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At least 217 records · Page 12Linked to original sources
PubMed2006

A prospective study of the immediate and delayed adverse events following intravenous immunoglobulin infusions.

AIM: To document the incidence of immediate and delayed adverse events (AE) following intravenous immunoglobulin (IVIG) infusion in children. METHODS: Immediate and delayed adverse events were prospectively recorded for 345 infusions in 58 children receiving IVIG for immunodeficiency (n = 33) or immunomodulation (n = 25). For each infusion adverse events were documented during the infusion and by follow up interview 4-7 days later. RESULTS: Immediate adverse events occurred in 10.3% and delayed adverse events in 41.4% of children treated during the study period. Three and a half per cent of the infusions were associated with immediate AE and 20.9% with delayed adverse events. Headache was the most common delayed AE, occurring in 24.1% of patients and 12.8% of infusions. CONCLUSIONS: Delayed adverse events to IVIG infusions are common in children. They occur more frequently than immediate adverse events and are the cause of significant morbidity. Recognition of the high frequency of delayed adverse events is important in the care of children receiving IVIG therapy.

Adolescent↗
PubMedDate not supplied

[Directory of diagnostic tests in primary immunodeficiencies].

The clinical and immunological characteristics that suggest diverse forms of primary immunodeficiency are discussed. Data on the hospitals that perform immunological, molecular and genetic tests for the diagnosis of most of the primary immunodeficiencies in Spain are presented.

Algorithms↗
PubMed1977

Effect of thymic factor on human lymphoid cells of umbilical cord blood and of children with T cell deficiency.

We report on the in vitro effect of a thymic factor (TF) extracted from pig thymuses, on human lymphoid cells from umbilical cord blood and from peripheral blood of 8 T cell-deficient patients. E rosette formation was not affected by TF when tested on cells from peripheral blood of normal adults. With cells from umbilical cord blood of 13 healthy, full-therm newborn babies, the difference between the percent (mean) of ERFCs before (16.31 +/- 11.13) and after (28.85 +/- 17.10) incubation with TF was statistically significant (p less than 0.05). In most samples, TF transformed about 10-20% of the cells. In the T cell-deficient group the increase in ERFCs of the peripheral blood lymphocytes, though consistent, was variable in degree from case to case. Our data indicate that precursor cells in some individuals with T cell deficiency are very sensitive to TF. Patients with highly responsive precursors appear to be the best candidates for a therapeutic approach with TF when thymus transplant is not possible.

Child↗
PubMedDate not supplied

Evaluation of possible causes of delayed hypersensitivity impairment in cancer patients.

The separate roles of malnutrition, advanced age, and stage of tumor growth as causes of impairment of delayed hypersensitivity response (DHR) was studied in 111 patients with solid tumors and in 56 nonneoplastic control patients matched for age, anatomical site of disease, degree of illness, and nutritional status. Pretreatment DHR to recall antigens (tuberculin, Candida, streptokinase-streptodornase, trichophyton) and to dinitrochlorobenzene in cancer patients with 9% anergic, 43% hypoergic, and 48% normoergic; the distribution of DHR in controls was not significantly different. In cancer patients, the serum albumin level showed an inverse correlation with the stage of tumor (p less than 0.01) and a positive correlation with the DHR (p less than 0.001); the serum albumin level was also in the controls positively correlated with the DHR (p less than 0.01), indicating that malnutrition in neoplastic or benign disease may cause depression of DHR. In well-nourished controls, age was inversely correlated with DHR (p less than 0.05), showing that aging itself may be another relevant cause of depression of DHR. The results of this study indicate that DHR in patients with solid tumors is similar to the DHR of nonneoplastic patients if matched for age, sex, and nutritional status. DHR impairment in cancer patients appears to be caused mainly by aging and by malnutrition due to the advanced progression of cancer.

Adult↗
PubMed2001

Postgrafting administration of granulocyte colony-stimulating factor impairs functional immune recovery in recipients of human leukocyte antigen haplotype-mismatched hematopoietic transplants.

In human leukocyte antigen haplotype-mismatched transplantation, extensive T-cell depletion prevents graft-versus-host disease (GVHD) but delays immune recovery. Granulocyte colony-stimulating factor (G-CSF) is given to donors to mobilize stem cells and to recipients to ensure engraftment. Studies have shown that G-CSF promotes T-helper (Th)-2 immune deviation which, unlike Th1 responses, does not protect against intracellular pathogens and fungi. The effect of administration of G-CSF to recipients of mismatched hematopoietic transplants with respect to transplantation outcome and functional immune recovery was investigated. In 43 patients with acute leukemia who received G-CSF after transplantation, the engraftment rate was 95%. However, the patients had a long-lasting type 2 immune reactivity, ie, Th2-inducing dendritic cells not producing interleukin 12 (IL-12) and high frequencies of IL-4- and IL-10-producing CD4(+) cells not expressing the IL-12 receptor beta(2) chain. Similar immune reactivity patterns were observed on exposure of donor cells to G-CSF. Elimination of postgrafting administration of G-CSF in a subsequent series of 36 patients with acute leukemia, while not adversely affecting engraftment rate (93%), resulted in the anticipated appearance of IL-12-producing dendritic cells (1-3 months after transplantation versus > 12 months in transplant recipients given G-CSF), of CD4(+) cells of a mixed Th0/Th1 phenotype, and of antifungal T-cell reactivity in vitro. Moreover, CD4(+) cell counts increased in significantly less time. Finally, elimination of G-CSF-mediated immune suppression did not significantly increase the incidence of GVHD (< 15%). Thus, this study found that administration of G-CSF to recipients of T-cell-depleted hematopoietic transplants was associated with abnormal antigen-presenting cell functions and T-cell reactivity. Elimination of postgrafting administration of G-CSF prevented immune dysregulation and accelerated functional immune recovery.

Acute Disease↗
PubMed2001

VEGF as a mediator of tumor-associated immunodeficiency.

Decreased immune function in cancer patients is well-characterized (1), and tumor cells have developed a variety of mechanisms to avoid anti-tumor immune responses (2-8). One mechanism for inhibition of immune cell function by tumors is the production of soluble factors, such as IL- 10, TNF, TGF-beta, and Vascular Endothelial Growth Factor (VEGF). The effects of these factors appear to be twofold: To inhibit effector function and to impair the development of immune cells by acting on earlier stages of immunopoiesis. Immune suppression by tumors is accomplished by a variety of cellular and molecular mechanisms, and virtually all branches of the immune system can be affected. VEGF and its receptors have profound effects on the early development and differentiation of both vascular endothelial and hematopoetic progenitors (9). It induces proliferation of mature endothelial cells and is an important component in the formation of tumor neovasculature (10). VEGF is abundantly expressed by a large percentage of solid tumors and this over-expression is closely associated with a poor prognosis (11,12). Some of the earliest hematopoetic progenitors express receptors for VEGF (13), and we have demonstrated that VEGF causes a defect in the functional maturation of dendritic cells (DC) from progenitors. This developmental defect is associated with impaired activation of NF-kappaB (14-17). This review describes research demonstrating that VEGF is not only important for tumor vascularization, but is also a key factor produced by solid tumors to inhibit recognition and destruction of tumor cells by the immune system.

Antibodies, Monoclonal↗
PubMed2005

The product: All intravenous immunoglobulins are not equivalent.

The first intravenous formulation of intravenous immunoglobulin (IGIV) was introduced in the United States in the early 1980s. At that time, the only indication was for treatment of primary immunodeficiency. By the mid-1990s, IGIV was mainly used for indications approved by the United States Food and Drug Administration, but as new indications are found, use of IGIVs is increasing. In fact, today, IGIV is mostly used for off-label indications. The specific characteristics of individual IGIV products must be directly addressed in the manufacturing process, as clinical efficacy may be affected. In addition, the safety profile of the ideal IGIV should be maximized by ensuring inactivation of the widest spectrum of viruses and prions. Some IGIV products are more suitable than others for certain patients; the challenge is to understand the different characteristics among products and select the most appropriate IGIV product for each patient. Convenience factors must be considered, for both the health care provider and the patient, without jeopardizing the more important features of the IGIV, such as tolerability and safety.

Carbohydrates↗
PubMed2005

The patient: Emerging clinical applications of intravenous immunoglobulin.

Intravenous immunoglobulin (IGIV) originally was used as prophylactic treatment of infections in patients with primary immunodeficiency disease. Today, administration of IGIV, due in large part to its immunomodulatory activity, has expanded to include a number of other disorders. Available data suggest that the accepted indications for IGIV will continue to expand. As the number of clinical applications for this therapy grows, so will market opportunities; current preparations will be modified and improved and new products introduced. Intravenous immunoglobulin therapy has improved the lives of many patients with immune-related disorders. Future applications will ideally advance this paradigm further.

Autoimmune Diseases↗
PubMed2005

Immunomodulatory function of orally administered thymosin alpha1.

OBJECTIVE: To investigate the immunological function of a yeast expression system for thymosin alpha1 (Talpha1). METHODS: A constructed Talpha1 yeast expression system was used to investigate the immunological function of orally administered Talpha1. Dried yeast containing three different concentration of Talpha1 was fed to normal Balb/c mice and other Balb/c mice whose immunities were inhibited in advance by cyclophosphamide. Synthesized Talpha1 peptide was used as positive control and dried yeast with empty plasmid was used as negative control. CD4(+) and CD8(+) levels were detected by flow cytometry assay. TNF-alpha, IFN-gamma, IL-2, IL-6 and IL-10 levels were detected by liquid chip. RESULTS: In normal Balb/c mice or immune inhibition Balb/c mice, CD8(+) levels were significantly increased. Especially in immune inhibition Balb/c mice, CD8(+) levels in synthesized Talpha1 group (18.77%+/-4.72%), small dose group (13.48%+/-6.17%) and large dose group (22.74%+/-1.09%) were significantly higher than that in empty yeast control group (7.49%+/-2.14%). CONCLUSION: Orally administered Talpha1 has its certain immunomodulatory function.

Administration, Oral↗
PubMed1987

Evaluation of immunity.

Immunodeficiency disease is rapidly increasing in frequency. The AIDS epidemic, the increasing use of transplantation with immunosuppression, the aggressive immunotherapy, the persistent deficiencies after bone marrow transplantation--all contribute to the astronomically increasing numbers of patients with host defense failure. This review has presented my viewpoint as to the approaches which can be utilized by practitioners with varying focal points to provide diagnosis and maximize the potential for a cure today or at least to provide the beginnings of understanding from which will come the cures of tomorrow.

Antigens, Surface↗
PubMed1979

Plasma protein patterns in health and disease.

The complex nature of protein metabolism has made interpretation of serum protein data a difficult task. Interpretive efforts can be facilitated by use of protein profiles which consist of quantitative immunochemical data combined with qualitative electrophoretic patterns. These profiles can be designed to clarify physiological relationships and emphasize pathological conditions through pattern recognition. This review will present protein profiles observed in acute, subacute, and chronic inflammation: liver diseases, protein losing disorders, plasma cell dyscrasias, humoral immune deficiencies, autoimmune diseases, genetic deficiency states, and other disorders. The value of consultative interaction and the use of combined profiles in the assessment of a patient's protein status will be covered. A discussion of protein patterns in normal individuals will include data on day-to-day, age- and sex-related variation. A section on management of protein data will present various approaches to profile reporting. Graphical report formats which minimize the time required for information transfer and simplify assimilation of results will be emphasized.

Adolescent↗
PubMed1992

The pathogenesis of AIDS lymphomas: a foundation for addressing the challenges of therapy and prevention.

The association between AIDS and a spectrum of malignancies relates to chronic, profound defects in both cellular and humoral mechanisms of immune surveillance. Ironically, as AIDS patients live longer in response to increasingly effective antiretroviral therapies, the incidence of AIDS-related malignancies will continue to rise. The emergence of non-Hodgkin's lymphomas (NHL) as a major sequela of HIV infection bears a striking relationship to depletion of CD4 lymphocytes, particularly below 50/mm3. The ability to interfere early in the course of active HIV infection with additional mechanisms that may promulgate transformed cell hyperproliferation and clonal expansion--growth factors, HIV itself or other viruses (Epstein-Barr, in particular), aberrant oncogene or tumor suppressor genes expression, factors that induce genetic instability or DNA damage or alter host or viral genome repair--might decrease the occurrence or prolong the time to development of AIDS-related malignancies. The development of antiretroviral strategies that confer long-term suppression of HIV activity and relative preservation of immune function are essential to the ultimate prevention of malignancies that arise as a consequence of HIV-induced immunosuppression.

Actuarial Analysis↗
PubMed1987

Induction of latent immunological memory in genetically nonresponsive mice.

C57BL/10 mice exhibit major histocompatibility complex linked nonresponsiveness to hen egg white lysozyme (HEL). When these animals are primed with HEL in Freund's complete adjuvant (FCA), their secondary splenic plaque forming cell responses to aqueous HEL challenge are minimal to nonexistent. This notwithstanding, we show here that concomitant priming with both HEL and keyhole limpet hemocyanin (KLH) leads to an enhanced response to the HEL component following secondary challenge with an HEL-KLH conjugate. This enhancing effect can be transferred by nylon wool nonadherent spleen cells from HEL/FCA primed animals. Adoptive transfer studies with fractionated spleen cell populations suggest also that B cells are primed in these animals. Thus, animals which are incapable of mounting a secondary response to this antigen nevertheless appear to be primed at both the T-cell and B-cell levels following exposure to the antigen in FCA. The implications of this finding are discussed.

Animals↗