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J Koistinen

Publications and source records attributed to J Koistinen.

At least 37 records · Page 2Linked to original sources
PubMed1992

Frequency of low erythrocyte porphobilinogen deaminase activity in Finland.

The frequency of low erythrocyte porphobilinogen deaminase (PBGD) activity was investigated in 2234 blood donors and in 30 patients with acute intermittent porphyria. The mean enzyme activities (+/- SD) were 3.38 +/- 0.58 U and 1.82 +/- 0.41 U, respectively. Eighteen blood donors without any history of symptoms of porphyria or haematological disease had low PBGD activity (less than 2.20 U), and they were studied further. All of them also had subnormal concentrations of the erythrocyte enzyme protein, as determined by an immunological method. Lymphocyte PBGD activity was within the normal range, but this parameter does exhibit a wide overlap between normal and porphyric values. Urinary excretion of porphobilinogen was moderately increased in two of the blood donors. In four of the 18 families of the blood donors with low PBGD activity several first-degree relatives had low erythrocyte enzyme activity, consistent with a dominant mode of inheritance. The 5-aminolaevulinic acid loading-test was normal in the blood donors with familial occurrence of low erythrocyte PBGD. It is concluded that inherited defects in erythrocyte PBGD occurred among Finnish blood donors with a frequency of about 1 in 500. The defects may be identical with those in acute intermittent porphyria (AIP), but other mechanisms are also possible, e.g. a mutation in the erythroid-specific part of the PBGD gene.

Adult↗
PubMed1991

Determination of anti-IgA antibodies with a flow cytometer-based microbead immunoassay (MIA).

A flow cytometer-based microbead immunoassay (MIA) was employed to detect anti-IgA antibodies in patients with IgA deficiency. 3 microns latex particles were coated with purified IgA and serum anti-IgA antibodies of the IgG class were detected with FITC-conjugated anti-human IgG. Antibodies against three different IgA preparations were tested from 22 patients samples as well as 20 controls and compared with a conventional enzyme-linked immunosorbent assay (ELISA) and a passive hemagglutination assay (HA). There was a very close correlation between the results obtained with the MIA and the ELISA assay and between MIA and the HA. Because of the low intra-assay variation and good linearity of the assay, the analysis of one single serum dilution was sufficient to determine the anti-IgA level of a patient and no titration series was required. We conclude that MIA is a satisfactory alternative method for routine anti-IgA antibody determinations. For laboratories already equipped with a flow cytometer the assay is cost effective.

Agammaglobulinemia↗
PubMed1989

Lack of evidence of HTLV-I antibodies in the Finnish population.

5,287 serum samples from 2 different sources in Finland, people possibly at risk and healthy blood donors, were tested for the presence of HTLV-I antibodies. No positive cases were found. The result suggests that this virus is not endemic in Finland. 10 cases gave repeatedly a low positive value in the enzyme immune assay (EIA) test but were confirmed negative with other tests that included western blot, passive agglutination and immunofluorescence. Four of these samples originated from healthy blood donors, 6 from other categories. Several of them showed restricted reactivity in western blots. Five HIV-positive sera, discovered during the study from people with possible risk factors, were also tested for HTLV-I but showed no reactivity.

Blood Donors↗
PubMed1989

IgG and IgA enhance the chrysotile-induced production of reactive oxygen metabolites by human polymorphonuclear leucocytes.

Chrysotile asbestos fibres induce a rapid generation of reactive oxygen metabolites by human polymorphonuclear leucocytes (PMNL) in vitro. This effect was markedly enhanced by the presence of 10-200 micrograms/ml of human gammaglobulin, purified polyclonal IgG, and monoclonal IgG and IgA myeloma proteins. Purified monoclonal IgD, IgM, kappa light chain proteins, and secretory IgA inhibited this chrysotile-induced response. No enhancing effect of IgG was observed when quartz dust or opsonized zymosan were used as stimulators of PMNL metabolism. The enhancing effect of IgG was shown to depend on opsonization of the asbestos fibre. We suggest that the IgG and IgA potentiating effect on the asbestos fibre-induced production of tissue-damaging reactive oxygen metabolites by inflammatory cells is dependent on a particle-specific binding of immunoglobulin to the fibre surface, with subsequent Fc receptor-mediated effects on cells. Such an interaction between certain immunoglobulins and asbestos may explain a number of in vivo phenomena in which immunological responses (hypergammaglobulinemia, circulating immune complexes, etc.) have been shown to relate to the progression of pulmonary asbestosis. The differences between various immunoglobulin classes and monoclonal immunoglobulins could represent an individual inflammation-modulating mechanism in the development of acute or chronic pulmonary asbestosis.

Asbestos↗
PubMed1988

Serum IgA deficiency and anti-IgA antibodies in pernicious anemia.

Three pernicious anemia (PA) patients with selective IgA deficiency and anti-IgA antibodies in their sera were followed for over 3 years. After instituting therapy with cyanocobalamin there was a slight increase in the anti-IgA antibodies. After 1 year the titers of anti-IgA antibodies in the sera of these patients declined significantly as compared to the values before treatment (P less than 0.02), and after 2 years one patient had no measurable anti-IgA antibodies, yet no IgA appeared in the serum of any of the three. Further, in a medium with no anti-IgA the lymphocytes of these patients were not capable of producing IgA in vitro. Thus, the reason for the IgA deficiency in PA appears to be linked to the function of B cells rather than to anti-IgA antibodies.

Adolescent↗
PubMed1987

Distribution of blood groups in the East African Somali population.

The results of a population survey on blood group distribution in Somalia, East Africa, are presented. Over 1,000 subjects were tested for most blood groups included in the survey. The sampling covered the whole country and was well in accordance with the population density as estimated by the recorded birth places of the subjects. Altogether, 46 blood group antigens were tested, partly common antigens within 11 of the major blood group systems, but also infrequent and very frequent antigens, some not tested before in Africa, were included. The results were compared with the available data for other related peoples and for populations from the same geographical area. The standard genetic distances were also applied in the comparison. The results suggest that only a minor component in the genetic constitution of the Somali population can be ascribed to Caucasian admixture. They are markedly in contrast with some earlier findings. During the survey we observed a previously unknown Rh gene complex occurring with a polymorphic frequency in Somalis.

Adult↗
PubMed1986

C-reactive protein in population samples.

The significance of C-reactive protein (CRP) was studied in three different sets of specimens. Raised levels (greater than 10 mg/l) were detected in 2.0% of 380 healthy blood donors from whom two blood specimens, taken at an interval of half a year, were tested. Except for two cases, only one of the two specimens was positive. Raised levels were found three times as frequently (in 6.6%) in a random middle-aged population sample consisting of 531 subjects. More than 40% of the raised levels could be connected to acute respiratory infections, and about 20% to smoking. Five of the 35 subjects (14%) in the population sample with elevated CRP had rheumatoid arthritis. The third set of sera comprised pre-illness specimens from 22 subjects who developed rheumatoid arthritis a few months to five years later. Although it had previously been proved that the majority of these sera contained rheumatoid factors, the CRP concentration was increased in one specimen only.

Acute Disease↗
PubMed1986

Suppressor factors generated from human mononuclear cells by means of purified myeloma proteins.

Peripheral blood mononuclear cells (PBMC) from normal human donors were cultured in Marbrook flasks in the presence of purified IgG or IgA myeloma proteins. The culture supernatants were tested for their ability to suppress pokeweed mitogen (PWM)- or Epstein-Barr virus (EBV)-driven Ig synthesis by normal PBMC. Two supernatants from PBMC cultured with IgG and one from PBMC cultured with IgA were tested and suppressed PWM-driven Ig synthesis as measured by a reverse haemolytic plaque assay and by quantitation of the Ig secreted into the culture medium of the PWM-driven cells. This suppression was not restricted to the Ig isotype of the 'inducing' myeloma protein, but was extended to IgG, IgA, and IgM. The suppressive effect could be absorbed out with human IgG.

Antibody Formation↗
PubMed1985

A necropsy study of Pi phenotypes, emphysema, and smoking.

Pi phenotypes, determined post mortem by isoelectric focusing and immunofixation, emphysema, assessed from inflation fixed specimens and smoking history were correlated in 186 hospital necropsies. It was possible to determine Pi phenotype in 98.4% of the specimens. Phenotype M occurred in 87.5%, MZ in a 8.1%, MS in 2.1% and FM in 0.5%. An expected association was found between smoking and emphysema but not between the Pi phenotypes and emphysema. Thus, while smoking is a major aetiological factor, the Pi MZ heterozygous state does not seem to predispose to structural emphysema. However, the small number of cases did not allow an estimation of the risk of smoking in Pi MZ heterozygous persons compared to those with the normal Pi phenotype.

Adult↗
PubMed1985

Cross-reactive idiotypes in immunoglobulin A-deficient sera.

Mice of inbred strains immunized with simple antigens can produce antibodies that share similar V regions, which result in serologic similarities called cross-reactive idiotypes (CRI). In this study, we considered the possibility that IgA-deficient humans, who are continuously immunized via the intestinal tract by dietary protein, might also produce antibodies sharing CRI. For this, anti-casein antibodies were isolated from the blood of 16 adult IgA-deficient donors (4 Finns and 12 North Americans) and an autologous anti-anti-casein from the blood of one of the Finnish donors. In addition, a heterologous anti-anti-casein was raised to the casein-anti-casein immune complexes of this donor. Comparing the activities of the two anti-idiotypes, it was found that both bind anti-casein in the region of the antigen binding site, but that each binds additional determinants not located within this region, with the heterologous reagent having more affinity for these latter determinants than the autologous anti-idiotype. Using both reagents in enzyme-linked immunosorbent assay inhibition assays, extensive cross-reactivities between anti-caseins were demonstrated. Using the autologous anti-idiotype, 5 of 16 anti-caseins were found to share CRI, and with the heterologous reagent 12 of 16 shared CRI. In both assays, the anti-caseins of Finnish donors displayed more cross-reactivity than those derived from Northern American donors. These studies show that specific, commonly shared CRI can be identified in this human system in which antibodies are raised as a result of natural immunization across the gastrointestinal mucosa.

Adult↗
PubMed1984

Increased frequency of HLA-A1 and -B8 in association with total lack, but not with deficiency of serum IgA.

HLA-A, B, C typing was performed on 37 unrelated healthy blood donors with selective deficiency (less than 0.05 g/l) or total lack (less than 0.00002 g/l) of serum IgA. A significant increase in HLA-B8 and A1 antigen frequency was found in the 15 individuals with lack of serum IgA. This was not observed among those 22, who had only deficiency of serum IgA (0.00002-0.05 g/l). The HLA antigen frequencies were compared to those of 900 randomly selected healthy blood donors. Increased frequency of HLA-A1 and B8 in association with total lack of serum IgA, but not with deficiency has not been demonstrated before. On the basis of this result it seems conceivable that lack of serum IgA may be caused by a different, perhaps genetically determined, mechanism than IgA deficiency.

Blood Donors↗
PubMed1981

Serum alpha-1-antitrypsin in patients with juvenile periodontitis.

alpha-1-Antitrypsin phenotypes and serum levels were determined in 19 patients with juvenile periodontitis in order to test whether reduced periodontal resistance in this disease is caused by decreased serum protease inhibitory capacity resulting from deficient alpha-1-antitrypsin phenotypes. The phenotyping of the patients' sera was performed by thin-layer isoelectric focusing in polyacrylamide gel. The quantitation of alpha-1-antitrypsin was performed using the radial immunodiffusion technique. All 19 patients displayed the most common phenotype M. Twelve patients had the subclass M1M1, two the M1M2 and five and M1M3. The alpha-1-antitrypsin levels in the patients' sera were within normal limits. The results do not support the hypothesis that deficient production of alpha-1-antitrypsin is causally related to juvenile periodontitis.

Adolescent↗
PubMed1981

Pulmonary apical fibrocystic disease. A serologic study.

Common aetiopathogenic factors were sought in 12 patients with progressive pulmonary apical fibrocystic changes, active human-type tuberculosis excluded. HLA-typing did not reveal any clear-cut trends; only the three patients with ankylosing spondylitis or Reiter's disease were HLA-B27 positive. Six patients had HLA-Cw3, which exceeds the prevalence in referents, antibodies, as well as other tissue antibodies, were mainly negative so that autoimmune aetiology is not likely. Similarly, antimicrobial antibodies were found occasionally, while low-titred influenza antibodies were positive in all patients. Serum proteins, immunoglobulins, rheumatoid factor and C-reactive protein were suggestive of chronic inflammation, as were low positive titres of smooth muscle antibodies in nine patients. In spite of the uniform clinical picture and course of the disease, no uniform aetiopathogenic factors were found, but possible unidentified slow- and low-grade viral or fungal infection is discussed.

Adult↗