BackgroundHidradenitis Suppurativa (HS) is a painful, chronic inflammatory skin disease. Global estimates of prevalence vary between 0.03% and 4% of the population.Our main aim was to determine HS prevalence in the Australian adult population focussing on the demographics, management pathways and diagnosis rate of individuals living with HS.MethodsIn this population-based cross-sectional study, 17,050 individuals representative of the Australian adult population were asked through face-to-face household interviews to answer a previously validated HS screening questionnaire with high diagnostic power. Individuals who screened positive were asked additional questions, including previous diagnosis of HS and number/type of physicians consulted regarding their condition.Results11,433 Australian residents answered the HS questionnaire, 88 screening positive for HS (0.77%; 95% CI 0.62–0.95). Considering the previously reported sensitivity (0.97) and positive predictive value (0.85) of the screening questionnaire, HS prevalence was estimated to be 0.67% (95% CI 0.53%-0.84%). 6 of 88 suspected HS individuals reported a pre-existing HS diagnosis (6.8%; 95% CI 3.2%-14.1%). 25.6% of the undiagnosed individuals suspected of having HS had not seen any clinicians regarding their boils; the remaining ones had consulted General Practitioners (96.7%), and clinicians from different specialties. Comparisons of individuals who screened positive for HS versus those who screened negative demonstrated statistically significant differences in gender (p = 0.0046), age (p<0.0001), BMI (p = 0.0307), smoking status (p<0.0001), employment status (p<0.0001) and income (p = 0.0321).ConclusionsThe prevalence of HS in Australia was estimated to be 0.67% (95% CI 0.53%-0.84%). The diagnosis rate amongst the suspected HS cases was low, which appeared to be due to a combination of patients not seeking help and decentralization of care. Individuals suspected of having HS were more likely to be females, young, obese, smokers, unemployed or at home duties and having lower annual personal income in comparison with individuals not suspected of having HS.

. Currently available pharmacological therapies treat arthritis inadequately. We have previously found that the kappa (K)‐opioid, U‐50,488H (trans‐(±)‐3,4‐dichloro‐N‐methyl‐N‐[2‐(1‐pyrrolidinyl) cyclohexyl]‐benzene‐acetamide methane sulphonate), possesses anti‐arthritic effects. In light of the finding that opioid receptors in the periphery are upregulated during inflammation, K‐opioids may represent a novel therapy for arthritis. The primary aim and unique feature of the present study is to investigate whether opioids exert their anti‐arthritic effects in the periphery. Thus, the dose‐effect relationship of a K‐opioid agonist, U‐50,488H was compared after both local and distant administration. Further, we tested whether the anti‐arthritic effects of this drug are stereospecific and receptor‐mediated by use of opioid antagonists. . Using an adjuvant model of arthritis in male Lewis rats, arthritis was judged by oedema, radiography and histological changes in the contralateral ankle of the hind limb. Treatment with (±)‐U‐50,488H for 3 days during disease onset and 3 days during established disease significantly attenuated arthritis, but the effects of (±)‐U‐50,488H on radiology and histology varied according to treatment time. Administration of (±)‐U‐50,488H during disease onset had a more marked effect on radiography, suggesting that treatment with that drug should be started early to prevent progressive joint destruction. Further, it was found that (±)‐U‐50,488H, administered for 3 days during the disease onset, either by direct subcutaneous injection into the inflamed paw or at a more distant site into the back of the neck, dose‐dependently attenuated arthritic damage as measured by an index which pooled all three variables. More importantly however, (±)‐U‐50,488H was approximately fourfold more potent as an ‘anti‐arthritic’ agent after local compared to distant subcutaneous injection (ED50; local vs distant: 5.8 ± 1.6 vs 19.5 ± 0.8 mg kg−1). . Equivalent doses of the (−)−enantiomer (20 mg kg−1 day−1) and the racemate (±) of U‐50,488H (40 mg kg−1 day−1), elicited a similar attenuation of arthritic parameters while the (+)‐enantiomer exacerbated arthritis, suggesting that the anti‐arthritic activity lies solely with the (−)−enantiomer. . Both the peripherally selective antagonist, naloxone methiodide, and the K‐selective antagonist, MR2266 ((−)−5, 9α‐diethyl‐2‐(3‐furylmethyl)‐2′‐hydroxy‐6,7‐benzomorphan), were able to reverse fully the peripheral anti‐arthritic effects of U‐50,488H, indicating that it exerts its effects through peripheral K‐opioid receptors. . Taken together, these results not only confirm our previous findings that demonstrate anti‐arthritic effects of U‐50,488H but they indicate that the opioid attenuation of experimental arthritis is mediated via peripheral K‐receptors in the arthritic joint. Peripherally acting K‐opioid agonists should lead to new therapies for arthritis.

Anti-arthritic effects of morphine are opioid receptor mediated but morphine use for this indication is restricted by its adverse effects.

The endogenous opioid system is often assumed to play a role in vulnerability to drug abuse. However, controversial results have been reported regarding the levels of enkephalins or preproenkephalin in neurons of rodent brains after opiate administration. The present study was performed to determine the extracellular levels of enkephalins and its physiological antagonist cholecystokinin (CCK), using in vivo microdialysis in freely moving rats after morphine-induced physical dependence or positive place conditioning. A large increase (340%) of Metenkephalin was observed in the periaqueductal gray matter, a structure involved in morphine withdrawal syndrome, in morphine-dependent rats. No change in CCK immunoreactivity occurred in these conditions. Moreover, using the conditioning place preference paradigm, we observed for the first time opposite changes of enkephalin outflow in the nucleus accumbens (NAc). Thus, an increase in enkephalin levels was observed in rats placed in the drug-associated compartment and a decrease in the saline-paired side. These changes in opioid peptides in the NAc may reflect an "emotional state" of the animals in relation to the expectation of drug reward (reinforcing effects of morphine). Moreover, the lack of regulation in CCK outflow suggests that CCK-opioid interactions in morphine dependence involve probably post-receptor events.