Biomedical subjects
A G Giovannoni
Publications and source records attributed to A G Giovannoni.
Galactorrhoea, hyperprolactinaemia, and protease inhibitors.
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Association between high serum prolactin levels and concomitant infections in HIV-infected patients.
Although prolactin (PRL) is now recognized as a cytokine and persistent immune activation is a common immunopathogenic feature of the human immunodeficiency virus infection (HIV), the circumstances associated with the onset of hyperprolactinemia during the course of this infection remain controversial. Given that PRL is able to exert not only endocrinologic effects but also immunologic influences, a study was conducted to investigate whether raised serum levels of PRL were more likely to prevail when HIV-infected patients developed concomitant infections. Serum PRL concentrations, as well as immunoglobulin isotypes, plasmatic viral burden, CD3+, CD4+, CD8+, CD19+, and natural killer (NK) cell counts were measured in 46 nonselected HIV-infected patients stratified on the basis of the presence or absence of clinically active concomitant infections. Serum PRL levels were significantly higher in patients presenting secondary infections as compared with the asymptomatic ones, with hyperprolactinemia being detected in 10/18 (55%) and 2/28 (7%) of these patient groups, respectively. Hyperprolactinemia was not related with viral burden, antiretroviral treatment, gender differences, or CD4+ cell counts. CD3+, CD4+, CD8+, and CD19+ cells were significantly lower in the group presenting active infections, whereas comparisons in NK cell counts, immunoglobulin levels and HIV viral burden revealed no differences between groups. These results provide evidence that hyperprolactinemia is more prevalent during the onset of secondary infections, which might have diagnostic and therapeutic consequences.
[Celiac disease and Budd-Chiari syndrome: infrequent association].
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[Hyperprolactinemia is a frequent finding in HIV infection but does not correlate with viral burden].
Although many authors have reported the finding of hyperprolactinemia during the course of HIV infection, the circumstances determining the rise of prolactin (PRL) concentrations in serum are poorly understood. To analyze the relationships between serum PRL and other clinical variables in HIV-infected patients, 46 HIV-infected patients and 17 seronegative controls were studied. Serum PRL concentrations were significantly higher in the HIV-infected group (p = 0.022). Furthermore, Serum PRL and serum IgG correlated positively (Rs = 0.42; p = 0.05, Spearman-Rank). On the contrary, serum PRL concentrations did not correlate with the plasmic viral burden (Rs 0.039; p = 0.841), Our data confirm that hyperprolactinemia is a frequent finding during the course of HIV infection, and that serum PRL are independent of viral replication kinetics. Considering that a positive correlation was found between serum PRL and immunoglobulins, it is possible that serum PRL might increase in response to non specific immunological activation, or even in response to immunological activation at the onset of infections.
[Immunological properties of prolactin].
A profound bi-directional interaction exists between the hormone prolactin and the immune system. Even the name "hormone" seems to be inadequate, since prolactin is clearly a growth factor and in fact it functions as an immune co-mitogenic cytokine using autocrine, paracrine and obviously endocrine mechanisms. Prolactin (PRL) stimulates lymphocyte proliferation in response to antigen and mitogens. In addition, prolactin is locally secreted by immune cells, and the pituitary production of prolactin is partially under the control of pro-inflammatory cytokines. These reciprocal influences imply the presence of specific receptors for prolactin in many immune cells, such as lymphocytes and other accessory cells. The PRL-binding to its receptor stimulates the synthesis and secretion of lymphocyte cytokines. In addition, it is a growth factor essential for at least one lymphoid cell line. The PRL-corresponding mRNA has been demonstrated in the cytoplasm of mitogen-stimulated lymphocytes, and the secretion of PRL has been well documented in lymphoid cells. Moreover, PRL acts on NK cells to induce their differentiation to prolactin-activated killer cells (PAK cells) in a dose-dependent way (activation at physiological concentrations, and cytotoxicity inhibition at tenfold higher concentrations). PRL also shows a well known capacity to induce IFN-gamma and IL-2 synthesis, suggesting their participation in the genesis of Th1-responses. These PRL immunological properties strongly support PRL as a cytokine. PRL involvement in both the normal immune response and in many pathological conditions raises important considerations regarding potential diagnostic and therapeutic applications.
Leg ischemia in a patient receiving ritonavir and ergotamine.
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Autoantibodies in human immunodeficiency virus-infected patients with and without concurrent hepatitis C infection.
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[Empirical anti-toxoplasma therapy in cerebral AIDS and Chagas disease. Presentation of 2 cases, review of the literature and proposal of an algorithm].
Trypanosoma cruzi is the responsible agent of Chagas disease and is endemic in extended areas of South and Central America. There are many previous reports indicating that T. cruzi frequently involves the central nervous system in AIDS patients. Here, we present two cases illustrating that neurological involvement caused by T. cruzi frequently shows a clinical picture similar to that caused by Toxoplasma gondil. Since in neurological Chagas disease early treatment has been associated with a better outcome and considering that the diagnosis is easily reached by the detection of the agent in the cerebrospinal fluid, we propose a new algorithm for the management of AIDS patients presenting neurological focal lesions in endemic areas for T. cruzi.