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Biomedical subjects

S Pollack

Publications and source records attributed to S Pollack.

At least 163 records · Page 9Linked to original sources
PubMed1989

High dose intravenous gammaglobulins in autoimmune disorders: mode of action and therapeutic uses.

Gammaglobulins administered intramuscularly have been used for more than 40 years to treat antibody deficiency states. In the last decade intravenous preparations were developed. They do not aggregate and contain IgG molecules with intact recognition and effector functions. These compounds are safe and only minor side effects were reported even when high doses were given. While studying their effect when given in high doses to hypogammaglobulinemic patients, an accidental finding was observed regarding their beneficial effect in idiopathic thrombocytopenic purpura (ITP). This observation led to many studies looking at the effect of high dose gammaglobulin in several other autoimmune diseases. While the effect in acute ITP is well established, there are encouraging reports in respect to the effect of intravenous gammaglobulin in many other disorders, but no final conclusion can be drawn due to the small numbers of cases studied. The mechanism by which intravenous gammaglobulin exerts its function is still unclear. It may work through the Fc receptor in the reticuloendothelial system, as an immunoregulator agent or interact in the idiotype-antiidiotype network. Intravenous gammaglobulin seems to be an important therapeutic tool in a large number of autoimmune disorders of various etiologies.

Autoantibodies↗
PubMed1989

Antigen stimulated IgM secretion by circulating B lymphocytes in patients with benign and malignant IgG gammopathy. Relationship to stage of disease.

In the present investigation antigen-driven (sheep red blood cells, SRBC) IgM antibody secretion by B lymphocytes of 22 MM (IgG kappa) patients and 15 patients with IgG kappa monoclonal gammopathy of undetermined significance (MGUS) was studied and compared to that of 20 age-matched healthy controls and five patients with Waldenstrum (IgM) macroglobulinemia (WM). Antibody production by cultured lymphocytes of MM and WM patients was significantly decreased, whereas in MGUS patients it fell within normal limits. We could divide MM patients into three subsets: those who secrete normal amounts of IgM in vitro (patients with the stable type); a second subset of patients whose B lymphocytes secreted low amounts of IgM (MM patients in remission); and a third subset of patients who manifested an intrinsic block of B cell differentiation into IgM-secreting cells (patients with the progressive stage). Sephadex G-10 adherent suppressor cells had no effect on antibody production in the stable and progressive types of disease, whereas in the remission stage they markedly inhibited IgM secretion. Measurement of antigen-driven IgM antibody secretion might help in the differentiation of MGUS and stable (smouldering) MM from frank (progressive) MM at diagnosis. It may also provide a tool for monitoring progression of disease and response to therapy.

Aged↗
PubMed1989

Humoral and cellular immune dysfunction in a patient with Bloom's syndrome and recurrent infections.

Immunological evaluation of a patient with Bloom's syndrome (BS) who suffered from recurrent bacterial and fungal infections, revealed low serum levels of IgG and high levels of IgM accompanied by an elevated proportion of surface membrane IgM positive B-lymphocytes and a decreased proportion of IgG positive B-cells. In vitro IgG secretion was also reduced whereas IgM production was normal. Although proportions of T-cell subsets were normal and proliferative responses to T-cell mitogens were adequate, a defective regulatory T-cell function for the generation of IgG was observed. Natural killer (NK) cell activity against K562 tumor cells was also decreased in this patient. The findings in this patient may suggest a maturation arrest of lymphocytes at an early developmental stage, and this may explain in part the increased susceptibility to infections.

Adolescent↗
PubMed1989

Interleukin-1 and interleukin-2 production by peripheral blood mononuclear cells of patients with rheumatoid arthritis.

Contradictory results have been reported concerning the secretion of interleukin-1 (IL-1) and interleukin-2 (IL-2) by mononuclear cells of rheumatoid arthritis (RA) patients. In the present study, peripheral blood mononuclear cells from 18 RA patients were stimulated in vitro to produce IL-1 and IL-2 and compared with monocytes of age-matched healthy control subjects. Endotoxin-stimulated monocytes of RA patients produced normal amounts of IL-1 compared with healthy controls (P = 0.5), whereas T-lymphocytes from the same patients produced decreased amounts of IL-2 compared with control T-lymphocytes (P less than 0.01). There was no difference in IL-1 or IL-2 production by mononuclear cells from patients with active or inactive disease. These findings could not be explained by concurrent therapy, and support the notion that defective immunoregulatory T-cell functions are involved in the pathogenesis of RA.

Adult↗
PubMed1989

Immunological investigations in 2 families with progressive diaphyseal dysplasia.

Immunological studies were done in members of 2 families with progressive diaphyseal dysplasia. In one family 10 patients and 5 healthy consanguineous relatives were studied, and in the second family one patient and 4 healthy consanguineous relatives were investigated. Evaluation included serum immunoglobulin and complement levels, peripheral blood mononuclear cell subpopulations and lymphocyte stimulation by mitogens. Immunoglobulin and complement levels were normal. All patients had markedly elevated proportions of OKM1 positive mononuclear cells and some of the healthy consanguineous relatives also exhibited the same abnormality. Proliferative responses of lymphocytes to phytomitogens were generally normal. This abnormality of mononuclear cell subset seems to serve as a marker of the disease and may reflect immune mechanisms involved in this disorder.

Adolescent↗
PubMed1988

P. falciparum infected erythrocytes are capable of endocytosis.

P. falciparum, an intraerythrocytic parasite, obtains nourishment primarily through phagocytosis of the host cytosol but also through the incorporation of extracellular small molecules which enter through the parasitized red cell's membrane via pores. Normal mature erythrocytes are incapable of endocytosis. Several lines of evidence suggest that extracellular large molecules may be taken up when the mature red cell is parasitized by P. falciparum, but direct evidence has been lacking. We now report the use of ferritin, an electron dense protein, to demonstrate endocytosis in P. falciparum infected red cells. Parasitized red cells incubated with ferritin internalize that macromolecule as demonstrated by electron microscopy. While normal red cells incubated with ferritin took up none of the tracer molecule, parasitized red cells internalized substantial amounts. In addition both ferritin and apoferritin inhibited the growth of P. falciparum in a dose dependent fashion, again indicating endocytosis of a macromolecule. These data indicate that P. falciparum can somehow stimulate the mature erythrocyte to engage in endocytosis. We also note that both infected and non-infected red cells in a culture in which P. falciparum is growing become abnormally sticky for ferritin. Moreover, parasitized red cells bind I125-transferrin while non-parasitized erythrocytes do not. These observations suggest that a soluble parasite product alters the red cell membrane in a non-global manner, causing selective effects in relation to different proteins.

Animals↗
PubMed1988

Pharmacologic studies of tardive dyskinesia.

Based on the results of two preliminary studies, we concluded that late-developing persistent drug-induced movement disorders are pharmacologically heterogeneous, and this heterogeneity is seen between individual patients (and groups of patients) as well as within body areas of individual patients; dystonic pathology has a distinct and more consistent response to pharmacologic stimulation than does nondystonic tardive dyskinesia (TD); and, although disturbances in dopamine and acetylcholine appear to be involved in these disorders, they do not in all cases exist in functionally opposite relationships. The observed pharmacologic heterogeneity in TD response reflects the limitations of the dopamine/acetylcholine model of TD, which oversimplifies the neuroanatomy of the basal ganglia and the pathophysiology of TD. The chemical and anatomical complexity of this region suggests that other neurotransmitter systems and neuronal circuits within and extending from the basal ganglia may be disturbed in the pathogenesis of TD.

Adult↗
PubMed1988

Inability to detect transferrin receptors on P. falciparum parasitized red cells.

The mechanism by which P. falciparum takes up iron from transferrin has been explored. Binding of 125I labelled transferrin to parasitized red cells at 37 degrees C is two-fold greater than to control cells; at 0 degrees C there is no significant difference. The binding is non-specific as judged from the following: it is not saturable; it is not limited to transferrin as lactoferrin (which has iron binding domains) and bovine serum albumin (which does not) also bind in excess to parasitized red cells. A transferrin receptor complex could not be demonstrated when parasitized red cells, to which 125I transferrin was bound, were solubilized in Triton X100. Previous observation showed that uptake of transferrin iron by parasitized red cells is not accompanied by equimolar uptake of transferrin protein. We therefore suggest that nonspecifically bound transferrin is endocytosed, that the protein is degraded and the iron selectively retained.

Animals↗
PubMed1988

Immunological studies of pancytopenia in visceral leishmaniasis.

We report three cases of combined anemia, neutropenia and thrombocytopenia in patients with visceral leishmaniasis (kala-azar). Using immunofluorescence techniques and the common antiglobulin (Coombs') test, we showed membrane-associated antiplatelet, antineutrophil and antierythrocytic IgG antibodies in all three cases. Treatment with sodium stibogluconate raised the patients' platelet, neutrophil and erythrocyte count. At that time no antibodies were detected on peripheral blood cells. Immunological studies performed on these patients did not show marked abnormalities except for reduced T-helper cells and elevated OKM1-positive cells, which normalized after recovery. As bone marrow suppression was not found, it is suggested that pancytopenia resulted from rapid destruction of antibody-coated blood cells. Whether these antibodies are specific is not clear.

Adolescent↗
PubMed1988

Hypersensitivity vasculitis induced by terbutaline sulfate.

Hypersensitivity vasculitis developed in a patient six days after therapy with terbutaline sulfate was initiated. The casual association between the drug and hypersensitivity vasculitis is based on the temporal relationship, a positive lymphocyte transformation test with terbutaline sulfate, and exclusion of other causes. This is, to the best of our knowledge, the first report of a leukocytoclastic vasculitic reaction to terbutaline sulfate.

Aged↗
PubMed1988

Pharmacologic characterization of tardive dyskinesia.

Tardive dyskinesia (TD) occurs in approximately 20% of patients treated chronically with antipsychotic drugs and constitutes a major public health problem. The cause of this disorder remains unknown, and no effective treatment has yet been found. The major etiologic theory (dopamine [DA] supersensitivity hypothesis) suggests that TD is the pharmacologic opposite of Parkinson's disease and implies that all patients with TD should respond uniformly to specific pharmacologic agents. Clinical research, however, has not borne this out. To evaluate pharmacologic response in TD syndromes, 15 patients underwent single dose acute administration of four different drugs: a DA agonist (bromocriptine 5 mg orally), a DA antagonist (haloperidol 5 mg intravenously), a cholinergic agonist (physostigmine 2 mg intravenously) and a cholinergic antagonist (benztropine 4 mg intravenously), individually in separate procedures at weekly intervals for four consecutive weeks in randomized order and under controlled double-blind conditions. Patients were evaluated for their clinical and endocrine responses. Pre- and post-drug administration TD exams were blindly rated. Results were not consistent with the DA supersensitivity theory; instead they demonstrated marked inter- and intrasubject variability in pharmacologic responses. Greatest uniformity in response was found among the tardive dystonic subjects, although this also was not consistent with a DA supersensitivity hypothesis. TD appears to be a pharmacologically heterogeneous condition, which may reflect the neurochemical complexity of the basal ganglia.

Adult↗