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Dermatitis artefacta is a disease characterized by self-inflicted skin lesions in fully aware patients. Mechanical and chemical devices are most commonly used to produce such injuries. Several psychological disorders like depression, obsessive compulsive disorders, hysteria, etc. are associated with this kind of disease. Most of the patients are young females aged between 15 and 30, but the diagnosis of dermatitis artefacta may even be made in pediatric patients or elderly people. Because of its rarity and the polymorphism of lesions, dermatitis artefacta is often a challenge for the clinicians. More difficulties might be due to the lack of cooperation in these patients, who usually refuse the dialogue with doctors and deny their primary role in damaging their skin. We present a case of an elderly woman who showed a peculiar pattern of deep excoriating lesions disseminated on the upper part of her body, with an evident state of depression. Diagnostic and therapeutic procedure, that is often long lasting and difficult in such cases, was made by teamwork of dermatologists, psychiatrists and psychologists, leading to steady control of impulses and full remission of cutaneous symptoms.

Different mitogens are involved in the pathogenesis of kidney damage after subtotal nephrectomy. One of them, TGF-beta, controls mesangial cell proliferation and interstitial fibrosclerosis. The transduction of the TGF-beta signal is controlled by intracellular signalling molecules such as Ras G monomeric proteins. Renal damage after subtotal nephrectomy (5/6 Nx) can be prevented by heparins, but so far no immunohistochemical correlation between TGF-beta, TGF-beta induced matrix molecules and Rho proteins has been investigated. Since the Ras transduction pathway has recently been associated with progression of renal damage, we evaluated the effect of heparan sulphate (HS) on the expression of TGF-beta, laminin, fibronectin and a Ras protein, RhoA, in the rat remnant kidney model.The immunoperoxidase technique was employed to reveal the antigens on 18 remnant kidneys from 5/6 nephrectomized rats, nine untreated and nine treated with oral HS, and on seven normal kidneys from sham-operated rats. Data were semiquantitatively analyzed by an image analyzer (Quantimet, Leica).The expression of the antigens was significantly higher in the remnant kidneys than in normals. The high TGF-beta, laminin, fibronectin and RhoA expression observed in subtotally nephrectomized rats suggests a role for these molecules in the pathogenesis of progressive renal damage. However, apart from RhoA, HS-treated rats had significantly lower levels of the antigens than the untreated rats.HS treatment is associated with significantly lower renal expression of TGF-beta, laminin and fibronectin, but not of RhoA. This suggests that the renal-protective effect of HS may be obtained by modulating the TGF-beta pathway, independently of RhoA-mediated transduction.

Hyperhidrosis is an idiopathic condition of exaggerated sweat production resulting in dramatic impairments of daily activities, social interactions and occupational activities. The aim of the present study was to evaluate correlation between a subjective (Dermatology Life Quality Index) and an objective (Minor test) criterion and to assess difference in their levels over time in patients affected by axillary hyperhidrosis treated with botulinum toxin type A. Nineteen patients received injections of 50 U of botulinum toxin type A per axilla. Patients were observed for 9 months after treatment. All patients showed great improvement of hyperhidrosis by Minor test and Dermatology Life Quality Index following treatment with botulinum toxin type A, with the effect persisting for 6-9 months. All patients demonstrated direct relationship between objective improvement documented by Minor test and quality of live improvement documented by Dermatology Life Quality Index after treatment with botulinum toxin type A.

The analysis of myenteric neurons is becoming increasingly important for the assessment of enteric nervous system injury and degeneration occurring in motor disorders of the gut. Limited information is presently available on the quantitative estimation of myenteric neurons and glial cells in paraffin-embedded colonic sections; additional data would be useful for diagnostic purposes. In this morphometric study, we performed immunohistochemistry to count myenteric neurons and glial cells in paraffin sections of human colon. Serial cross sections of formalin-fixed paraffin-embedded full-thickness normal human left colon (n = 10, age-range: 50-72 years) were examined. HuC/D and S100beta antigens were found to be the best markers for the detection of neurons and glial cells, respectively. Significant correlations were noted between the numbers of neurons/glial cells and the respective myenteric ganglion areas. These findings suggest that HuC/D-S100beta-immunostained paraffin cross sections of human colon can be regarded as valuable tools for the quantitative estimation of myenteric neurons and glial cells. Based on the present method, only a limited number of paraffin sections are needed for reliable quantitative assessments of myenteric ganglion cells, thus allowing fast and simple approaches in the settings of the histopathological diagnosis of colonic motility disorders and retrospective evaluations of pathological archival tissue specimens.

Beta(3)-adrenoceptor agonists protect against experimental gastric ulcers. We investigated the effects of the beta(3)-adrenoceptor agonist SR58611A on 2,4-dinitrobenzene sulphonic acid-induced colitis in rats and analysed the expression of beta(3)-adrenoceptors in the colonic wall. SR58611A was administered orally (1-10 mg kg(-1)) for 7 days, starting the day before induction of colitis. Colitis was assessed by macroscopic and histological scores, tissue myeloperoxidase activity, interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) levels. Reverse transcription-polymerase chain reaction and immunohistochemical analysis were used to examine the expression of beta(3)-adrenoceptors. SR58611A significantly reduced the severity of colitis as well as the tissue levels of TNF-alpha, IL-1beta and IL-6. Colitis was associated with a decreased expression of beta(3)-adrenoceptor mRNA in the mucosal/submucosal layer of distal colon and this reduction was not affected by SR58611A. Immunohistochemical analysis revealed beta(3)-adrenoceptors within the muscularis externa, in myenteric neurons and nerve fibres and in the submucosa. beta(3)-Adrenoceptor immunoreactivity was decreased in inflamed tissues compared to controls, particularly in the myenteric plexus; this reduction was counteracted by SR58611A. Amelioration of experimental colitis by the selective beta(3)-adrenoceptor agonist SR58611A suggests that beta(3)-adrenoceptors may represent a therapeutic target in gut inflammation.

This study examines the role played by cyclooxygenase (COX) isoforms (COX-1 and -2) in the regulation of colonic neuromuscular function in normal rats and after induction of colitis by 2,4-dinitrobenzenesulfonic acid (DNBS). The expression of COX-1 and COX-2 in the colonic neuromuscular layer was assessed by reverse transcription-polymerase chain reaction and immunohistochemistry. The effects of COX inhibitors on in vitro motility were evaluated by studying electrically induced and carbachol-induced contractions of the longitudinal muscle. Both COX isoforms were constitutively expressed in normal colon; COX-2 was up-regulated in the presence of colitis. In normal and inflamed colon, both COX isoforms were mainly localized in neurons of myenteric ganglia. In the normal colon, indomethacin (COX-1/COX-2 inhibitor), SC-560 [5-(4-chloro-phenyl)-1-(4-methoxyphenyl)-3-trifluoromethylpyrazole] (COX-1 inhibitor), or DFU [5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone] (COX-2 inhibitor) enhanced atropine-sensitive electrically evoked contractions. The most prominent effects were observed with indomethacin or SC-560 plus DFU. In the inflamed colon, SC-560 lost its effect, whereas indomethacin and DFU maintained their enhancing actions. These results were more evident after blockade of noncholinergic pathways. In rats with colitis, in vivo treatment with superoxide dismutase or S-methylisothiourea (inhibitor of inducible nitric-oxide synthase) restored the enhancing motor effect of SC-560. COX inhibitors had no effect on carbachol-induced contractions in normal or DNBS-treated rats. In conclusion, in the normal colon, both COX isoforms act at the neuronal level to modulate the contractile activity driven by excitatory cholinergic pathways. In the presence of inflammation, COX-1 activity is hampered by oxidative stress, and COX-2 seems to play a predominant role in maintaining an inhibitory control of colonic neuromuscular function.