Ovarian 25OH-vitamin D production in young women affected by polycystic ovary syndrome.

INTRODUCTION: Vitamin D is involved in the regulatory mechanisms of ovarian function and is frequently low in PCOS patients. Since obesity and hyperinsulinemic state negatively influenced vitamin D levels, therefore, we evaluated the production of vitamin D at the ovarian level only in lean and normoinsulinemic PCOS subjects. Basal, GnRH analogue-induced ovarian production of 25OH-vitamin D (VitD) and a direct sampling at ovarian vein level were investigated. METHODS: Basal and GnRH analogue-induced hormone levels were evaluated at peripheral level in 45 subjects, aged 18-39 years, and in 22 healthy women with age- and BMI-matched as controls. In 12 PCOS patients, undergoing laparoscopy, a venous sampling at both peripheral and ovarian level was further done. All subjects presented low VitD levels, appropriate to the season and with no difference between PCOS and control subjects. RESULTS: GnRH analogue significantly stimulated plasma LH, FSH, 17-OHP and estradiol secretion (p from < 0.05 to < 0.001 vs basal levels), whereas no effect was observed on both serum AMH and VitD concentrations in all groups. A significant difference (p < 0.006), between peripheral and ovarian veins, was observed in both AMH and estradiol levels in PCOS subjects, while no gradient of VitD was detected. CONCLUSIONS: All patients presented with low VitD levels. The absence of any VitD variation, both at basal and after GnRH analogue administration, or at peripheral-ovarian vein gradient, suggests no pituitary-ovarian axis involvement in VitD production or its direct ovarian production in lean and normoinsulinemic PCOS subjects.

Diagnostic relevance of IgE sensitization profiles to eight recombinant Phleum pratense molecules.

BACKGROUND: Grass pollen-related seasonal allergic rhinoconjunctivitis (SARg) is clinically heterogeneous in severity, comorbidities, and response to treatment. The component-resolved diagnostics disclosed also a high heterogeneity at molecular level. Our study aimed at analyzing the characteristics of the IgE sensitization to Phleum pratense molecules and investigating the diagnostic relevance of such molecules in childhood. METHODS: We examined 1120 children (age 4-18 years) with SARg. Standardized questionnaires on atopy were acquired through informatics platform (AllergyCARD™). Skin prick tests were performed with pollen extracts. Serum IgE to airborne allergens and eight P. pratense molecules (rPhl p 1, rPhl p 2, rPhl p 4, rPhl p 5b, rPhl p 6, rPhl p 7, rPhl p 11, rPhl p 12) were tested by ImmunoCAP FEIA. RESULTS: The analysis of IgE responses against eight P. pratense molecules showed 87 profiles. According to the number of molecules recognized by IgE, the more complex profiles were characterized by higher serum total IgE, higher grass-specific serum IgE, and higher number and degree of sensitization to pollens. The most frequent IgE sensitization profile was the monomolecular Phl p 1. Sensitization to Phl p 7 was a reliable biomarker of asthma, whereas Phl p 12 of oral allergy syndrome. Sensitization to Phl p 7 was associated with a higher severity of SARg, and complex profiles were associated with longer disease duration. CONCLUSIONS: In a large pediatric population, the complexity of IgE sensitization profiles against P. pratense molecules is related to high atopic features although useless for predicting the clinical severity. The detection of serum IgE to Phl p 1, Phl p 7, and Phl p 12 can be used as clinical biomarkers of SARg and comorbidities. Further studies in different areas are required to test the impact of different IgE molecular profiles on AIT response.

Endotypes of pollen-food syndrome in children with seasonal allergic rhinoconjunctivitis: a molecular classification.

BACKGROUND: Pollen-food syndrome (PFS) is heterogeneous with regard to triggers, severity, natural history, comorbidities, and response to treatment. Our study aimed to classify different endotypes of PFS based on IgE sensitization to panallergens. METHODS: We examined 1271 Italian children (age 4-18 years) with seasonal allergic rhinoconjunctivitis (SAR). Foods triggering PFS were acquired by questionnaire. Skin prick tests were performed with commercial pollen extracts. IgE to panallergens Phl p 12 (profilin), Bet v 1 (PR-10), and Pru p 3 (nsLTP) were tested by ImmunoCAP FEIA. An unsupervised hierarchical agglomerative clustering method was applied within PFS population. RESULTS: PFS was observed in 300/1271 children (24%). Cluster analysis identified five PFS endotypes linked to panallergen IgE sensitization: (i) cosensitization to ≥2 panallergens ('multi-panallergen PFS'); (ii-iv) sensitization to either profilin, or nsLTP, or PR-10 ('mono-panallergen PFS'); (v) no sensitization to panallergens ('no-panallergen PFS'). These endotypes showed peculiar characteristics: (i) 'multi-panallergen PFS': severe disease with frequent allergic comorbidities and multiple offending foods; (ii) 'profilin PFS': oral allergy syndrome (OAS) triggered by Cucurbitaceae; (iii) 'LTP PFS': living in Southern Italy, OAS triggered by hazelnut and peanut; (iv) 'PR-10 PFS': OAS triggered by Rosaceae; and (v) 'no-panallergen PFS': mild disease and OAS triggered by kiwifruit. CONCLUSIONS: In a Mediterranean country characterized by multiple pollen exposures, PFS is a complex and frequent complication of childhood SAR, with five distinct endotypes marked by peculiar profiles of IgE sensitization to panallergens. Prospective studies in cohorts of patients with PFS are now required to test whether this novel classification may be useful for diagnostic and therapeutic purposes in the clinical practice.

Sertoli-Leydig cell tumors: hormonal profile after dynamic test with GnRH analogue: triptorelin represents a useful tool to evaluate tumoral hyperandrogenism.

We report the case of a 15-year-old woman with signs of hyperandrogenism affected by a Sertoli-Leydig cell tumor (SLCT). In our patient, blood analysis showed a high testosterone (T) level (T: 8.53 nmol/L; nv < 1.87 nmol/L) while the GnRH-analogue test demonstrated an exaggerated secretion of 17-hydroxyprogesterone (OHP), T, and androstenedione (A) by the ovary after stimulation. We compared the GnRH-analogue test of our patient with that obtained in a group of normal and healthy women (no. 8 subjects, 16-26 years old), men (no. 4 subjects, 18-28 years old), and in a group of PCOS patients with age and body weight compared. We found in our patient a value of OHP, 17-beta estradiol (E2) and T, from 2 to 18 times higher than healthy women. When we compared our patient with healthy men, we differently observed a comparable response of T. The response of our patient was also comparable with that observed in the PCOS group for E2. During the post-surgical follow up, the GnRH-analogue test of our patient showed a response of OHP, T, and E2 comparable with that of the PCOS group. The GnRH-analogue test is a useful tool to characterize steroidogenesis in SLCT.

Gonadal function in males with autoimmune Addison's disease and autoantibodies to steroidogenic enzymes.

Steroidogenic enzyme autoantibodies (SEAbs) are frequently present and are markers of autoimmune premature ovarian failure (POF) in females with autoimmune Addison's disease (AAD). The prevalence and significance of SEAbs in males with AAD have not yet been defined. We studied the prevalence of SEAbs in a large cohort of males with AAD and assessed the relationship between SEAbs positivity and testicular function. A total of 154 males with AAD (mean age 34 years) were studied. SEAbs included autoantibodies to steroid-producing cells (StCA), detected by immunofluorescence, and steroid 17α-hydroxylase (17α-OHAbs) and side chain cleavage enzyme (SCCAbs) measured by immunoprecipitation assays. Gonadal function was evaluated by measuring follicle-stimulating hormone (FSH), luteinizing hormone (LH), total testosterone (TT), sex hormone-binding globulin (SHGB), anti-müllerian hormone (AMH) and inhibin-B (I-B). Twenty-six males, 10 SEAbs((+)) and 16 SEAbs((-)), were followed-up for a mean period of 7·6 years to assess the behaviour of SEAbs and testicular function. SEAbs were found in 24·7% of males with AAD, with the highest frequency in patients with autoimmune polyendocrine syndrome type 1 (APS-1). The levels of reproductive hormones in 30 SEAbs((+)) males were in the normal range according to age and were not significantly different compared to 55 SEAbs((-)) males (P > 0·05). During follow-up, both SEAbs((+)) and SEAbs((-)) patients maintained normal testicular function. SEAbs were found with high frequency in males with AAD; however, they were not associated with testicular failure. This study suggests that the diagnostic value of SEAbs in males with AAD differs compared to females, and this may be related to the immunoprivileged status of the testis.

Markers of eosinophilic and neutrophilic inflammation in bronchoalveolar lavage of asthmatic and atopic children.

BACKGROUND: Recent studies performing fiberoptic bronchoscopy in children have improved our understanding of asthma pathophysiology. Eosinophilic, but also neutrophilic, inflammation has been described in asthma, but the relationship with atopy was incompletely investigated. The aim of this study is to examine inflammatory cells and mediators in children with asthma compared to the appropriate controls, i.e. atopic children without asthma and children with no atopy or asthma. Moreover, asthmatic children were analysed separately based on the presence of atopy and stratified by age. METHODS: We recruited 191 children undergoing fiberoptic bronchoscopy for appropriate indications: 91 asthmatics (aged 1.4-17 years), 44 atopics without asthma (1.6-17.8 years) and 56 nonasthmatic nonatopic controls (1.4-14 years). In bronchoalveolar lavage, total and differential cell counts and inflammatory mediators, including ECP, eotaxin, IL-8 and TNFalpha, were analysed. RESULTS: Eosinophils and ECP levels were increased in asthmatic children when compared to controls (P = 0.002 and P = 0.01, respectively), but also atopic children without asthma had increased ECP levels compared to controls (P = 0.0001). Among asthmatic children, eosinophils and ECP levels were not different between atopic and nonatopic individuals. Neither neutrophils nor the related mediators (IL-8 and TNFalpha) differed significantly in the three groups. This pattern of inflammation was observed in both preschool and school-aged asthmatic children. CONCLUSIONS: This study suggests that markers of eosinophilic, but not neutrophilic inflammation, are increased in asthmatic children and also in atopic children without asthma. Of interest, in asthmatic children, the activation of the eosinophilic response is not solely because of the presence of atopy.

Neurological complications of celiac disease and autoimmune mechanisms: preliminary data of a prospective study in adult patients.

Antibodies to gangliosides and Purkinje cells have been reported in patients with celiac disease (CD) with neuropathy and ataxia, respectively. Whether these antibodies are pathogenic is not clear. The response of neurological symptoms and antibody titers to a gluten-free diet is still controversial. The objective of our study was to assess whether neurological manifestations in CD patients correlate with antibody titers and a gluten-free diet.Thirty-five CD patients (9 males, 26 females, mean age 37.1 +/- 12.6 yrs) were followed prospectively. At initial evaluation, 23 were on a gluten-free diet, 12 were not. At recruitment and during follow-up, patients underwent neurological and electrophysiological evaluation. IgG, IgM, and IgA anti-ganglioside antibodies were assayed by ELISA; anti-neuronal antibodies were assessed by immunohistochemistry and Western blot. Four patients, all males, had electrophysiological evidence of neuropathy; three had been on a gluten-free diet for several months, and one was newly diagnosed. One had reduced tendon reflexes; another complained of distal paresthesias. With regard to anti-ganglioside antibodies, three patients had a moderate increase in antibodies without symptoms or signs of neuropathy. No patients had ataxia or cerebellar dysfunction, although in four patients reactivity to neuronal antigens was found. In 17 patients, an electrophysiological follow-up (mean duration of follow-up, 9 months) showed no changes. In conclusion, the preliminary results of this prospective study indicate that neuropathy, usually subclinical, may accompany CD. Antibody titers do not seem to correlate with neurological symptoms/signs or diet. Ongoing follow-up will help confirm these data and clarify the role, if any, of antibodies in neurological involvement in CD.

CAR-3 and CA 19-9 serum levels in pancreatic cancer: any differences between two epitopes of the same mucin-like glycoprotein?

The aim of this study was to compare the utility of two recently identified tumour markers of pancreatic cancer, CA 19-9 and CAR-3, and to ascertain the roles of some factors influencing both antigens. CA 19-9 and CAR-3 were measured in sera of 18 control subjects, 27 patients with pancreatic cancer, 25 with chronic pancreatitis, and 29 with extra-pancreatic diseases. CA 19-9 and CAR-3 were, respectively, found to be increased in 85 per cent and 44 per cent of patients with pancreatic cancer, 28 per cent and 0 per cent with chronic pancreatitis and 72 per cent and 28 per cent with extra-pancreatic diseases. The ROC curves showed that, for any serum value considered, CA 19-9 is more effective than CAR-3 in discriminating between pancreatic cancer and control subjects and chronic pancreatitis. With the combined use of both antigens the results were no better than those given by CA 19-9 alone. Correlations were found between liver function tests and CA 19-9 levels and between cholestasis indices only and CAR-3 values. Our findings show that CAR-3 is not a sufficiently reliable marker of pancreatic cancer, due to its low sensitivity. Nor does it offer any more information than CA 19-9. Both assays are influenced, at least in part, by the extent of the neoplasia. Cholestasis which can greatly influence a serum glycoproteic marker such as CA 19-9, was found also to affect, to a lesser extent, CAR-3, an epitope on the same mucin molecule.

Oxygen derived free radicals in patients with chronic pancreatic and other digestive diseases.

To ascertain modifications in the activation products derived from oxygen free radicals in patients with chronic pancreatic and extra-pancreatic diseases, lipid peroxide activity was measured in the sera of 40 control subjects, 28 patients with pancreatic cancer, 49 with chronic pancreatitis, and 53 with extra-pancreatic diseases. In 142 of the subjects, elastase 1, amylase, and pancreatic isoamylase activities were also determined. Increased lipid peroxide activities were found in some patients with both chronic pancreatic and extra-pancreatic diseases. Patients with chronic pancreatitis studied during relapse had higher activities of lipid peroxides than those without active disease. No difference was found between the values in patients with pancreatic cancer with liver metastases and those without. Correlations were found between lipid peroxides and both amylase and pancreatic isoamylase activities; no correlation was detected between lipid peroxides and elastase 1. In benign biliary tract disease a correlation was detected between lipid peroxides and alanine aminotransferase and alkaline phosphatase activities. In all patients, however, a correlation was found between alkaline phosphatase and lipid peroxide activities. It is concluded that activation of oxygen derived free radicals occurs in chronic pancreatic as well as in extra-pancreatic disease; it seems to reflect the degree of inflammation.

Evaluation of the Incstar Cyclo-Trac sp kit for the determination of cyclosporine in blood.

We measured cyclosporine in whole blood samples from renal and heart transplant patients by high performance liquid chromatography and by two radioimmunoassays with use of specified monoclonal antibodies. In particular, we evaluated the analytical performance of a new specific radioimmunoassay with an iodinated tracer. The reproducibility of the method is satisfactory (within-run CV 7.1 to 9.5% and between-run CV 7.2 to 10.3%). The limit of detection is 10.3 micrograms/L and the analytical recovery between 99 and 114%. The results obtained with samples from both renal heart transplant patients agree well with those obtained by HPLC and by a specific RIA that uses a tritiated tracer.

Tear and serum soluble leukocyte activation markers in conjunctival allergic diseases.

PURPOSE: To measure markers of leukocyte activation in patients with an exclusively ocular inflammatory or bacterial disease. METHODS: Neutrophil myeloperoxidase, eosinophil cationic protein, eosinophil neurotoxin, and soluble interleukin-2 receptor were measured in serum and tears of 17 patients with allergic vernal keratoconjunctivitis, seven with atopic keratoconjunctivitis, 11 with seasonal allergic conjunctivitis, seven with giant papillary conjunctivitis, 13 with rosacea blepharokeratoconjunctivitis, seven with bacterial conjunctivitis, and 13 normal subjects as controls. RESULTS: In serum of patients with vernal and atopic keratoconjunctivitis, levels of eosinophil cationic protein, eosinophil neurotoxin, and interleukin-2 receptor were significantly increased compared with control subjects but were not correlated with the severity of ocular symptoms. In tears of patients with vernal and atopic keratoconjunctivitis and seasonal allergic conjunctivitis, as well as in the nonallergic diseases, rosacea blepharokeratoconjunctivitis and bacterial conjunctivitis, levels of eosinophil cationic protein, neurotoxin, and interleukin-2 receptor were significantly increased compared with control subjects. The highest values of these markers were found in vernal keratoconjunctivitis samples. Neutrophil myeloperoxidase was significantly increased in vernal and atopic keratoconjunctivitis, rosacea blepharokeratoconjunctivitis, and bacterial conjunctivitis. In vernal keratoconjunctivitis, tear markers were correlated to the clinical score of the disease, but not with cytology. CONCLUSIONS: Tear histamine was measured in 10 allergic patients after allergen challenge. Although none of the above markers can be considered specific to a single disease, their measurement may still be useful for the quantification of local cell activation in ocular inflammatory diseases.

Serum-mediated relaxant response to toluene diisocyanate (TDI) in isolated guinea-pig bronchi.

The present study was designed to evaluate whether pre-incubation with serum, obtained from both control and toluene diisocyanate (TDI)-immunized guinea-pigs, modified the contractile response to TDI in isolated guinea-pig bronchial rings. Guinea-pigs were anaesthetized and the main bronchi dissected in two rings. Bronchial rings were incubated with normal or immune serum (100 microl ml(-1) for 2 h) and dose-response curves to TDI (0.03-1000 microM) were studied isometrically. Before serum incubation, in eight bronchial rings, epithelium was removed by rubbing the luminal surface gently with a gauze. In control rings, TDI produced a concentration-dependent contraction, whereas in rings pre-incubated with either normal or TDI-immune serum, it produced a concentration-dependent relaxation. Relaxation was 101.4 (SEM 17.4)% and 94.9 (SEM 21)% of the relaxation induced by isoproterenol (1 mM) respectively with normal and TDI-immune serum. Similarly to the pre-incubation with serum, pre-incubation with albumin produced a concentration-dependent relaxation to TDI. Serum-induced relaxant response to TDI was not affected by capsaicin desensitization, it was only partially inhibited by an NK1-tachykinin antagonist, whereas it was blocked by indomethacin. In bronchial rings without epithelium, pre-incubated with serum, TDI caused contraction at highest doses, while it still induced relaxation at the lowest doses. This study shows that one or more components of the serum modify the contractile response to TDI in isolated guinea-pig bronchi. In bronchial rings without epithelium serum was able to inhibit the contration induced by low doses of TDI.

Deoxyribonuclease I serum activity in pancreatic cancer.

In patients with pancreatic cancer deoxyribonuclease I (DNase I) serum levels were compared with those of other known pancreatic enzymes. Serum deoxyribonuclease I, elastase 1, immunoreactive trypsin, amylase and phospholipase A2 were determined in 40 healthy controls, 28 patients with pancreatic cancer, 49 with chronic pancreatitis and 40 with extra-pancreatic diseases. The analysis of variance showed a significant difference among groups for serum DNase I values. However, none of the 3 groups of patients had a mean deoxyribonuclease I value higher than that of the healthy controls. In pancreatic cancer and chronic pancreatitis patients, increases in the 4 pancreatic enzymes values were found in percentages that were higher than those for DNase I. A significant correlation was found between DNase I and phospholipase A2, but not between DNase I and elastase 1, immunoreactive trypsin and amylase serum activities. The findings indicate that deoxyribonuclease I serum determination is an even less satisfactory index of pancreatic malignancy than the other pancreatic enzymes. Rather than expressing pancreatic damage, any variations in this enzyme appear more likely to reflect an aspecific phenomenon.

[Frequent occurrence of diabetes mellitus after corticosteroid treatment in mixed cryoglobulinemia. An HCV-related complication?]. / Frequente insorgenza di diabete mellito dopo trattamento cortisonico nella crioglobulinemia mista. Una complicanza HCV-correlata?

The hepatitis C virus (HCV) infection is characterized by a variety of extra-hepatic manifestations in many individuals. Among these, diabetes mellitus (DM) can be included, as such a metabolic disorder has been demonstrated to be more frequent in chronic hepatitis C than in liver disease due to other causes. Recently, we have observed that most patients affected with HCV-associated mixed cryoglobulinemia (13 out of 15, 86.7%), that were at baseline normoglycemic, developed DM following corticosteroid treatment (prednisone > 25 mg/daily) for at least three months. Conversely, when we consider a control group including 36 HCV negative patients affected with various immunomediated disorders, i.e., systemic lupus erythematosus, myasthenia gravis, poly/dermatomyositis and chronic inflammatory demyelinating polyneuropathy, that were initially normoglycemic, corticosteroid induced DM (prednisone > 25 mg/daily for at least three months) occurred only in 16.7% of subjects. Moreover, in other two HCV positive patients suffering from myasthenia gravis, prolonged corticosteroid treatment was complicated by DM. These data, that are still unclear from a pathophysiologic viewpoint, seem to indicate corticosteroid induced DM as a further, unusual extra-hepatic manifestation of the HCV infection.

[Basal and postprandial blood gastrin in peptic ulcer. The physiopathological aspects in relation to different sites of the lesion]. / La gastrinemia basale e post-prandiale nella malattia ulcerosa peptica. Considerazioni fisiopatologiche in relazione alla differente localizzazione della lesione.

A different pathophysiological mechanism is widely accepted for gastric and duodenal ulcer. In particular, the exact role of gastrin in the determinism of non hormono-dependent peptic ulcer disease is not completely clarified. Therefore, the aim of present study was to analyse fasting and post-prandial serum gastrin levels in 99 duodenal ulcer patients, 17 gastric ulcer patients and 11 subjects presenting an association of gastric and duodenal ulcer. The possible correlation between post-prandial gastrin concentrations and basal and maximal acid output in the 3 fasting serum gastrin levels appear not different among the 3 classes of patients, while post-prandial gastrin concentrations are statistically higher at 15 minutes in duodenal ulcer patients and in subjects with the association of gastric and duodenal ulcer as compared to gastric ulcer patients. Mean fasting and stimulated gastrin levels are higher in gastric ulcer females than in males during the entire test and with statistically difference at 30 minutes. The concentrations of the hormone are not different in males of the 3 groups of patients at basal time, while are statistically lower at 15 and 30 minutes in gastric ulcer males compared to the males with duodenal ulcer and the association of the localization. Finally, positive correlation has been observed between BAO and MAO and post-prandial gastric concentrations in the 3 groups of patients, while there is an inverse correlation between the previous parameters as regards sex, both in gastric and duodenal ulcer.

[Basal and postprandial blood gastrin in peptic ulcer. The physiopathological considerations in relation to different locations of the lesion]. / La gastrinemia basale e post-prandiale nella malattia ulcerosa peptica. Considerazioni fisiopatologiche in relazione alla differente localizzazione della lesione.

A different pathophysiological mechanism is widely accepted for gastric and duodenal ulcer. In particular, the exact role of gastrin in the determinism of nonhormone-dependent peptic ulcer disease has been completely clarified. The aim of the present study was to analyse fasting and postprandial serum gastrin levels in 99 duodenal ulcer patients, 17 gastric ulcer patients and 11 subjects presenting an association of gastric and duodenal ulcer. The possible correlation between postprandial gastrin concentrations and basal and maximal acid output in the 3 groups of patients has also been investigated. Fasting serum gastrin levels do not appear different among the 3 classes of patients, while postprandial gastrin concentrations are statistically higher at 15 minutes in duodenal ulcer patients and in subjects with the association of gastric and duodenal ulcer as compared to gastric ulcer patients. Mean fasting and stimulated gastrin levels are higher in gastric ulcer females than in males during the entire test and with a statistically significant difference at 30 minutes. The concentrations of the hormone are not different in males of the 3 groups of patients at basal time, while they are statistically lower at 15 and 30 minutes in gastric ulcer males compared to those with duodenal ulcer and the association of the localization. Finally, positive correlation has been observed between B.A.O. and M.A.O. and postprandial gastrin concentration in the 3 groups of patients, while there is an inverse correlation between the previous parameters as regards sex, both in gastric and duodenal ulcer.

[Role of serum markers and or various clinical parameters in the diagnosis of pancreatic carcinoma]. / Ruolo dei marcatori sierici e di alcuni parametri clinici nella diagnosi di carcinoma pancreatico.

This study was performed to ascertain the role of serum markers and simple clinical data in detecting pancreatic cancer and in distinguishing this malignancy from chronic pancreatitis and other gastrointestinal diseases. Serum CA 19-9, tissue polypeptide antigen and carcinoembryonic antigen were measured in 38 control subjects, 37 patients with pancreatic cancer, 39 with chronic pancreatitis and 44 with extra-pancreatic diseases mainly of gastrointestinal origin. Clinical data recorded included age, sex, presence of pancreatic calcifications, weight loss, pain, jaundice, alcohol abuse, diabetes mellitus. Serum markers gave a correct allocation of the subjects in 48.1% of the cases with pancreatic cancer patients correctly predicted in 62.2%. Clinical data correctly diagnosed 74.2% of subjects. Chronic pancreatitis was identified in 84.6% of the cases and pancreatic cancer in 64.9%. The first clinical variables selected were pain and age. The addition of serum markers to clinical data did not enhance accuracy of the results. We conclude that the diagnosis of chronic pancreatic diseases should first be suspected on the basis of accurately recorded simple clinical data; serum markers seem to be only occasionally useful. Since indicative clinical data and serum markers become positive in the advanced phases of pancreatic cancer, early diagnosis of this malignancy still remains an objective to reach.

Sex hormone changes in post-menopausal women with primary biliary cirrhosis (PBC) and with cryptogenic chronic liver disease.

Sex hormones and sex hormone binding globulin (SHBG) have been studied in 32 female post-menopausal patients (16 with Primary Biliary Cirrhosis (PBC) and 16 with cryptogenic chronic liver disease (CLD). Dehydroepiandrosterone-sulfate (DHEA-S) serum levels were significantly higher in PBC compared to CLD subjects (p less than 0.005). In PBC DHEA-S concentration was higher in precirrhotic than in cirrhotic patients (p less than 0.02). SHBG was raised in both PBC and CLD patients but higher in CLD compared to PBC subjects (p less than 0.002). PBC reveals a sex hormone pattern similar to post-menopausal subjects with breast cancer. These results suggest that sex hormone alteration is present in females with different types of liver disease, but the metabolic pattern is not due to liver disease per se.

Plasma lipids and inflammation in active inflammatory bowel diseases.

BACKGROUND: Ulcerative colitis (UC) and Crohn's disease (CD) can cause metabolic and inflammatory alterations. AIM: To evaluate the relationships between inflammatory parameters, plasma lipids and phospholipid fatty acid (FA) composition in patients with active UC and CD. METHODS: Diet, the Harvey-Bradshaw Activity Index (HBAI), inflammatory parameters, lipoproteins and FA composition were assessed in 60 CD and 34 UC. RESULTS: No differences in clinical parameters were observed in the two groups. Total cholesterol correlated inversely with the number of bowel movements in both groups and directly with BMI in UC. Arachidonic acid correlated inversely with HBAI in UC and total and HDL cholesterol were inversely related to C-reactive protein (CRP) in CD while HDL correlated with CRP in UC. Docosapentaenoic acid was the only polyunsaturated n-3 FA that was correlated to CRP in both groups. Total cholesterol was independently associated in the multiple regression analysis with the number of bowel movements and systemic inflammation. CONCLUSIONS: Total and LDL cholesterol were lower in the active UC and CD than in the healthy subjects and were correlated with the systemic inflammatory status. Phospholipid FA composition was correlated to the systemic inflammatory status, but was unrelated to dietary intake and intestinal disease activity.

Variations in fibrinolytic parameters and inhibin-A in pregnancy: related hypertensive disorders.

BACKGROUND: The mechanisms leading to pregnancy-related hypertensive disorders, and pregnancy-induced hypertension (PIH) and pre-eclampsia (PE) in particular, are still not clear. Diagnostic criteria are clinical because specific markers of the condition are lacking. A role of the fibrinolytic system has been suggested. OBJECTIVES: We aimed to evaluate the behavior of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), PAI-2, and the placental hormone inhibin-A in women with a normal pregnancy vs. women with pregnancies complicated by PIH or PE. METHODS: Blood samples were drawn between the 25th and 30th gestational week (GW) and between the 31st and 36th GW in order to assay t-PA, PAI-1, PAI-2 and inhibin-A; routine biochemical exams, ultrasonography umbilical artery pulsatility index (PI), placental weight and newborn weight were measured. RESULTS: In pregnancies complicated by hypertensive disorders, PAI-1 levels were higher than in controls and increased significantly after the 25th GW, especially in PE, as did inhibin-A. PAI-2 levels were significantly lower after the 30th GW in patients with PIH and PE. The PAI-1/PAI-2 ratio was significantly higher in PE patients than in controls as of the 25th GW, but only after the 30th GW in patients with PIH. Inhibin-A was significantly correlated with fibrinolytic parameters, and inversely with newborn weight. Receiver-operator characteristic curves for PAI-1 and inhibin-A showed a high sensitivity and specificity for PE. PAI-2 correlated with newborn and placental weight, and inversely with PI of the umbilical artery. CONCLUSIONS: Fibrinolytic tests (especially PAI-1) and inhibin-A monitoring during pregnancy may help in the early diagnosis of pregnancy-related hypertensive disorders.