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Background The susceptibility of patients with chronic plaque psoriasis and the risks or benefits related to the use of biological therapies for COVID-19 are unknown. Few data about prevalence, clinical course and outcomes of COVID-19 among psoriatic patients were reported. The aims of this study were 1) to assess the prevalence and severity of COVID-19 in psoriatic patients treated with biologic agents during the first phase of the emergency (22 February to 22 April 2020) in Italy, and 2) to report the clinical outcomes of patients who have been exposed to individuals with confirmed SARS-CoV-2 infection. Methods Patients with moderate-to-severe chronic plaque psoriasis, aged ≥18 years and undergoing treatment with biologic agents as of 22 February 2020, were eligible to be included in PSO-BIO-COVID study. Demographic and clinical characteristics of patients using any biologic for psoriasis treatment between 22 February and 22 April 2020 were registered. For all confirmed or suspected cases of COVID-19, data about concomitant disease, ongoing therapies, and comorbidities were also reported. Results A total of 12,807 psoriatic patients were included in the PSO-BIO-COVID study. In this cohort twenty-six patients (0.2%) had a swab confirmation of SARS-CoV-2 infection. Eleven patients required hospitalization and two died. 125 of 12807 patients (1.0%) with exposure to a patient with COVID-19 under quarantine or active health surveillance, were reported. Conclusion The incidence of COVID-19 observed in our cohort of psoriatic patients (0.2%) is similar to that seen in the general population (0.31%) in Italy. However, the course of the disease was mild in most patients. Biological therapies may likely lessen "cytokine storm" of COVID-19, which sometimes lead to multiple organ failure, ARDS, and death.

Topical treatment is the mainstay for mild or moderate psoriasis, but patients are generally little satisfied. Calcipotriol/betamethasone dipropionate (Cal/BD) cutaneous foam has shown to improve signs and symptoms in plaque psoriasis patients. This study assessed patient's satisfaction with Cal/BD foam in a real-life Italian dermatological clinical practice. A multicenter, 4-week observational prospective cohort study enrolled, in 17 Italian dermatology clinics, adult patients with plaque psoriasis on the body and/or scalp. Treatment satisfaction was assessed by 9-item Treatment Satisfaction Questionnaire for Medication (TSQM-9), preference over previous treatments by Patient Preference Questionnaire (PPQ), and change in disease state by Psoriasis Area Severity Index (PASI). Overall 256 patients were eligible, with a mean (SD) age of 55.6 (15.4) years, 59.4% were males. Psoriasis severity was mild in 52.0% of patients, moderate in 43.3%, and severe in 4.7%. Scalp involvement was present in 36.7% of patients. Previous antipsoriatic treatments had been received by 80.5% of patients. TSQM-9 median (25th-75th percentile) scores were 83.3 (66.7-88.9) for effectiveness, 77.8 (66.7-88.9) for convenience, and 78.6 (64.3-92.9) for global satisfaction. Mean (SD) PASI value decreased from 7.3 (4.8) to 2.1 (2.7) after 4 weeks. More than 90% of patients previously treated for psoriasis evaluated the Cal/BD foam more effective, easier to use and better tolerated compared to previous topical treatments at PPQ. This observational study provides real-life evidence of a high level of satisfaction with effectiveness and convenience of the Cal/BD foam in a cohort of plaque psoriasis patients, with an objective improvement in PASI.

Psoriasis is a multifactorial chronic inflammatory skin disease characterized by erythemato-squamous lesions with a chronic relapsing course. The desease clinical activity (PASI) and the patient's quality of life (DLQI) are the main elements to assess for setting up a correct therapeutic management.The aim of the study was to evaluate the management of the patient with moderate-severe psoriasis in therapy with biological drugs and to establish the difference in the achievement of PASI 90 and DLQI 0-1 between a group of patients treated with only biological drugs and a group of patients receiving biologic therapy in combination with a topical ointment.We conducted a prospective, observational real-life study enrolling 60 patients with moderate to severe psoriasis and divided in two groups: Group A patients treated with biological drugs, Group B patiens treated with biological drugs in association with an ointment composed of betamethasone, salicylic acid and ammonium sulpho-ichtyolate, applied 2 times a day. PASI and DLQI were evaluated at study beginning (T0) for both study groups, after 12 weeks (T3) for sample in therapy with biological drugs and after 24 weeks (T6) for sample in co-medication therapy.The two-way ANOVA method was used to evaluate the standard deviations (SD): at T3 and T6 Group B obtained a significant PASI reduction and improvement of DLQI (* p value0.05) compared to Group A.Our study shown that the patients treated with biologics in co-medication with topical therapy reached a significantly higher PASI and DQLI compared with those treated with only biologics. Furthermore we observed that the association with topical oinment showed more efficacy in the treatment of areas such as palm-plantar region, that is often difficult-to-treat region, even for biologic drugs.

Basal cell carcinoma (BCC) is the most frequent skin cancer and is characterized by slow growth, even if it can be locally invasive and rarely metastasizes. Many different phenotypic presentations and histopathologic subtypes have been described, and the current guidelines subdivide BCCs into low-risk (nodular and superficial) and high-risk subtypes (micronodular, infiltrating, and morphoeic BCC and those with squamous differentiation). Dermoscopy allows the identification of the features associated with these different subtypes. Compared with the low-risk forms of BCC, more aggressive ones tend to undergo more frequently incomplete surgical excision and perineural invasion, so the identification of these lesions before surgery is extremely important. The gold standard of treatment is surgery, particularly for the H region of the face and infiltrative lesions, but other options are available and selected according to many variables, including body area, age, comorbidities, and clinical, dermoscopic, and histopathological features of the lesion. Moreover, the possible complications of surgical approaches, namely healing defects, failure of skin grafts, and wound infection, should be considered. In this review we discuss the management of BCC localized on the face and scalp, according to the currently available treatment options.

Objective-Arginase can reduce NO availability. In this study, we explored arginase as a determinant of endothelial dysfunction in small arteries from obese patients and its relationship with aging and microvascular remodeling. Approach and Results-Small arteries were dissected after subcutaneous fat biopsies and evaluated on a pressurized micromyograph. Endothelium-dependent vasodilation was assessed by acetylcholine, repeated under L-NAME (NG-nitro-L-arginine-methyl ester), N(ω)-hydroxy-nor-l-arginine (arginase inhibitor) and gp91ds-tat (NADPH [nicotinamide adenine dinucleotide phosphate oxidase] oxidase inhibitor) in vessels from young (age 30 years) control and obese subjects. Media-lumen ratio and amount of vascular wall fibrosis were used as markers of vascular remodeling. Amount of vascular superoxide anions and NO production were determined with immunofluorescence, whereas arginase expression was quantified using Western blot and quantitative polymerase chain reaction. Obese and older age groups had lower vascular NO, as well as higher media-lumen ratio, wall fibrosis, intravascular superoxide, and blunted inhibitory effect of L-NAME on acetylcholine versus controls and younger age groups. N(ω)-hydroxy-nor-l-arginine restored the acetylcholine-induced vasodilation in young and, to a lesser extent, in old obese subjects. This effect was abolished by addition of L-NAME. Gp91ds-tat increased the vasodilatory response to N(ω)-hydroxy-nor-l-arginine in old obese. Superoxide anions and arginase I/II levels were higher in the vascular wall of obese versus controls. Conclusions-Arginase contributes to microvascular endothelial dysfunction in obesity. Its impact is reduced by aging because of higher levels of vascular oxidative stress. Obesity is accompanied by accelerated microvascular remodeling, the extent of which is related to the amount of arginase in the vascular wall. © 2018 American Heart Association, Inc.

Questo nuovo testo di istologia, destinato alle lauree triennali è stato redatto tenero conto dell'evoluzione della disciplina e delle necessità formative delle lauree triennali sanitarie, ognuna delle quali richiede uno specifico insegnamento.

Aims. Cyclooxygenase isoforms (COX-1, COX-2) have been implicated in the development of fibrosis at gastrointestinal sites. Under bowel inflammation, transforming growth factor beta (TGF-beta) has been identified as the main regulator of fibrotic remodelling. The present study investigated the effects of cyclooxygenase inhibitors on pro-fibrotic signalling mediated by the TGF-beta/SMAD pathway in experimental colitis. Methods. Colitis was induced in rats by intrarectal 2,4-dinitrobenzenesulfonic acid (DNBS, 30 mg/rat in 0.25 ml ethanol 50%). After 6 days, systemic [body and spleen weight] and tissue inflammatory parameters [macroscopic and microscopic damage] were assessed. Three days before colitis assessment, the animals were treated daily with indomethacin (IND, non-selective COX-1/COX-2 inhibitor, 2 mg/kg), SC-560 (SC, selective COX-1 inhibitor, 2.5 mg/kg), or celecoxib (CEL, selective COX-2 inhibitor, 1 mg/kg) by intragastric gavage. At the time of sacrifice, functional and molecular tests were carried out. Peristaltic activity of control and inflamed colonic segments was studied in vitro by a modified Trendelenburg set-up. Collagen fibers (Van Gieson) and elastic fibers (orcein) were examined by histochemistry. The expression of molecular factors involved in TGF-beta signalling (TGF-beta, RhoA and SMAD6, as well as phosphorylated SMAD2, p38, ERKs and JNK), and cellular proliferation and apoptotis (PCNA, Akt and caspase-3) was analyzed by western blot. Results. Animals with colitis displayed an impairment of colonic peristalsis, as shown by a significant decrease in compliance and maximal ejection pressure, as well as an increase in the threshold pressure and luminal volume required to trigger peristalsis. Moreover, histochemistry showed an increased deposition of collagen fibers in parallel with a dramatic decrease in elastic fibers. IND, SC and CEL inhibited collagen deposition, and reverted the loss of elastic fibers. In the inflamed/fibrotic colon, western blot analysis revealed an increased expression of TGF-beta, PCNA, caspase-3, pAkt, p-p38, RhoA and pSMAD2. By contrast, the expression of SMAD6, pERKs and pJNK was reduced. In this setting, IND, SC and CEL counteracted the increased expression of TGF-beta, RhoA, pSMAD2 and p-p38, and partly reverted the reduced expression of SMAD6. Conclusions. In the DNBS model of colitis, bowel fibrosis is associated with impaired colonic peristalsis and alterations in the expression of factors driven by activation of TGF-beta signalling. The pharmacological blockade of COX-1 and COX-2 is able to counteract the fibrotic remodelling of inflamed colon, and this action appears to depend on the modulation of TGF-beta-dependent SMAD signalling, particularly through an induction of the inhibitory protein SMAD6 and a reduction of the phosphorylated status of SMAD2.

Parkinson’s disease (PD) is characterized by degeneration and loss of dopaminergic nigrostriatal neurons, responsible for neurologic symptoms. Besides motor signs, most PD patients experience gastrointestinal (GI) disturbances, including dyspepsia and constipation, which impair severely their quality of life. The pathophysiology of digestive disturbances in PD is largely unknown, but recently a link between PD and colonic inflammation has been observed in human biopsies [1]. Our study aims at evaluating some inflammatory patterns in colonic whole wall in a rat model of PD. PD was induced in rats by unilateral injection of 6-idroxydopamine (6-OHDA) into two sites of the right medial forebrain bundle. Studies were carried out 28 and 56 days after treatment on full-thickness samples from distal colon. The following parameters were examined: tissue malondialdehyde (MDA), an index of membrane lipid peroxidation; tumor necrosis factor (TNF), an index of inflammatory cytokine release; inflammatory cells (eosinophils, mast cells); glial fibrillar acid protein (GFAP) and substance P (SP) expression in myenteric ganglia by immunohistochemical staining. At both time points 6-OHDA-induced nigrostriatal denervation was associated with significant increase in: a) tissue levels of MDA (membrane oxidative stress) and TNF (tissue inflammation); b) density of eosinophil and mast cell in tunica mucosa and submucosa (inflammatory infiltration); b) GFAP expression in myenteric ganglia of tunica muscularis (enteric glia activation); c) SP expression in myenteric neurons, which is compatible with an enhanced tachykinenergic motor control as shown by preliminary functional studies on colonic muscle strips from PD rats. Our findings suggest that experimental PD, elicited by nigrostriatal dopaminergic degeneration, is associated with an inflammation of the colonic wall involving all layers. These results support the view that peripheral enteric neuroinflammation may account for GI motor dysfunctions in PD., Italian Journal of Anatomy and Embryology, Vol 119, No 1 (Supplement) 2014

Psoriasis is a systemic inflammatory immune-mediated skin disease. Recently a relationship with metabolic syndrome in terms of psoriasis severity and response to therapy was observed.We performed an open-label randomized controlled study to evaluate the role of a nutraceutical containing Q10 coenzyme, Krill-oil, lipoic acid, resveratrol, Vitis vinifera seed oil, vitamin E and selenium in addition to etanercept therapy for patients affected by psoriasis and metabolic syndrome. Forty patients were enrolled and divided into two arms, one receiving only etanercept, one other receiving also the neutraceutical. After a period of 3 months (T1) a second evaluation of the considered parameters was performed.At T1 statistically significant differences were detected in HDL cholesterol and triglycerides values both comparing the two arms and in the nutraceutical arm.Our results show that the dietary addiction of the nutraceutical to the etanercept therapy in patients affected by both psoriasis and metabolic syndrome could help to restore the normal lipid profile.

Intestinal fibrosis in inflammatory bowel disease is a dynamic, multifactorial process, which involve multiple cell types and interconnected events [1]. Angiogenesis is a hallmark of active gut disease and closely related to fibrogenetic processes. Endothelial cells and pericytes of neovessels have been found to be able to differentiate into fibroblasts and can be considered good candidates for fibrogenesis also in the intestinal tract [2]. This study was aimed to study whether the fibrotic processes occurring within the tunica muscularis of UC patients are associated with vascular remodeling. Full-thickness left colonic samples were obtained from patients with established, severe and pharmacologically unresponsive UC, who underwent bowel resection. Routine histology, histochemistry and immunohistochemistry were conducted in paraffin cross-sections. Collagen and elastic fiber distribution was evaluated within the tunica muscularis by both histochemical and immunohistochemical assays. The vascular network pattern was analyzed by revealing the expression of CD31, CD105 and nestin by immunofluorescence applied to laser confocal microscopy. A significant increase in collagen fibers and a decrease in elastin content were detected in the tonaca muscularis of UC inflamed colon, as compared with controls. In particular, enhanced collagen deposition were found at level of the longitudinal muscle and circular muscle layer, and in perivascular spaces. By contrast, elastic fiber pattern was significantly decreased throughout the whole muscle compartment. Increased blood vessel density was observed in the colonic tunica muscularis of UC samples compared with samples from healthy control individuals. In particular, the neovessels of inflamed colon showed the activation of both endothelial cells and pericytes, which overexpressed CD105 and nestin, respectively. A significant vascular remodelling (i.e., angiogenesis, endothelial proliferation and pericyte activation) has been observed in the fibrotic tunica muscularis of colon from UC patients. On the basis of the present findings, it is possible to argue that cells of newly formed vessels within the tunica muscularis may contribute to the UC-associated fibrosis by cell transition to mesenchymal phenotype., Italian Journal of Anatomy and Embryology, Vol 118, No 2 (Supplement) 2013