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Biomedical subjects

D Catalano

Publications and source records attributed to D Catalano.

At least 37 records · Page 2Linked to original sources

[Essential thrombocythemia in pregnancy. A case report and general considerations].

Essential thrombocythemia is a rare disease of unknown etiology characterized by an abnormal increase in the platelet count which cannot be explained by other identifiable causes such as malignancy, infection, chronic inflammatory diseases or other myeloproliferative disorders. It rarely affects people less than 50 years of age and may be associated with hemorrhagic or thrombotic tendencies. A care of pregnancy complicated by essential thrombocythemia treated with aspirin, antiaggregating agent, throughout pregnancy and with hydroxyurea, a platelet lowering drug is reported. Also examine are some pathogenetic and therapeutic aspects of the thrombotic tendency secondary to elevated platelet count in pregnancy.

Adult↗

[The role of transvaginal ultrasonography in the screening of ovarian tumors].

BACKGROUND: From January 1992 to March 1996, 1987 women underwent vaginal sonography screening, at the Department of Obstetrics and Gynaecology of the II Faculty of Medicine and Surgery "Federico II" in Naples. This mass screening aimed at early diagnosis of ovarian cancer. METHODS: Patients included in this investigations were all asymptomatic and had no pelvic abnormalities. Each ovary was measured in three planes and ovarian volume was calculated using the prolate ellipsoid formula. In premenopausal women, ovaries were normal if their volume was of > or = 18 cm3 and if they were hypoechogenic or anechogenic. In postmenopausal women a normal ovary was defined as having a volume of > or = 8 cm3 and a uniformly hypogenic internal structure. RESULTS AND CONCLUSIONS: In thirty-five premenopausal women was detected an abnormal volume of the ovaries. Forty-six postmenopausal women had abnormal vaginal sonograms. In this investigations vaginal sonography has permitted the detection of about 4.88% ovarian tumors in asymptomatic women, so that, it can be considered a more accurate and direment screening method for ovarian cancer than abdominal sonography.

Adult↗

Alcohol-induced regulation of nuclear regulatory factor-kappa beta in human monocytes.

Acute ethanol exposure has the capacity to modulate immune functions, particularly, to down regulate monocyte production of inflammatory cytokines. However, the intracellular mechanisms for these effects of ethanol are yet to be understood. Considering that nuclear regulatory factor-kappa beta (NF-kappa B)/Rel is a common regulatory element of the promoter region of the inflammatory cytokine genes, herein, we tested the hypothesis that acute ethanol affects NF-kappa B activation in human monocytes. Adherence-isolated monocytes showed constitutive DNA binding activity of NF-kappa B. A clinically relevant dose (25 mM) of acute ethanol treatment in vitro increased NF-kappa B binding activity in monocytes with a preferential induction of the inhibitory, p50/p50, NF-kappa B/Rel homodimer, and resulted in no induction of the p65/p50 heterodimer. In contrast, lipopolysaccharide stimulation primarily induced the p65/p50 heterodimer that has been shown to result in gene activation. Thus, such unique activation of the inhibitory p50/p50 homodimer by acute ethanol treatment may result in inhibition rather than activation of NF-kappa B-regulated inflammatory cytokine genes. Consequently, these results suggest that physiologically relevant concentrations of ethanol may affect production of inflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 by disrupting NF-kappa B signaling in monocytes.

Adolescent↗

[Changes in fetal karyotype in non-immune hydrops fetalis].

BACKGROUND AND METHODS: Among the pregnant patients who underwent an amniocentesis at our department of prenatal diagnosis (Division of Gynecology and Obstetrics of the University "Federico II" in Naples) from 1989 to 1996, 16 patients were affected by non-immune hydrops faetalis associated with chromosomal diseases. RESULTS: The karyotype test revealed at an ultrasound exam of the fetus that 11 cases were affected by trisomy 21, 4 cases by Turner syndrome and one case by trisomy 18. This study took into consideration all the pathogenetic factors and the diagnostic problems of non-immune hydrops faetalis in fetus affected by associated chromosomal associated anomalies. CONCLUSIONS: Since the incidence of the chromosomal anomalies on fetus affected by non-immune hydrops foetal is was very high, there was the necessity to carry out a routine karyotype test if the ultrasonography revealed anomalies of the hydrops, during the first three months of pregnancy.

Abnormalities, Multiple↗

Human monocyte IL-10 production is increased by acute ethanol treatment.

Immune alterations after acute ethanol treatment are characterized by abnormal monocyte mediator production and antigen presentation capacity. Here, we tested the hypothesis that some of the regulatory effects of ethanol on monocyte functions are mediated by elevated M phi IL-10 production. Physiologically relevant in vitro doses of ethanol (25-100 mM) resulted in significantly increased IL-10 secretion by normal blood monocytes after 18 h stimulation. We found that monocyte IL-10 production induced by either ethanol or LPS increased at 10 h, maximized at 18 h and decreased by 40 h post-stimulation. Furthermore, ethanol significantly augmented LPS-induced monocyte IL-10 secretion at 18 h. Data also show that ethanol-induced changes in monocyte IL-10 mRNA levels mirror those seen at the protein levels. Greater IL-10 levels and IL-10 induction by LPS in adherent compared to non-adherent M phi imply that adherence is an important co-stimulator for IL-10 production in human M phi. We further showed that cyclooxygenase inhibitor treatment augments M phi IL-10 production suggesting that elevated PGE2 (and cAMP) is not necessary for IL-10 induction by ethanol or LPS in isolated M phi. Finally, our data demonstrate that ethanol-induced elevated M phi IL-10 contributes to the decreased M phi TNF-alpha production seen after acute ethanol treatment. However, observation of an ethanol-induced decrease in TNF-alpha mRNA as early as 1.5 h after stimulation indicate that ethanol has an additional, IL-10 independent, effect on M phi TNF-alpha production. These results suggest that elevated monocyte-derived IL-10 can contribute to the monocyte as well as other immune abnormalities after acute ethanol uptake.

Alcoholic Intoxication↗

Regulation of human monocyte functions by acute ethanol treatment: decreased tumor necrosis factor-alpha, interleukin-1 beta and elevated interleukin-10, and transforming growth factor-beta production.

We and others have previously shown that even acute ethanol exposure has the capacity to modulate immune functions, particularly monocyte functions. Herein, we tested the hypothesis that acute ethanol treatment inhibits inflammatory, while increasing inhibitory cytokine production in human blood monocytes that, in turn, could contribute to the overall immune abnormalities seen after alcohol use. Our data show that in vitro treatment of blood monocytes with a physiologically relevant dose of alcohol (25 mM) results in significantly decreased induction of tumor necrosis factor-alpha (TNF alpha) and interleukin (IL)-1 beta by bacterial stimulation of either Gram-positive [staphylococcal enterotoxin B (SEB), 1 microgram/ml of SEB] or Gram-negative [lipopolysaccharide (LPS), 1 microgram/ml of LPS] origin both at the protein and mRNA levels. In contrast, acute ethanol treatment induces monocyte production of mediators with immunoinhibitory potential, including transforming growth factor-beta and IL-10. We further show that ethanol not only induces monocyte/macrophage (Mø) IL-10 and transforming growth factor-beta, but even augments bacterial (both LPS and SEB) stimulation-induced production of both of these cytokines. IL-10 is a potent inhibitor of Mø TNF alpha production. We found that ethanol-induced elevation in Mø IL-10 levels contributes to the decreased Mø TNF alpha production to bacterial challenge in ethanol-exposed Mø. However, mRNA levels for TNF alpha are downregulated as early as 1.5 hr after ethanol treatment, suggesting that ethanol likely has an IL-10 independent, direct effect on early signaling events of TNF alpha induction.

Adult↗

Relapse of acute lymphoblastic leukemia during pregnancy.

A young woman had a late relapse from acute lymphoblastic leukemia during her first pregnancy at the 17th week of gestation and decided not to interrupt the pregnancy. A partial remission was obtained with mild chemotherapy (vincristine and prednisone) in a month, then the treatment was intensified, but only partial remission was achieved. A cesarean section was performed at the end of the 7th month, with the delivery of a normal male infant. The patient died of refractory leukemia 9 months later. The baby is now 3 years old with no medical problems. This case suggests that: a) pregnancy might be associated with an increased risk of relapse in women in continuous complete remission from leukemia; b) chemotherapy, even intensive, can be safely administered to pregnant women without damaging the fetus, after the first trimester.

Adult↗

Inhibition of superantigen-induced T cell proliferation and monocyte IL-1 beta, TNF-alpha, and IL-6 production by acute ethanol treatment.

Alcohol use has been shown to decrease monocyte antigen presentation capacity and inflammatory cytokine production, thereby increasing susceptibility to infections. Here, we demonstrate that in vitro acute treatment of normal monocytes with pharmacological doses of ethanol can decrease superantigen [Staphylococcus enterotoxins B (SEB) and A (SEA)]-induced T cell proliferation. Furthermore, ethanol treatment (25-100 mM) significantly inhibited SEA- or SEB-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 in monocytes. Ethanol-induced down-regulation of monocyte TNF-alpha, IL-1 beta, and IL-6 occurred at both the protein and mRNA levels. Additional data suggest that ethanol can decrease IL-1 beta mRNA stability. Furthermore, experiments using cycloheximide indicate that de novo protein synthesis is required for the inhibitory effect of ethanol on SEB-induced IL-1 beta mRNA production. Finally, ethanol treatment decreased HLA-DR expression in monocytes, suggesting that ethanol treatment can compromise monocyte stimulation by down-regulating the SEB-binding capacity of monocytes. These results suggest that acute ethanol treatment can interfere with monocyte activation by SEB at multiple steps. Consequently, decreased superantigen-induced polyclonal T cell activation and inflammatory monokine production would contribute to an impaired immune response to bacterial challenge with superantigens after acute alcohol intake.

Adult↗

Acute ethanol consumption synergizes with trauma to increase monocyte tumor necrosis factor alpha production late postinjury.

The hypothesis that acute ethanol uptake plus trauma can synergize to increase immunosuppression was tested. We found that, unlike non-alcohol-exposed patients, patients with acute alcohol use prior to trauma have a transient decrease in monocyte tumor necrosis factor alpha (TNF alpha) production during the very early postinjury (0-3 days) period. However, TNF alpha production by these alcohol-exposed patients' monocytes (M0) became hyperelevated late postinjury (> 9 days). Consequently, these massively elevated M0 TNF alpha levels can contribute to posttrauma immunosuppression after acute alcohol use. We also demonstrate that normal monocyte activation with the superantigen, Staphylococcus enterotoxin B (SEB), results in a preferential induction of cell-associated M0 TNF alpha production, described as characteristic of immunosuppressed trauma patients. Acute in vitro ethanol treatment down-regulated the elevated TNF alpha production by trauma patients' M0 after either SEB, muramyl-dipeptide (MDP), interferon-gamma plus MDP, or lipopolysaccharide (LPS) stimulation. Both SEB- and LPS-induced TNF alpha mRNA induction was inhibited by acute alcohol treatment in normal M0, indicating that ethanol can regulate cytokine gene expression. An additional immunosuppressive effect of acute ethanol's stimulation was suggested by its induction of elevated transforming growth factor beta production in trauma patients' activated M0.

Adult↗

Regulatory potential of ethanol and retinoic acid on human monocyte functions.

Retinoic acid (RA), a metabolic product of vitamin A, has been shown to affect a variety of immune functions, including monocytes. Monocyte functions and mediator production are also modulated by ethanol exposure. This study demonstrates that therapeutic doses of RA (0.1-10 microM) significantly increase transforming growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic cells, and in human peripheral blood monocytes. We have previously reported TGF beta induction by ethanol in human M theta. Combination of RA stimulation with acute in vitro ethanol treatment, however, resulted in significantly lower M theta TGF beta production than TGF beta levels induced by RA alone (p < 0.003). Down-regulation of M theta TGF beta production by ethanol was tested at the concentration range of 25-150 mM and occurred both at high and low RA concentrations (10-0.1 microM). In contrast to its inhibitory effect on RA-induced M theta TGF beta production, ethanol augmented TGF beta production induced by muramyl dipeptide (20 micrograms/ml), suggesting that ethanol can either up- or down-regulate M theta TGF beta production, depending on the costimulatory factors. RA also induced a moderate increase in M theta tumor necrosis factor-alpha (TNF alpha) production, which was down-regulated by ethanol both at the level of secreted and cell-associated TNF alpha. In addition to regulation of cytokine production, both RA and ethanol decreased expression of CD4 on THP-1 cells. The degree of inhibition of CD4 expression by RA was more significant than by ethanol, but RA-induced decrease in CD4 expression was not significantly affected by the combined stimulation with ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)

CD4 Antigens↗

[Needle aspiration of ovarian cysts. Our experience].

80 patients underwent ultrasound guided cyst puncture of ovarian cysts. Six patients were pregnant and in four of them needle aspiration was executed through the transvaginal tract. The sediment aspirated was examined by a cytologic method and when possible it was also correlated to a histological test. Technique and results have been dealt with. No relevant complication was found. Finally, the echoguided (induced) needle aspiration is a simple and safe method to treat benign ovarian cysts in fertile women. It is particularly advisable in pregnancy and in patients for whom both laparascopy and traditional surgery are not practicable.

Adult↗