Could colorimetric method replace the individual minimal erythemal dose (MED) measurements in determining the initial dose of narrow‐band UVB treatment for psoriasis patients with skin phototype III–V?

Background Assessment of minimal erythemal dose (MED) for individual patients has been used to guide the narrowband Ultraviolet B (NB‐UVB) phototherapy, which sometimes causes discomfort and additional time. The L* value (the lightness of color in Commission Internationlale de l’Eclairge L*a*b* color scale) measured by colorimeter was shown to be useful for predicting sensitivity to NB‐UVB irradiation. Objective To compare the efficacy and safety of NB‐UVB phototherapy between 50% of MED and colorimetric L* value starting dose regimens for skin phototype III–V Korean patients with psoriasis. Method Twenty seven patients determined starting doses based on colorimetric L* value, and 27 patients based on 50% of MED. Since correlation analysis showed that L* value had the most significant association with MED compared with skin phototypes, a*, and b* values, we designated starting doses of L* value regimen as follows: 300 mJ/cm² (L* >66), 400 mJ/cm² (62 < L*≤66), and 500 mJ/cm² (L*≤62). Results There was no significant difference between two groups in clinical efficacy including response rate, mean number of sessions, duration of treatment, maximum dose and cumulative dose until achieving the state of near clearance. The proportion of adverse effects was not also significantly different. Conclusions NB‐UVB starting dose determination based on colorimetric L* value was comparable with conventional MED based regimen in efficacy and safety for skin phototype III–V patients. Since it provides much convenience and ease for both patients and physicians, colorimetric L* value could partly substitute the MED checking methods in NB‐UVB phototherapy.     

Do the filarial lymphoedema patients’‘3 months recall’ on acute dermato‐lymphangio‐adenitis (ADLA) correlate with streptococcal serology?

Aim The aim of this study was to know the correlation of patients’ 3 months recall on acute dermato‐lymphangio‐adenitis (ADLA) with anti‐streptolysin O (ASO) serology and its application as a tool to know the burden of ADLA in the community. Methods Fifty‐nine lymphoedema (LE) patients and 27 age matched controls were clinically assessed for LE and the occurrence of ADLA during the previous 3 months was obtained by recall. After obtaining the informed consent, 2 mL of venous blood sample was collected and ASO was quantified in Olympus AU400 auto‐analyzer. Results When the results were computed as two groups, controls and LE patients with no reported ADLA and LE patients with reported ADLA (by 3 months recall), the ASO positivity and ASO titre was significantly higher in the later group (P < 0.05). When the results were computed as three groups, controls with no reported ADLA, LE patients with no reported ADLA and LE patients with reported ADLA, the ASO titre was significantly higher in LE patients reported ADLA (P < 0.05). Conclusion As ASO was measured in post‐infection phase, we relied on the ASO titre for making conclusion. Patients’ 3 months recall on ADLA correlates with the ASO titre and therefore, it could be considered as a tool to measure the burden of ADLA in the community. Multicentre community‐based studies are needed to ascertain the findings.     

Acute Crohn’s colitis with lobular panniculitis – metastatic Crohn’s?

One of the common lesions in Crohn's colitis is erythema nodosum, a septal panniculitis that may appear before diagnosis or in conjunction with flare up. We report a case of Crohn's colitis where the presenting sign was neutrophilic lobular panniculitis with few granulomas. The possibility that this case represents a forme fruste of metastatic Crohn's is suggested. As skin biopsies are not usually performed by gastroenterologists in erythema nodosum-like skin lesions in Crohn's patients it may well be that the incidence of lobular panniculitis is higher than reported in the literature.     

Does massage postapplication improve moisturizer’s efficacy? A 2‐week regression study

Background Combining massage with moisturizer application is a popular technique in beauty spa sessions. The subjective positive psychological effects of massage with moisturizer application in hand and face beauty treatment are documented by many people attending spa sessions. The aim of this study was to objectively evaluate the effect of local effleurage massage as an external intervention on moisturizer efficacy. Methods In a regression‐type study of 2‐week, twice‐daily application followed by 1 week of regression, 13 female subjects applied “off the shelf” moisturizer twice daily on both forearms followed by 1 min superficial massage for one forearm randomized among subjects. The influence of massage after moisturizer application on skin barrier properties was evaluated by noninvasive measurements of transepidermal water loss (TEWL), skin capacitance, and skin elasticity at baseline, day 7, and day 14 during the treatment phase, and day 21 following a 1‐week regression period, in which no moisturizer and no massage were performed on forearms. Results The tested “off the shelf” moisturizer in both “massage” and “no‐massage” application protocols caused a comparable progressive improvement in skin hydration level and barrier permeability over the 2‐week treatment period, which was maintained during the 1‐week regression (no moisturizer) period. In addition, skin elasticity was similarly improved by both application protocols. Conclusion In this long‐term study, the daily performance of massage after moisturizer application was not an effective external intervention for enhancing moisturizer efficacy.     

Does interleukin‐33 level correlate with the activity of Pemphigus vulgaris?: A case‐control study

Pemphigus is a group of immune‐mediated blistering diseases of skin and mucus membrane caused by destruction of the intercellular junction (desmosomes) by autoantibodies. Pemphigus vulgaris (PV) is considered the most common type of all pemphigus family. Various cytokines play a major role in pemphigus pathogenesis. Interleukin‐33 (IL‐33) role has been studied in various autoimmune diseases as; psoriasis and rheumatoid arthritis, yet it has not been studied in Egyptian patients with PV. The study aimed to evaluate the possible role of IL‐33 in PV by assessing its level in the serum using ELISA and to detect its correlation with activity score using Pemphigus Disease Area Index (PDAI). Forty‐four patients with PV and 36 age and sex‐matched healthy controls were enrolled in the study. After full history taking and complete dermatological examination, the severity score was calculated using PDAI, then serum samples were taken from each patient and control subjects and subjected to quantitative measurement of serum IL‐33 using ELISA. Serum level of IL‐33 is significantly raised in PV patients compared to control subjects (P‐value = .007). The level of IL‐33 was found to be strongly correlated with the activity of the disease measured by PDAI. IL‐33 might have a role in PV pathogenesis as shown by its rising level in PV patients. In addition, serum level of IL‐33 is strongly correlated with the activity of PV. Thus, we suspect that IL‐33 can be used as marker for monitoring PV severity and measuring treatment efficacy.     

‘Activation‐induced cell death’: a special program able to preserve the homeostasis of the skin?

The 'activation-induced cell death' (AICD) is a molecular system leading to death of antigen-activated T lymphocytes, in order to avoid accumulation of harmful cytokine-releasing cells. This article reviews both the molecular mechanisms working in AICD and the role played by such mechanisms in preventing a number of skin diseases. Specifically, because AICD removes activated and autoreactive T cells through a CD95-/CD95-L-mediated suicide, skin diseases were scrutinized in which such valuable machinery could be lacking. Indeed, at least some inflammatory skin diseases, including psoriasis and atopic dermatitis, can be sustained by an increased survival of activated T lymphocytes associated with deficient CD95-/CD95-L-mediated AICD of such strong pro-inflammatory cells. In addition, autoreactive skin diseases, including, e.g. alopecia areata, lichen planus and other lichenoid tissue reactions, can be related to autoreactive T lymphocytes which could be unable to undergo CD95-/CD95-L-mediated AICD. Finally, a lack of AICD may be executive even in favoring cutaneous T cell lymphoma. Thus, because inflammatory, autoreactive and neoplastic skin diseases can be associated with a deficient CD95-/CD95-L-mediated suicide of activated T cells, AICD is likely to represent a fundamental program to preserve the homeostasis of the skin. Therapeutic approaches able to restore the AICD machinery promise to successfully treat such relevant skin diseases.     

Can the brain inhibit inflammation generated in the skin? The lesson of α‐melanocyte‐stimulating hormone

The neuro-immuno-cutaneous-endocrine network is not a simple construct featuring organ systems intimately involved in the bridge between body and mind. Mind-body influences are bi-directional and the skin should be considered an active neuroimmunoendocrine interface, where effector molecules of neuropeptides act as common words used in a dynamic dialogue between brain, immune system and skin. Gamma-melanocyte stimulating hormone (gamma-MSH), one of the principal neuroimmunomodulating peptides, seems to exercise some control on the cutaneous inflammatory process, through a central action mediated by descending anti-inflammatory neural pathways and via local direct influence on inflammatory cells infiltrating the dermis, such as monocytes, macrophages and neutrophils. Gamma-MSH down-regulates the production of proinflammatory cytokines, while the production of the anti-inflammatory cytokine IL-10 is stimulated by gamma-MSH. Finally, gamma-MSH seems to regulate the expression of surface molecules in immunocompetent cells. Thus, further studies may lead to the use of gamma-MSH as an important anti-inflammatory agent in clinical dermatology.     

Is there a ‘gut–brain–skin axis’?

Please cite this paper as: Is there a ‘gut–brain–skin axis’? Experimental Dermatology 2010; 19: 401–405. Abstract: Emerging evidence arising from interdisciplinary research supports the occurrence of communication axes between organs, such as the brain–gut or brain–skin axis. The latter is employed in response to stress challenge, along which neurogenic skin inflammation and hair growth inhibition is mediated. We now show that ingestion of a Lactobacillus strain in mice dampens stress‐induced neurogenic skin inflammation and the hair growth inhibition. In conclusion, we are introducing a hypothesis, encouraged by our pilot observations and resting upon published prior evidence from the literature, which amalgamates previously proposed partial concepts into a new, unifying model, i.e. the gut–brain–skin axis. This concept suggests that modulation of the microbiome by deployment of probiotics can not only greatly reduce stress‐induced neurogenic skin inflammation but even affect a very complex cutaneous phenomenon of (mini‐) organ transformation, i.e. hair follicle cycling. These observations raise the intriguing prospect that feeding of just the right kind of bacteria can exert profound beneficial effects on skin homoeostasis, skin inflammation, hair growth and peripheral tissue responses to perceived stress.     

Opioids and the skin – where do we stand?

Abstract:  The common ectodermal origin of the skin and nervous systems can be expected to predict likely interactions in the adult. Over the last couple of decades much progress has been made to elucidate the nature of these interactions, which provide multidirectional controls between the centrally located brain and the peripherally located skin and immune system. The opioid system is an excellent example of such an interaction and there is growing evidence that opioid receptors (OR) and their endogenous opioid agonists are functional in different skin structures, including peripheral nerve fibres, keratinocytes, melanocytes, hair follicles and immune cells. Greater knowledge of these skin-associated opioid interactions will be important for the treatment of chronic and acute pain and pruritus. Topical treatment of the skin with opioid ligands is particularly attractive as they are active with few side effects, especially if they cannot cross the blood–brain barrier. Moreover, cutaneous activation of the opioid system (e.g. by peripheral nerves, cutaneous and immune cells, especially in inflamed and damaged skin) can influence cell differentiation and apoptosis, and thus may be important for the repair of damaged skin. While many of the pieces of this intriguing puzzle remain to be found, we attempt in this review to weave a thread around available data to discuss how the peripheral opioid system may impact on different key players in skin physiology and pathology.     

Is the human skin a pheromone‐producing organ?

It is controversial whether or not humans convey specific compounds within their body odours which can potentially affect the physiology and behaviour of others. Such compounds are called pheromones and have been discovered in many other species, including mammals. It has been suggested that humans might have a special organ within their nose that can transmit such chemosensory information. However, the evidence for this organ is highly questionable. In any case, the main olfactory system is a highly diverse system, capable of transmitting pheromonal information. So far, no single substance has been found that acts as a chemical messenger for erotic attraction. On the other hand, studies investigating the pheromonal properties of natural complex body odour have proven that it does deliver information about the sender and that it has an effect on the physiology and likely behaviour of other humans. Its significance for human mating preferences probably lies not in driving them to choose the right mate but rather in warning them not to choose the wrong one.     

Melanotropic peptides: more than just ‘Barbie drugs’ and ‘sun‐tan jabs’?

While ultraviolet radiation (UVR) is a major cause of skin ageing and carcinogenesis, public pursuit of a novel tanning strategy circumventing the need for UVR is increasingly reported in the media and scientific press. This involves the subcutaneous self‐administration of unregulated products labelled as melanotan I and/or II, synthetic analogues of α‐melanocyte stimulating hormone (α‐MSH), as obtained via the internet, tanning salons and gyms. The Medicines and Healthcare products Regulatory Authority has recently raised awareness of the public health risk of transmission of blood‐borne viruses from the needle sharing that may occur, and of the potential impurity of these products. Dermatologists should also be aware that these agents can complicate the clinical presentation of patients with pigmented lesions; their use may be suspected in unexpectedly tanned individuals with rapidly pigmenting naevi. Meanwhile, the regulated α‐MSH analogue afamelanotide (Clinuvel Pharmaceuticals Ltd, Melbourne, Australia) is showing promise for its photoprotective potential, and is undergoing phase II and III clinical trials in people with photosensitivity disorders and those prone to nonmelanoma skin cancer. The photoprotective and other biological effects of α‐MSH analogues await full determination.     

Does adjuvant alpha‐interferon improve outcome when combined with total skin irradiation for mycosis fungoides?

BACKGROUND: Patients with mycosis fungoides (MF) experience frequent disease recurrences following total skin electron irradiation (TSEI) and may benefit from adjuvant therapy. OBJECTIVES: To review the McGill experience with adjuvant alpha-interferon (IFN) in the treatment of MF. METHODS: From 1990 to 2000, 50 patients with MF were treated with TSEI: 31 with TSEI alone and 19 with TSEI + IFN. Median TSEI dose was 35 Gy. In the TSEI + IFN group, IFN was given subcutaneously at 3 x 10(6) units three times per week starting 2 weeks prior to start of TSEI, continued concurrently with the radiation and for an additional 12 months following TSEI. The TSEI alone group included 16 men and 15 women with a median age of 61 years (range 31-84). The TSEI + IFN group included 14 men and five women with a median age of 51 years (range 24-83). Clinical stage was IA, IB, IIA, IIB, III and IVA in 2, 9, 4, 8, 1 and 7 patients of the TSEI group and 0, 3, 3, 7, 4 and 2 patients of the TSEI + IFN group. RESULTS: Median follow up for living patients was 70 months. All patients responded to treatment. Complete response (CR) rate was 65% following TSEI and 58% following TSEI + IFN (P = 0.6). Median overall survival (OS) was 61 months following TSEI and 38 months following TSEI + IFN (P = 0.4). Acute grade II-III dermatitis was seen in all patients. Fever, chills or myalgia were seen in 32% of patients treated with TSEI + IFN. CONCLUSIONS: Concurrent IFN and TSEI is feasible, with acceptable toxicity. Even when controlling for disease stage, the addition of IFN did not appear to increase CR rate, disease-free survival or OS.