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Lower serum zinc in Chronic Fatigue Syndrome (CFS): relationships to immune dysfunctions and relevance for the oxidative stress status in CFS.

The present study examines serum zinc concentrations in patients with chronic fatigue syndrome (CFS) versus normal volunteers. Serum zinc levels were determined by means of an atomic absorption method. We found that serum zinc was significantly lower in the CFS patients than in the normal controls. There was a trend toward a significant negative correlation between serum zinc and the severity of CFS and there was a significant and negative correlation between serum zinc and the subjective experience of infection. We found that serum zinc was significantly and negatively correlated to the increase in the alpha2 protein fraction and positively correlated to decreases in the expression of mitogen-induced CD69+ (a T cell activation marker) on CD3+ as well as CD3+CD8+ T cells. These results show that CFS is accompanied by a low serum zinc status and that the latter is related to signs of inflammation and defects in early T cell activation pathways. Since zinc is a strong anti-oxidant, the present results further support the findings that CFS is accompanied by increased oxidative stress. The results of these reports suggest that some patients with CFS should be treated with specific antioxidants, including zinc supplements.

Adult↗

Prospective study of post-partum thyroid immune dysfunctions in type 1 diabetic women and in a healthy control group living in a mild iodine deficient area.

Second to diabetes mellitus, thyroid diseases are the most common endocrinopathies seen in pregnancy. The incidence of post-partum thyroid dysfunction (PPTD) in women with type 1 diabetes mellitus is three-fold increased. We determined the incidence of thyroid abnormalities in a well-defined group of young subjects with type 1 diabetes and in an age-matched healthy controls during and six months after pregnancy in an area of mild iodine deficiency. Twenty-five out of twenty-eight pregnant women completed the study. Fifteen were affected by type 1 diabetes and ten were controls. Our protocol of study consisted of four evaluations of each subject: in the first, in the second trimester, at delivery and six months after. At each control the patients were submitted to physical examination, thyroid ultrasonography, and determination of fT3, fT4, TSH, Antithyroglobulin antibodies (TgAbs), Antithyroperoxidase antibodies (TPOAbs). The variation of thyroid volume is statistically significant in both the diabetics and in the controls during the different times of observations. Four out of the fifteen diabetic pregnant patients (27%) developed a thyroid disease: two cases of post-partum thyroiditis (PPT) and two cases of euthyroid benign nodular goiter, as confirmed by cytological examination. Two out ten controls (20%) developed positive antibodies (TPO Abs and TgAbs) since the first observation and showed an autoimmune thyroiditis six months after delivery. Both of them showed a familial history of thyroid disease. Our study suggests that in an area of mild iodine deficiency the incidence of thyroid autoimmunity in pregnant women is similar, whether diabetic or not; moreover, thyroid volume is increasing in the diabetics as much as in the non diabetics during pregnancy.

Adult↗

Age-related immune dysfunction in health and in human immunodeficiency virus (HIV) disease: association of age and HIV infection with naive CD8+ cell depletion, reduced expression of CD28 on CD8+ cells, and reduced thymic volumes.

Older age is a strong predictor of accelerated human immunodeficiency virus (HIV) disease progression. We investigated the possible immunologic basis of this interaction by comparing older (>/=45 years) and younger (</=30 years) HIV-infected adults with simultaneously enrolled, aged-matched, healthy volunteers. Cross-sectional comparisons suggested age-associated reductions in naive CD8(+) cells and in the expression of CD28(+) on CD8(+) cells among both HIV-infected subjects and control subjects. Opposite patterns of CD4(+) and CD8(+) cell differences were apparent between these subject groups. HIV infection, but not age, was associated with impairments in delayed-type hypersensitivity responses, lymphoproliferation, and spontaneous apoptosis and with alterations in expression of chemokine receptors CCR5 and CXCR4. Reduced thymic volumes were associated with age and with HIV infection among younger, but not older, subjects. Because of their common association with age and HIV disease, naive CD8(+) cell depletion, diminished CD28 expression on CD8(+) cells, and reduced thymic volumes are possible correlates of the interaction of age with HIV disease.

Adolescent↗

Immune dysfunction in rabbits associated with chronic administration of enemas and rectal insemination.

NZ rabbits were treated with various combinations of enemas and intrarectal insemination (1 or 3 ml of semen a week) to investigate the effects of intestinal uptake and immunogenicity of seminal components and of an unrelated antigen, bovine serum albumin (BSA), given simultaneously. For 5 months the treatment was limited to enemas and/or semen, and total immunoglobulins and antisperm and antilymphocyte antibodies were determined. Then, without interruption of the treatments, the animals received two courses of three consecutive daily intrarectal administrations of BSA, and the humoral response was determined 7 days after each course of administration. Only 1 of 18 intrarectally inseminated animals responded with production of antisperm antibodies; none had antilymphocyte antibodies. Total immunoglobulins, however, were significantly increased in animals receiving enemas alone (p less than 0.02) or followed by insemination (p less than 0.05). The humoral response to BSA was significantly (p less than 0.01) enhanced by prior administration of enemas but was moderately reduced by simultaneous administration of semen, in a dose-related fashion.

Animals↗

Endometriosis: abnormal endometrium and dysfunctional immune response.

This review highlights recent studies that illuminate the role of the immune system in endometriosis. The findings are discussed in the framework of a model which proposes that endometriosis reflects an immunological selection process. Endometrial cells, which are inherently resistant to apoptosis and immune-mediated elimination, acquire the capacity to utilize the products of an activated immune system to establish ectopic foci of disease. Cyclical inflammatory/immune cell stimulation that fails to eliminate ectopic endometrial implants results in progressive immunological derangement and associated pathophysiological changes which are characteristic of the disease.

Endometriosis↗