Search

Abstract Background Chlamydophila pneumoniae and Mycoplasma pneumoniae are associated with acute exacerbation of bronchial asthma (AEBA). The aim of this study was to evaluate the correlation between these acute bacterial infections and the severity of AEBA. Methods We prospectively analysed consecutive patients admitted to the Emergency Department with acute asthma exacerbation. In every patient peak expiratory flow (PEF) measurement was performed on admission, and spirometry during follow-up. Serology for Chlamydophila and Mycoplasma pneumoniae was performed on admission and after 4–8 weeks. Results Fifty-eight patients completed the study. Acute atypical infections (AAI) was observed in 22/58 cases; we found single acute C. pneumoniae in 19 cases, single acute M. pneumoniae in 2 cases, and double acute infection in one case. Functional impairment on admission was greater in patients with AAI than in patients without AAI (PEF 205 ± 104 L/min vs 276 ± 117 p = 0.02) and persisted until visit 2 (FEV1% 76.30 ± 24.54 vs FEV1% 92.91 ± 13.89, p = 0.002). Moreover, the proportion of patients who presented with severe AEBA was significantly greater in the group with AAI than in the group without AAI (15/22 vs 12/36, p = 0.01; OR 4.29, 95% CI 1.38–13.32). Conclusion Our data suggest an association between acute atypical infection and a more severe AEBA.

Background: Chlamydophila pneumoniae and Mycoplasma pneumoniae are associated with acute exacerbation of bronchial asthma (AEBA). The aim of this study was to evaluate the correlation between these acute bacterial infections and the severity of AEBA.Methods: We prospectively analysed consecutive patients admitted to the Emergency Department with acute asthma exacerbation. In every patient peak expiratory flow (PEF) measurement was performed on admission, and spirometry during follow-up. Serology for Chlamydophila and Mycoplasma pneumoniae was performed on admission and after 4-8 weeks.Results: Fifty-eight patients completed the study. Acute atypical infections (AAI) was observed in 22/58 cases; we found single acute C. pneumoniae in 19 cases, single acute M. pneumoniae in 2 cases, and double acute infection in one case. Functional impairment on admission was greater in patients with AAI than in patients without AAI (PEF 205 +/- 104 L/min vs 276 +/- 117 p = 0.02) and persisted until visit 2 (FEV1% 76.30 +/- 24.54 vs FEV1% 92.91 +/- 13.89, p = 0.002). Moreover, the proportion of patients who presented with severe AEBA was significantly greater in the group with AAI than in the group without AAI (15/22 vs 12/36, p = 0.01; OR 4.29, 95% CI 1.38-13.32).Conclusion: Our data suggest an association between acute atypical infection and a more severe AEBA. [ABSTRACT FROM AUTHOR]

Background: Sildenafil is used for pulmonary hypertension treatment and its use is safe in chronic heart failure (HF) patients., Aims: To analyze the effects of sildenafil on lung mechanics, gas diffusion, exhaled nitric oxide (eNO) at rest and during exercise in chronic HF. We did so to evaluate if sildenafil prevents exercise-induced pulmonary edema formation., Methods: We studied 22 chronic HF males. We measured after a single dose of placebo, sildenafil (25 mg) and sildenafil (100 mg), lung diffusion (DLCO), molecular diffusion (DM), pulmonary capillary volume (VC), eNO, all at rest and during exercise, standard pulmonary function, and maximal cardiopulmonary exercise., Results: At rest sildenafil improved pulmonary mechanics and DLCO from 23.1+/-6.3 ml/mmHg/min to 23.9+/-6.4 (25 mg, p<0.05) and to 25.3+/-6.7 100 mg, p<0.02). Sildenafil (100 mg) prevents edema formation (highest DM/VC during exercise). At rest eNO was low and not affected by tested drugs. With light exercise eNO was higher with sildenafil 100 mg. Peak VO(2) increased with sildenafil from 1376+/-331 ml/min to 1471+/-375 (25 mg, p<0.01) and 1524+/-461 (100 mg, p<0.02). Peak VO(2) increase was related to DLCO improvement., Conclusion: In chronic HF sildenafil increases exercise performance, improves lung mechanics and gas diffusion and prevents exercise-induced pulmonary edema formation probably by restoring NO pathways.

Mansonella perstans filariasis is widely present in Africa and equatorial America and its pathogenicity has been recently reconsidered. Although M. perstans infection has been considered a minor filariasis, remaining asymptomatic in most of infected subjects, more recent studies have shown that M. perstans is capable of inducing a variety of clinical features, including angioedemas, swellings like the "Calabar swellings" of loiasis, pruritus, fever, headache, pain in bursae and/or joint synovia, or in serous cavities. It is likely that some of the pathological changes observed are induced by the immune response to the infection. Eosinophilia is present in many cases of infection. Moreover M. perstans filariasis is difficult to be treated. Effective treatment is lacking and there is no consensus on optimal therapeutic approach. The most commonly used drug is diethylcarbamazine (DEC) that is however often ineffective. Although other drugs have been tried (e.g. praziquantel, ivermectin), none has proven to be reliably and rapidly effective. Mebendazole seemed more active than DEC in eliminating the infection, with a comparable rate of overall responses. Thiabendazole evidenced a small, but significant activity against the infection. Combination treatments (DEC plus mebendazole) resulted in a significantly higher activity compared with the single drugs.

Mansonella perstans filariasis is widely present in Africa and equatorial America and its pathogenicity has been recently reconsidered. Effective treatment is lacking and there is no consensus on optimal therapeutic approach. We present the results of a new combination treatment against M. perstans filariasis. Two cases of M. perstans filariasis were treated with the combination of diethylcarbamazine (DEC) and thiabendazole. The treatment was able to significantly reduce microfilaria burden in a case and to achieve complete clearance of blood microfilariae in another case.

Objective: Thrombosis is rare in the young, but can cause severe psychological distress that influences the quality of life and the coping capacities of these patients. This study was meant to increase the understanding of self-perception, social and family functioning and ways of coping with the disease in young patients after an episode of thrombosis., Methods: Seven questionnaires spanning social and family functioning and ways of coping with disease were completed by 50 patients < or = 45 years of age after a first episode of venous or arterial thrombosis. Data were compared with those of 39 healthy individuals with similar age, sex and level of education., Results: Compared to healthy controls, young patients with thrombosis had lower self-esteem, showed higher impairment in social activities and in familial relationships, and used more frequently coping strategies. Most patients used all coping strategies, preferring the more active ones, but more patients than controls used the passive ones, particularly "avoidance" and "religiosity". A correlation was found between the frequency of use of passive or negative coping strategies and some of the psychological, social and familial dimensions that scored more negatively. Greater psychological impairment and differences in coping styles were found in women compared with men and in individuals < 34 years compared with those > or = 34 years., Conclusions: Young individuals with thrombosis develop psychological changes that influence their behaviour, quality of life and coping. This is particularly evident in women and in young patients. Physicians dealing with thrombosis should be aware of this situation and offer psychological support.

Background: Few data are available about the long-term outcome of renal transplantation in patients with systemic lupus erythematosus (SLE)., Methods: Between June 1982 and 2004, a total of 33 adults with lupus nephritis received 35 kidney allografts. Outcomes of these grafts and those of 70 controls matched for age, sex, and donor source who underwent transplantation during the same period were compared., Results: Mean follow-up after renal transplantation was 91 +/- 59 months for patients with lupus and 90 +/- 64 months for controls. Actuarial 15-year patient (80% versus 83%) and death-censored graft survival rates (69% versus 67%) were not significantly different between patients with lupus and controls. Risks for acute and chronic rejection, arterial hypertension, and infection were not different between the 2 groups. Mean serum creatinine levels also were similar in the 2 groups at the last follow-up visit. Intravascular thrombotic events occurred in 9 patients with SLE (26%) and 6 controls (8.6%; P = 0.038). In the SLE group, 6 of 7 antiphospholipid (aPL) antibody-positive versus 3 of 17 aPL antibody-negative patients experienced thrombotic events ( P = 0.015). Recurrence of lupus nephritis was documented in 3 renal grafts (8.6%), but no graft was lost because of recurrent lupus nephritis., Conclusion: Long-term patient and graft survival probabilities were similar in patients with SLE and matched controls. The risk for thrombotic complications was greater in patients with SLE, particularly aPL-positive patients. Nephritis recurred in less than 10% of patients with SLE and did not influence graft survival.

The indications and the choice of renal replacement therapy for lupus patients are similar to those for other uremic patients. However, lupus patients can pose some particular problems. First, 10-28% of patients needing dialysis can have a partial renal function recovery. Therefore, the clinician has to decide whether to administer a rescue treatment, risking side-effects, or to reduce immunosuppression precluding a potential recovery. Many patients on regular dialysis show subdued biological and clinical activity. Others can show a hectic disease activity, particularly in the 1st year. In these cases, treatment is difficult, as vigorous immunosuppression can expose uremic patients to severe side-effects. The presence of circulating antiphospholipid antibodies (aPL) can favor thrombosis or stenosis of vascular access (VA). Renal transplantation is the best therapy for most lupus patients with end-stage renal failure. Many, but not all, studies have reported similar patient and graft survival rates in lupus and in non-lupus transplant recipients. The results are much better with living donor transplantation. Patients with aPL, black patients and those on long-term dialysis have a higher graft failure risk. Candidates with active lupus and/or those with significant iatrogenic morbidity should be advised to wait 6-12 months before transplantation. The recurrence risk of lupus nephritis ranged between 2% and 30% in different studies. The histological picture does not usually show severe features. Antiplatelet agents or anticoagulation can be advised for aPL patients.

Human Vgamma9/Vdelta2(+) T lymphocytes participate in the immune response against intracellular pathogens through the secretion of type-1 cytokines and chemokines and by killing of infected cells. Little is known of the effects by type-2 differentiation of gamma delta cells on these functions. Here, we report that bona fide naive cord blood-derived gamma delta lymphocytes expanded in vitro with the mycobacterial antigen isopentenyl pyrophosphate (IPP) can be differentiated as either type-1 or type-2 cells, in the presence of an appropriate cytokine milieu. Instead, peripheral gamma delta cells from PPD-negative healthy adults displayed a type-1 cytokine profile, i.e. IPP-stimulated secretion of IFN-gamma, but not of IL-4 and IL-10. Moreover, they released the macrophage inflammatory protein (MIP)-1beta, but not IL-8 nor the Th2 chemoattractants I-309 and TARC (thymus and activation-regulated chemokine). This cytokine profile was not significantly affected by in vitro culture in Th2 polarizing conditions. Only in one case out of seven were peripheral gamma delta cells fully differentiated to type-2 lymphocytes, characterized by sustained IL-4 and IL-10 production, along with secretion of substantial amounts of IL-8, I-309 and TARC. Type-2 gamma delta T lymphocytes preferentially expressed the co-stimulatory molecule CD30; conversely, no skewing in chemokine receptor expression was observed. Both polarized populations displayed high levels of CXCR3 in the absence of CCR3, CCR4 and CCR5. Finally, type-1, but not type-2, gamma delta T lymphocytes killed IPP-pulsed U937 cells and displayed elevated perforin content. Overall, our data suggest that type-2 differentiation of gamma delta T lymphocytes profoundly affects both their effector functions and their potential to recruit the appropriate leukocyte subsets to the sites of inflammation.