a lesser extent, with myocardial infarction. As such, the results are analogous to what has already been reported in French white, Japanese, and Welsh coronary patients.

T lymphocyte subset abnormalities in peripheral blood from patients with the Guillain-Barré syndrome

T lymphocytes are probably of pathogenic importance in many autoimmune diseases. Recently, deviations of circulating T-helper (CD4 +) subpopulations have been noticed. Blood samples from 12 patients with Guillain-Barré syndrome (GBS) were studied with flow cytometry during their disease to define circulating T cell populations. The proportion of T-helper cells (CD4 +) was decreased (mean value 41±15%, P = 0.01) and the proportion of T cytotoxic/suppressor cells (CD8 +) was increased (35±18%, P = 0.0006) as compared to the control group of healthy blood donors (47±8% and 26±7% respectively). The CD4 + population is divided into the helper/inducer (CD4 + CD29 +) and suppressor/inducer (CD4 + CD45RA +) subsets. which normally are equally distributed (mean values in our control group were 45±15% and 44±15%, respectively). In patients with GBS, the helper/inducer (CD4 + CD29 +) subset was increased (54±10%, P = 0.05) and the suppressor/inducer (CD4 + CD45RA +) subset was decreased (31±9, P = 0.005) compared to the controls. The proportion of activated HLA-DR-expressing T cells was increased (7±8%, P = 0.005) as compared to control (3±3%). The total proportions of T cells (CD2 +), B cells (CD19 +) and natural killer (NK) cells (CD56 +) were similar in pateints and controls. The CD4 + and CD8 + populations, as well as the activated HLA-DR + T cells, normalized during the disease course. The derivations within the CD4 + population also tended to normalize, but even at follow up after 6–33 (mean 23) months, some abnormalities remained. In conclusion, we confirm previous reports of T cell activation in peripheral blood from patients with GBS. A new finding is the derivation of T helper subpopulations with an increased helper/inducer (CD4 + CD29 +) subset and a decreased suppressor/inducer (CD4 + CD45RA +) subset, which indicates a possible autoimmune character of GBS.

Hepatitis B virus DNA in serum and liver is commonly found in Chinese patients with chronic liver disease despite the presence of antibodies to HBsAg.

Sera from 410 patients from the Wuhan area in the central part of China with the diagnosis of chronic liver disease were analyzed for markers of hepatitis B, C and D virus infections. All sera, plus liver biopsy specimens from 188 of the patients, were also tested for hepatitis B virus DNA by polymerase chain reaction. Sixty-eight percent were HBsAg positive in serum, whereas 29% showed markers of past hepatitis B virus infection. Hepatitis B virus DNA was detected in all HBeAg-positive sera but also in 58% of patients with HBe antibody. In the liver specimens of the corresponding patient groups, 97% and 78%, respectively, were hepatitis B virus DNA positive. However, more noteworthy was that of the HBsAg-negative/HBs-antibody positive patients 30% had detectable hepatitis B virus DNA in serum and 32% had hepatitis B virus DNA in liver tissue, whereas in a control group of healthy blood donors, of which 90% had HBs antibody, none was hepatitis B virus DNA positive. Our results demonstrate that among patients with chronic liver disease, infections with hepatitis B virus or hepatitis B virus-related virus(es) may frequently occur without being revealed by conventional serological methods. Hepatitis C and D viruses seem to be of only minor importance in the pathogenesis of chronic liver disease in this part of China.

Oligoclonal immunoglobulins in HIV infection.

We tested 150 patients infected with human immunodeficiency virus (HIV) for the presence of oligoclonal bands in serum, prompted by reports that these abnormal proteins may have prognostic significance. Sixty HIV-negative individuals from "at-risk" groups were tested along with 80 HIV-negative, healthy blood donors for the presence of these bands. All sera were tested by isoelectric focusing, because it is more sensitive for this purpose than more-conventional electrophoretic techniques. In the HIV-positive group, 61% of the sera had oligoclonal bands; in the HIV-negative "at-risk" group, 36% had bands. No bands were detectable in sera from the healthy blood-donor group. Some patients were also followed for differing periods throughout their infection, and changes in their oligoclonal banding patterns could not be correlated with disease progression. The fact that oligoclonal bands were found to be present without HIV infection in a substantial number of individuals from within the "at-risk" groups leads us to conclude that the presence of oligoclonal bands in HIV infection is of limited prognostic significance.

The role of serology in the diagnosis of Campylobacter pylori infection.

Circulating antibodies to Campylobacter pylori in patients with campylobacter-associated gastritis are sufficiently specific to allow serodiagnosis of this condition. This is possible by various techniques, the most convenient being enzyme-linked immunosorbent assay. Applications of serodiagnosis are in two areas--in clinical practice, where proper evaluation is still required, and in epidemiology. Here serodiagnosis shows the prevalence of C. pylori in the general population and in specific population groups. A study of C. pylori and dyspeptic symptoms in a group of healthy blood donors showed a significant association between C. pylori and history of peptic ulceration. However in most donors the gastritis was clinically silent.

Fluidity of intact erythrocyte membranes. Correction for fluorescence energy transfer from diphenylhexatriene to hemoglobin

Membranes of intact erythrocyte were labeled by the fluorescent probe 1,6-diphenyl-1,3,5-hexatriene (DPH) using an improved labeling procedure described previously (Plášek J. and Jarolím, P. (1987) Gen. Physiol. Biophys. 6, 425–437). The relationship between the steady-state DPH fluorescence anistoropy r and the mean corpuscular hemoglobin concentration (MCHC) was studied. Fluorescence anisotropy increased with increasing MCHC. A linear dependence of r = 0.0026 ( MCHC) + 0.113 was obtained which enabled us to measure the fluidity of intact red cell membranes. Without this correction for fluorescence quenching by hemoglobin, incorrect conclusions about membrane fluidity could be made. This fact is demonstrated in a group of pyruvate kinase deficient patients compared with a group of healthy blood donors.

Enzyme-linked immunosorbent assay for immunoglobulin G subclass antibodies specific for enterobacterial Re core glycolipid in healthy individuals and in patients infected by gram-negative bacteria.

An enzyme-linked immunosorbent assay was developed to study the subclass distribution of immunoglobulin G (IgG) specific to the core glycolipid (CGL) of the Re mutant of Salmonella minnesota R595 in serum samples from individuals with an IgG response toward these antigens. In a group of healthy blood donors, we detected predominantly the IgG2 and IgG1 subclasses. In a group of patients in an intensive care unit who developed infectious complications due to gram-negative bacteria, the anti-CGL IgG activity was due mainly to the IgG2 and IgG3 subclasses. In all serum samples found to be IgG positive, the assay for anti-CGL IgG2 was positive. This subclass was revealed to play a predominant role in patients displaying a seroconversion or a significant rise in their antibody response toward CGL. IgG4 was found or appeared only in patients with confirmed bacteremia. In addition, we observed a drop in anti-CGL IgG2 before the death of patients undergoing a septic shock or an irreversible organ failure, suggesting that the anti-CGL IgG2 activity could be used as a marker of the evolution of the illness in this group of patients.

Bordetella pertussis infection: a cause of persistent cough in adults.

An enzyme-linked immunosorbent assay (ELISA) for Bordetella pertussis-specific immunoglobulin (Ig)A antibody in serum was used to demonstrate B. pertussis infection. The upper limit of normal for the assay (mean + 3 SD) was established by testing sera that had been collected from a group of healthy blood donors. All 13 patients with clinical whooping cough from whom B. pertussis was isolated and 25.7% of 218 adults, who were aged 18-81 years, who were referred to a consultant physician for the investigation of a persistent cough, had elevated levels of IgA to B. pertussis. The study confirms the B. pertussis IgA ELISA as a sensitive test for the diagnosis of B. pertussis infections and that these infections cause respiratory illness, in particular, persistent cough in adults.

Depression of cellular immunity after open-heart surgery

Using a whole blood test system we investigated cell-mediated immunity in 45 patients undergoing open-heart surgery. The peripheral blood lymphocytes were stimulated with the nonspecific mitogens phytohemagglutinin, concanavalin A and pokeweed mitogen, one bacterial recall antigen, tuberculin PPD, and one viral antigen, herpes simplex virus. The patients were tested three times: pre-operatively, and seven days and 2 wks post-operatively. There were no significant differences between a control group of healthy blood donors and the patient group tested pre-operatively. However, seven days after operation we observed a clear decrease of the reactions to all stimulants. Two weeks after operation there was an increase of lymphocyte proliferation data in regard to tuberculin PPD and herpes simplex virus. Concerning the nonspecific mitogens PHA and PWM, there was only a tendency of an increase. We believe that two weeks after operation is too short an interval to notice a full normalization of the cellular immune functions. In comparison with the conventional system of isolated lymphocytes, the whole blood technique is advantageous in investigating cell-mediated immunity, particularly if the patient groups are large.

Histamine levels in stored human blood.

The histamine content in plasma samples obtained from a group of healthy blood donors, from blood stored in citrate-phosphate-dextrose supplemented with adenine (CPDA) packs for up 28 days, and from the side arm of a transfusion line was measured by radio-enzymatic assay. Healthy donors had a mean plasma histamine content of 0.79 ng per ml. Blood stored in CPDA initially showed a similar histamine level (0.69 ng/ml on day 3 of storage), but there was a progressive rise with time, and at 28 days, the level was 20.5 ng per ml. The increase in histamine is best described by a positive exponential and may be explained by a process whereby the plasma histamine level increases the degree of histamine release from blood cells. The histamine levels in the blood infused into patients tended to be higher than those found in the stored units of the same age, if these packs were less than 7 days old. This may have been caused by the unit becoming warmer during transfusion. We speculate that the histamine levels in the older units of stored blood were high enough to cause or augment transfusion reactions and that the storage age of blood may have a bearing on the incidence of transfusion reactions.

Malignant hypertension and HLA antigens.

Thirty-two patients with malignant hypertension and terminal uremia and a group of 1263 healthy blood donors were studied regarding the incidence of different HLA antigens. HLA-Bw35; Cw4 antigens were found to be significantly more frequent in the group of patients with malignant hypertension than in the group of healthy individuals. The frequency of HLA-Bw35 in a group of 60 non-uremic patients with biopsy-proven glomerulonephritis and without malignant hypertension was also studied and found equal to the group of healthy blood donors. There was no overrepresentation of IgA nephritis among the HLA-Bw35 positive patients with glomerulonephritis, but advanced vascular lesions were more common among these than among patients with other HLA antigens.