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OBJECTIVE: Heart failure (HF) has been associated with increased risk of fragility fractures. Indeed, most literature data on fractures were based on an historical and clinical approach focused on the identification of peripheral fractures, whereas the risk of vertebral fractures in this clinical setting is still unclear. DESIGN: Cross-sectional study. AIM: To evaluate the prevalence and determinants of radiological thoracic vertebral fractures in patients with HF. METHODS: The study includes 1031 elderly hospitalized patients (491 females and 540 males; median age, 75 years; range, 65-90; 430 patients with HF) who were evaluated for the presence of thoracic vertebral fractures by quantitative morphometric analysis, using chest X-ray routinely performed in the diagnostic work-up of HF. RESULTS: Vertebral fractures were found in 166 patients (16.1%), the prevalence being significantly higher in patients with HF as compared with those without HF, both in females (30.9 vs 15.8%; P<0.001) and in males (16.4 vs 7.4%; P=0.001). The association between HF and vertebral fractures remained statistically significant (odds ratio, 2.14; 95% CI, 1.25-3.66; P=0.01) even after adjustment for age, sex, loop diuretic therapy, anticoagulant therapy, proton pump therapy, coexistent chronic obstructive pulmonary disease, diabetes mellitus, renal insufficiency, and chronic liver diseases. In patients with HF, vertebral fractures were positively correlated with female sex, duration of HF, ischemic heart disease, cigarette smoking, and treatment with anti-osteoporotic drugs, and inversely correlated with left ventricular ejection fraction. CONCLUSIONS: Hospitalized patients suffering from HF are at higher risk of vertebral fractures than patients without HF in the same clinical context.

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BACKGROUND: Some clinical studies have demonstrated that skin tests for ß-lactam antibiotics may cause more adverse reactions than skin tests for common allergens. OBJECTIVE: To assess the risk of systemic reactions from penicillin skin testing, based on a pre-test categorization of patients, in order to establish an appropriate strategy for preempting and dealing with cases. METHODS: A case series of 175 patients with a suspected allergy to penicillin was reviewed, and patients were classified as having a low or high probability of allergic sensitization to penicillin, according to their clinical history. For every group, the rate and the increase in the relative risk (RRI) of systemic reactions by skin testing were calculated. The results were compared to those reported in the available literature. RESULTS: In our case series of 175 patients, 52 were classified as having a high probability of being allergic to penicillin, according to their clinical history. Five systemic reactions to skin testing were observed, and these were exclusively in this group (9.61%, RRI = 479). In agreement with the literature, patients with a high likelihood of penicillin allergy showed an increase of up to 10% in the occurrence of systemic reactions at skin testing; in patients who had had severe allergic reactions, this figure was up to 20%. CONCLUSIONS: The RRI of systemic reactions by skin testing is proportional to the pre-test probability of a true immediate hypersensitivity reaction to ß-lactam antibiotics. In the present case series, only patients with high pre-test probability were at risk, and this group should therefore be skin tested and monitored in a hospitalization regimen, where resuscitation staff and access to an emergency room are immediately available.

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BACKGROUND: Specific IgG4 dosing against food is proposed to the public by a lot of commercial laboratories as a reliable method to diagnose food intolerance. Actually, few data on IgG4 responses to foods in adults are available in the literature. In this study we evaluated the clinical utility of specific IgG4 dosing against food in adult patients with suspected food allergy/intolerance. METHODS: A case series of 73 adult patients with suspected food allergy and clinical manifestations of chronic urticaria or other allergy-supposed skin symptoms were tested for specific IgG4 against foods. An open food challenge was carried out for all IgG4-positive food. All positive open tests were controlled by double-blind placebo-controlled food challenge. RESULTS: Forty-five patients (62%) were IgG4 positive for a number of foods, mainly egg, milk, casein and wheat. None of the patients with IgG4-positive testing showed adverse reactions, neither immediate nor delayed, to the corresponding food. CONCLUSIONS: In adult patients, testing for specific IgG4 lacks clinical utility for the diagnosis of food allergy or intolerance. Dosing of IgG4 should not be part of the diagnosis and therapy of adult patients with allergy-like skin diseases.

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BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are a frequent cause of hypersensitivity reactions, therefore, in clinical practice, it's important to find safe and effective substances. OBJECTIVE: To evaluate the tolerability of etoricoxib and its subsequent actual use and safety at home. METHODS: Etoricoxib tolerance was assessed by single-blind-placebo-controlled oral challenges and its subsequent use was checked by a standardized telephone call. The test was performed in 139 subjects (83 single NSAID reactors and 56 multiple NSAID reactors). RESULTS: The drug was not tolerated in 4 cases (2.8%) causing wheals on the face area in 3 single reactors and a severe generalised reaction occurring three hours after the intake of a therapeutic dose in a multiple reactor. The phone calls showed that 64 (52.8%) patients did not take etoricoxib, mostly due to the fear of adverse effects; in 5 cases (4.2%), the practitioner prescribed a different NSAIDs. Only 52 (43%) subjects took etoricoxib after oral challenges; all tolerated the drug but 2 single reactors, who reported a very mild labial oedema. CONCLUSION: Our study confirmed the good long-term tolerability of etoricoxib in patients with a history of hypersensitivity to other NSAIDs without differences between single and multiple reactors. Nonetheless, in NSAID-intolerant subjects this drug should be first challenged in specialised centres due to the risk ofsevere reactions.

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The aim of this study was to evaluate alcohol abstinence in alcoholics and their family relationships after a year of treatment. The 100 alcoholics recruited were divided into two groups: ALC, where treatment consisted of clinical control and meetings of with the family consulting together with their relatives at the Centre for Study and Treatment of Alcoholism and CAT, where treatment consisted of clinical control and weekly attendance together with their relatives at Alcoholics-in-Treatment-Clubs (CAT). The clinical condition of the sample was assessed by laboratory data. The subjects were given an MQ-Quant questionnaire, based on an artificial neural network (ANN) model, which analyses the communicative fatigue of their interactions. The same examination was applied after 1 year excluding patients relapsed and their relatives. Psycho-medical-social treatment by the attendance of alcoholics and their families into a Multifamily Community induces alcohol abstinence of about 79%. This percentage is greater than psycho-medical treatment carried out in the Centre of Alcoholism for ALC group (50%). We observed a significant difference between the communicative fatigue of the ALC group compared to the CAT group.

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The present study attempted to establish whether long term abstinence from alcohol restores the stimulatory effects on GH secretion of gamma-aminobutyric acid (GABA) and gamma-hydroxybutyric acid (GHB) that are absent during the first month of alcohol withdrawal. Six 4-year abstinent alcoholic subjects--already tested with GHB 4 years earlier, and seven age- and weight-matched normal controls, were tested p.o. with 800 mg sodium valproate (a drug that enhances endogenous GABA activity), 10 mg baclofen (a GABA(B) receptor agonist), 25 mg/kg body-weight GHB, or a placebo. The blood samples for growth hormone (GH) assay were taken every 30 min for the next 150 min. Placebo administration did not modify GH secretion in any subject. All drugs induced a significant increase in serum GH levels in normal controls. GH secretion in abstinent alcoholics did not change after baclofen or sodium valproate administration, whereas the GH response to GHB was similar to that observed in normal controls. The data confirm previous observations which suggest that different neuroendocrine mechanisms underlie GABA and GHB control of GH secretion. The data also indicates that the GHB--but not the GABA--stimulated pathway returns to normal in alcoholics after 4 years abstinence.

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To investigate whether sodium sensitivity of blood pressure participates in the relationship of arterial hypertension to chronic alcohol consumption, 30 alcoholics detoxified from 6 to 12 months and 30 teetotaler controls underwent a dietary sodium manipulation study. They received a daily 55 mmol sodium diet for 7 days, followed by a 260 mmol sodium diet for 7 days. Changes in 24-hour urinary sodium excretion between the end of each period were similar in alcoholics and controls (202+/-16 SEM mmol and 227+/-11, respectively). Plasma renin activity in alcoholics was lower than in controls at both low (2.4+/-0.4 ng angiotensin I/mLxh(-1) versus 3. 7+/-0.2, P<0.003) and high sodium intake (0.47+/-0.10 versus 0. 82+/-0.10, P<0.05), with smaller variations in alcoholics (-1.9+/-0. 3 versus -2.9+/-0.2, P<0.009). In alcoholics, alteration in sodium intake was followed by greater changes in both systolic and mean blood pressure (ambulatory blood pressure monitoring), which rose by 10.6+/-2.2 mm Hg and 7.3+/-1.5 versus 4.7+/-1.4 and 3.9+/-1.0 in controls, respectively (P<0.03 for systolic and P<0.05 for mean blood pressure). The ratio of changes in mean blood pressure to those in 24-hour urinary sodium excretion was higher in alcoholics (0.044+/- 0.011 mm Hgxmmol(-1) versus 0.018+/-0.0041, P<0.005). Our data show that in detoxified alcoholics, there is an abnormal response of both blood pressure and plasma renin activity to variations in salt intake similar to that in sodium-sensitive arterial hypertension. The precise relationship between the sodium sensitivity of blood pressure in detoxified alcoholics and the long-term influence of alcohol on blood pressure remains to be elucidated.

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In order to study the effects of exposure to heat, cardiovascular and hormonal responses were measured in 10 male cocaine addicts (after 4 weeks and 1 year of abstinence) and in 10 normal men. Subjects sat for 30 minutes in a sauna room. Hormonal (ACTH, beta endorphin, (beta EP) met enkephalin (met-enk), prolactin (PRL), cortisol) and cardiovascular parameters (heart rate, systolic and diastolic blood pressure) were measured before and after heat exposure. Basal levels of ACTH, beta EP, Met-Enk and cortisol were similar in normal and in cocaine addicts, whereas plasma PRL values were higher in drug abusers after long-term abstinence. All the examined hormones, with the exception of Met-Enk, were significantly raised in normal control subjects at the end of sauna. In contrast, no significant hormonal response to hyperthermia was observed in cocaine addicts either after 4 weeks and 1 year of abstinence. No changes were detected in heart rate and blood pressure in each group, indicating that the cardiovascular adaptive responses to hyperthermia in cocaine addicts was unaltered. The results of the present study provide evidence of an impairment of the hormonal response to hyperthermia in cocaine abusers. In conclusion, cocaine abuse produces alteration in the hypothalamic-pituitary function which persists after a long period of abstinence.

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BACKGROUND: To gain a better insight into the alterations of the hypothalamic-pituitary-adrenal axis in alcoholism, we evaluated the ACTH response to nicotine inhaled from cigarette smoking (two nonfilter cigarettes in succession within 10 min) in nine nonalcoholic men and nine age- and weight-matched alcoholic men who had been addicted to alcohol for at least 8 years. All subjects were regular cigarette smokers. METHODS: Alcoholic men were tested after 2 weeks of abstinence, when the possible interferences because of alcohol assumption or the acute withdrawal period had completely ceased, and again after 12 weeks of abstinence. RESULTS: At both 2 and 12 weeks of abstinence, basal plasma ACTH and cortisol levels were not significantly different in the alcoholic men from those observed in the control group. In the control group subjects, cigarette smoking induced a striking increase in the circulating concentrations of ACTH and cortisol, with peak responses 1.4 and 1.5 times higher than baseline at 20 and 30 min, respectively. In contrast, no significant ACTH/cortisol increase was observed in alcoholic subjects at any time after cigarette smoking in any test. CONCLUSION: These data suggest that alterations of nicotinic cholinergic transmission occur in the control of ACTH secretion in the alcoholic men, providing further evidence of modification of the hypothalamic-pituitary-adrenal axis in alcoholism.

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OBJECTIVE: To evaluate, in chronic alcoholics, the effects of accompanying diet on the release of insulin (IRI) and glucagon (IRG) and on the hepatic glucose production. METHOD: We evaluated variations of the response to the infusion of arginine into 16 male and 8 female chronic alcoholics divided into three groups of eight subjects each before and after three weeks of treatment with: (1) an isocaloric diet plus 200 g/day of ethanol; (2) an hypocaloric diet without alcohol (17.5 kcal/kg/day); and (3) an isocaloric diet (35 kcal/kg/day). Statistical evaluation was done by Kruskall-Wallis ANOVA and by Wilcoxon matched-pairs signed rank test. RESULTS: After isocaloric diet plus ethanol both IRI/IRG ratios and plasma glucose during arginine testing remained unmodified; after the hypocaloric diet IRI/IRG remained unmodified and the arginine-induced plasma glucose rise was slightly but significantly reduced; after the isocaloric diet there was a strong decrease of the arginine-induced plasma glucose rise because of a significant increase in the insulin/glucagon ratio. CONCLUSIONS: In chronic alcoholics the replacement of the usual hypocaloric diet with an isocaloric one while maintaining alcohol consumption does not modify the metabolic response to arginine administration; the hypocaloric diet without alcohol increases insulin and glucagon release and slightly decreases liver glycogenolysis; the replacement of the usual hypocaloric diet with an isocaloric one together with alcohol withdrawal stimulates insulin, inhibits glucagon release and lowers glycogenolysis much more than observed with hypocaloric diet alone.

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Alcohol abuse is commonly associated with reduced bone mass and osteoporosis as a consequence of both systemic and direct cellular effects. To clarify some of the pathways by which alcohol exerts its actions directly on bone cells, we investigated the formation of early osteoblast progenitors (colony-forming units for fibroblasts; CFU-F) in long-term murine and human bone marrow cultures exposed to ethanol and to its main metabolite, acetaldehyde. In murine bone marrow cultures, obtained from Swiss female mice, ethanol inhibited CFU-F formation (maximal reduction +/- SEM: 50 +/- 2%; p < 0.01) at concentrations ranging from 0.04% to 0.6% that are similar to those reached in vivo in alcoholics. Acetaldehyde strongly reduced CFU-F formation at concentrations of 0.004% and 0.02%, and completely abolished it at the dose of 0.06%. Similarly, ethanol (at concentrations > or =0.02%) and acetaldehyde (from 0.004% to 0.06%) significantly decreased the number of CFU-F in human bone marrow cultures; the mean reduction observed with ethanol was 63 +/- 12% (p < 0.05), whereas acetaldehyde completely prevented CFU-F formation at the concentration of 0.06%. These in vitro observations were confirmed by the in vivo findings that the CFU-F formation in bone marrow cultures from nine young, chronic, noncirrhotic alcoholics was significantly reduced (70 +/- 15%), compared with seven age-matched normal subjects (p < 0.01). In addition, acetaldehyde inhibited cell proliferation in human osteoblastic cells (MG-63 and HOBIT cell lines), whereas ethanol reduced proliferation only in MG-63 cells. Our results indicate that ethanol and acetaldehyde may directly inhibit the osteoblastogenic potential of the bone marrow, and this effect may contribute to the decreased bone formation observed in alcoholics.

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During cocaine addiction the hypothalamus-pituitary axis is widely affected and a blunted response of thyroid stimulating hormone (TSH) to thyroid releasing hormone (TRH) consistent with a hyperthyroid state has been observed. Since the thyroid status can affect the release of growth hormone (GH) the authors evaluated TSH and GH responses to TRH in cocaine addicts at the time of drug withdrawal and 30 days after. Twenty-six male cocaine addicts and 11 healthy male control subjects agreed to participate in the study. TRH and placebo tests were performed at random at 5 day intervals at the time of drug withdrawal and after 30 days. In drug addicts, at the time of the first test basal plasma levels of freeT3, freeT4 and TSH were normal, but the TSH response to TRH was impaired. After 30 days of cocaine abstinence basal freeT4 plasma levels were significantly lower, and TSH levels and the TSH response to TRH were higher than in the first test. At the first examination, basal GH concentrations were similar in cocaine addicts and in control subjects and GH did not respond to TRH. After 30 days of abstinence, basal GH plasma levels were unmodified, but the TRH became stimulatory of GH release in cocaine-deprived, but not in control subjects. In conclusion, in cocaine addicts, drug withdrawal is associated with a condition of subclinical hypothyroidism that makes the GH-releasing machinery sensitive to TRH.

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The present study was performed in order to establish, with a simple and safe neuroendocrinological test, whether alcoholism is associated with alterations in sensitivity to benzodiazepines. For this purpose, we tested the stimulatory effects of diazepam on GH secretion. An intravenous bolus of 10 mg diazepam was injected in 51 (33-51-year-old) alcoholic men after at least 5 weeks of abstinence and in 20 age- and weight-matched normal controls. On a different occasion, a control test with placebo (physiological saline) was performed in the same subjects. Diazepam but not placebo administration induced a striking increase of GH secretion in the normal controls. In contrast, neither diazepam nor placebo treatment significantly changed the basal serum GH levels in alcoholic men. These data show that alcoholism is associated with disrupted benzodiazepine activity on the hypothalamic-pituitary control of GH secretion. The simplicity of the diazepam GH-releasing test makes the drug suitable for clinical research in alcoholism.

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In order to establish possible alterations in the gamma-aminobutyric acid (GABA)ergic control of growth hormone (GH) secretion in alcoholics, 800 mg sodium valproate (a drug enhancing endogenous GABA activity), 10 mg baclofen (a GABA(B) receptor agonist) or a placebo were given orally to nine normal men (age 38-48 years) and nine 2-4-week-abstinent alcoholics (age 35-50 years; duration of alcohol consumption 3-6 years). Blood samples for GH assay were taken every 30 min for the next 150 min. Both drugs induced a significant increment in serum GH levels in the normal controls; mean peak was 7.2 and 3.27 times higher than baseline after sodium valproate and baclofen, respectively. In contrast, GH secretion in alcoholic patients did not change after baclofen or sodium valproate administration. Placebo administration did not modify GH secretion in any subject. In concurrence with previous reports showing alterations of GABAergic neurotransmission in the central nervous system of patients affected by alcoholism, these data show the loss of the GABAergic mechanism(s) underlying the GH response to sodium valproate and/or baclofen action in alcoholism.

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BACKGROUND: The aim of the present study was to establish whether the persistence of residual beta-cell activity after long-term diabetes mellitus (DM) exerts a protective role on luteinizing hormone (LH) secretion. METHODS: The LH responses to stimulation with gonadotropin-releasing hormone (Gn-RH) (100 microg in an i.v. bolus) or naloxone (4 mg injected in an i.v. bolus, followed by the constant infusion of 8 mg in 2 h) were measured in C-peptide-positive (CpP) and C-peptide-negative (CpN) normally menstruating women with short-term (group 1 < 3 years, CpP n = 11, CpN n = 11) or long-term (group 2 > 10 years, CpP n = 11, CpN n = 11) DM and in age-matched normal control subjects (n = 11). RESULTS: Gn-RH induced significant increments in LH secretion in all groups. Significant LH responses to naloxone were observed in all groups, except in group 2 CpN patients. However, the LH response to either Gn-RH or naloxone was significantly lower in group 1 CpN, group 2 CpP and group 2 CpN patients than in the normal control subjects. Furthermore, the LH response was significantly lower in group 2 CpP than in group 1 CpP patients and in group 2 CpN than in group 1 CpN subjects. CONCLUSIONS: These results indicate a role for both deficiency in residual endogenous insulin secretion and duration of diabetes in the derangement of LH secretory control. The data suggest that the protective role exerted by residual beta-cell activity on LH secretion during the early years of DM diminishes with time elapsed after the onset of diabetes mellitus.

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In order to establish whether nitric oxide (NO) is involved in the regulation of basal and/or TRH- or metoclopramide (MCP)-stimulated PRL secretion, normal male subjects were treated i.v. with the NO-synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) (40 mg/kg injected plus 50 mg/kg infused over 60 min) in basal conditions (N.7 subjects) or just before the PRL releasing hormone TRH (20 or 200 microg iv) (N.7 subjects) or the antidopaminergic agent MCP (1 or 10 mg iv) (N.7 subjects). In control experiments, subjects received normal saline instead of L-NAME. The administration of L-NAME modified neither the basal secretion of PRL, nor the PRL release induced by TRH (20 or 200 microg) or MCP (1 or 10 mg). These data suggest that in humans, NO is not involved in the control of PRL release at the anterior pituitary level.

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Chronic alcohol consumption profoundly affects hypothalamic-pituitary function. The present study was performed in order to establish whether alcoholism modifies the effects of melatonin (MEL) on the neuroendocrine control of growth hormone (GH) secretion. For this purpose, the effects of oral administration of 12 mg MEL or placebo on basal and hypoglycemia-stimulated GH secretion were tested in nine (40-52-year-old) alcoholic men after 10-31 days of abstinence and in nine age- and weight-matched normal controls. Hypoglycemia was induced with an intravenous bolus injection of 0.15 IU/kg body weight of insulin. MEL but not placebo administration induced a small, but significant increase in basal GH secretion in the normal controls. In contrast, neither MEL nor placebo treatment significantly changed the basal serum GH levels in alcoholic men. Both groups showed a similar hypoglycemic pattern after insulin administration. The GH response to insulin-induced hypoglycemia was significantly lower in alcoholic than in normal subjects. MEL administration significantly reduced hypoglycemia-induced GH rise in the normal controls, but not in alcoholic patients. These data show that alcoholism not only reduces the GH response to insulin-induced hypoglycemia, but also abolishes MEL actions on basal and hypoglycemia-stimulated GH secretion.

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This study discusses the effect of gammahydroxy butyric acid (GHB) on growth hormone (GH) secretion changes in cocaine addicts. Ten male cocaine users and 10 normal controls were tested with a single oral administration of GHB at a dose of 25 mg/kg body weight. Cocaine addicts were tested before and after 30 days of abstinence. All subjects underwent a control with a placebo. Basal GH levels were similar in normal controls and cocaine users and remained unmodified during the control test. In the normal control subjects, plasma GH levels rose significantly after the administration of GHB; in contrast, plasma GH concentrations failed to increase after GHB treatment in cocaine addicts. These data show that a chronic abuse of cocaine induces alterations of the GABAergic system which were unmasked by the absent GH response to GHB.

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Chronic alcohol drinking causes profound alterations in hypothalamic-pituitary function. In the present study, endocrine [corticotropin (ACTH), beta-endorphin, cortisol, and met-enkephalin] and cardiovascular (blood pressure) changes in response to hyperthermic stress (sauna at 90 degrees C for 30 min) were evaluated in 25 normal men (25 to 50 years old) and in 48 male alcoholic subjects (34 to 56 years old) after 5 weeks of abstinence. Significantly lower increments in systolic blood pressure were observed in alcoholics than in control subjects. Furthermore, alcoholics showed lower ACTH, beta-endorphin, and cortisol increments in response to sauna than normal controls. In contrast, sauna-induced hyperthermia did not change significantly the circulating met-enkephalin levels in either normal controls or chronic alcoholics. These data suggest that an impairment in the adaptive response to stress affects alcoholic men even after a few weeks of abstinence from alcohol.

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Alcoholism is sometimes associated with a blunted thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH; peak minus baseline < 5 mIU/liter), despite basal TSH and thyroid hormone levels within the normal range. In light of the inhibitory effect of somatostatin on TSH secretion, we examined whether this condition is caused by an increased hypothalamic somatostatinergic tone in alcoholic subjects. To answer this question, 16 euthyroid male alcoholics (aged 38 to 50 years) with normal [n = 8; normal responder alcoholics (NRAs)] or blunted [n = 8; low responder alcoholics (LRAs)] TSH response to TRH were selected in a preliminary TRH test (200 micrograms in an intravenous bolus). In addition, 8 age- and weight-matched normal men were tested with TRH and used as normal controls (NCs). NCs and alcoholic patients showed similar basal serum TSH, free triiodothyronine, and free thyroxine levels. All subjects were tested again with TRH, 60 min after treatment with 180 mg of pyridostigmine orally. According to selection criteria, NCs and NRA groups showed similar TSH responses to TRH, whereas TRH-induced TSH rise was strikingly lower in LRAs than in NCs and the NRA group. Pyridostigmine did not change the basal levels of TSH in any group, whereas it enhanced in a similar manner the TRH-induced TSH rise in the NC and NRA groups. No significant change in the TSH response to TRH was observed in LRA patients after pyridostigmine treatment. These data argue against the possibility that an enhanced somatostatinergic tone is responsible for the blunted TSH response to TRH observed in some alcoholic patients. This phenomenon might be attributed to alcohol-related defects of stimulated pituitary thyrotroph secretory capacity in some individuals, possibly due to genetic vulnerability and/or the toxic effects of prolonged alcohol abuse.

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