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Introduction The most common cancers in the UK are keratinocyte cancers (KCs): the combined term for basal cell carcinomas (BCCs) and cutaneous squamous cell carcinomas (cSCCs). Registration of KC is challenging due to high numbers and multiplicity of tumours per person. Methods We provide an updated report on the descriptive epidemiology of trends in KC incidence for the resident populations of UK countries (England, Northern Ireland, Scotland and Wales) using population‐based cancer registry and pathology report data, 2013–18. Results Substantial increases in cSCC incidence in England, Scotland and Northern Ireland can be detected for the period of 2013–18, and the incidence of cSCC also increased in Wales from 2016 to 2018. In contrast, however, the pattern of annual change in the incidence of BCC across the nations differs. In England, the incidence of BCC declined slightly from 2016 to 2018, however, the overall trend across 2013–18 is not statistically significant. In Scotland, the incidence of BCC shows some variability, declining in 2017 before increasing in 2018, and the overall trend across 2013–18 was also not statistically significant. In Northern Ireland, the incidence of BCC increased significantly over the study period, and in Wales, the incidence of BCC increased from 2016 to 2018. One in five people will develop non‐melanoma skin cancers (NMSC) in their lifetime in England. This estimate is much higher than the lifetime risk of melanoma (1 in 36 males and 1 in 47 females born after 1960 in the UK), which further highlights the burden of the disease and importance of early prevention strategies. Conclusions We highlight how common these tumours are by publishing the first ever lifetime incidence of NMSC. Additionally, the first time reporting of the age standardised incidence of KC in Wales further confirms the scale of the disease burden posed by these cancers in the UK. With approximately one in five people developing NMSC in their lifetime, optimisation of skin cancer prevention, management and research are essential.

Skin cancer is the commonest cancer in the UK. Skin cancer referrals via the two-week wait (urgent suspected cancer) pathway outnumber any other suspected malignancy.1, 2 The commonest skin cancers are keratinocyte cancers (KCs) which represents Basal Cell Carcinomas (BCC) and Cutaneous Squamous Cell Carcinomas (cSCC). Accurate KC incidence reporting is crucial for healthcare planning.

Summary During pregnancy, the mother undergoes changes to sustain and enable normal growth and development of the fetus. Common physiological changes include linea nigra, fibroepithelial polyps, striae, spider angioma, palmar erythema and pruritis gravidarum. However, there are some changes that are purely pathological, and these are termed the pregnancy-specific dermatoses (PSDs). The PSDs occur during pregnancy or in the immediate postpartum period. They do not include the various benign conditions or pre-existing dermatoses and tumours that may present or worsen with pregnancy. They do include a number of distinct and identifiable conditions: atopic eruption of pregnancy (AEP), polymorphic eruption of pregnancy (PEP), intrahepatic cholestasis of pregnancy (ICP) and pemphigoid gestationis (PG). These are a heterogeneous group of skin conditions characterized by pruritis and inflammatory changes. In addition, pruritis gravidarum is sometimes considered pathophysiological and thus part of this group, rather than a physiological process. Each of these conditions has a distinct, but not fully understood, pathogenesis. The mechanisms leading to PSD may be a reflection on the hormonal and immunological changes associated with pregnancy. AEP and PEP are benign conditions, and although they can cause distress to the mother, they are otherwise minor. However, ICP and PG are more serious conditions, and both carry the potential for serious risks to both the mother and the fetus. Thus, the pathophysiology of these latter two conditions is considered in more detail in the following article.

Various cutaneous signs presenting in childhood, for example cafe-au-lait macules, may have systemic cancer associations. Indeed, this may be the first manifestation of the underlying cancer predisposition. The syndromes covered in this review fall into four main categories: (i) DNA damage processing defects including Fanconi anaemia, ataxia telangiectasia, Bloom syndrome, Rothmund-Thomson syndrome, constitutional mismatch repair defects and xeroderma pigmentosum; (ii) signalling pathway defects, including naevoid basal cell carcinoma and Costello syndromes; (iii) primary immunodeficiency syndromes; and (iv) syndromes that do not fit this molecular classification, such as X-linked dyskeratosis congenita. This review focuses on the dermatological findings of these conditions. Some of these conditions exhibit a milder heterozygous phenotype and this should be elicited in the family history. Where the dermatological findings are subtle, a targeted family history can provide clues towards making a diagnosis. Nondermatological features of each condition are summarized too, together with molecular testing strategies, which will direct genetic counselling and screening. This review will enable the dermatologist and other clinicians in the early recognition and molecular confirmation of underlying cancer-predisposing syndromes. This allows the possibility of surveillance and prevention strategies to be initiated in a timely manner, in affected children and other at-risk family members.

Many syndromes predisposing to cancer have dermatological features, which, although often subtle, will alert the clinician to the possibility of systemic malignancy. Many of these conditions are hereditary and are therefore also of relevance to the families of these patients. Early detection and appropriate genetic counselling is vital, as this will allow the patient and their relatives to be screened appropriately. This review will provide an overview of dermatological features of several cancer-predisposing syndromes divided according to organ system, describing the main clinical features and presentation of the selected syndromes.

Classical acupuncture focuses primarily on treating the person, and secondarily treating the illness. The "symptoms" are regarded as "branch" expressions of a "root" (constitutional) imbalance. Different root imbalances can produce the same symptoms. Five patients with eczema, for example, may reveal five distinct root imbalances and would all be treated very differently. Because acupuncture treats the whole person, it has something to offer almost every condition. In many cases, acupuncture aims to bring about a complete cure; in others, it aims to manage the problem. Acupuncture remains a substantial part of the traditional Chinese medicine, which is used to treat many conditions including acne, alopecia, dermatitis, pruritus, psoriasis, rosacea, systemic lupus erythematosus, urticaria, herpes zoster, chicken pox, impetigo, leprosy, vitiligo, and tinea. This review introduces the historical context of acupuncture within Chinese medicine and how it relates to skin disease. Specifically, a key question is, what can we learn from the ancients with regard to their use of acupuncture as part of a holistic system of medicine, and how does this relate to the practice of modern dermatology?

The precursor protein proopiomelanocortin (POMC) produces many biologically active peptides via a series of enzymatic steps in a tissue-specific manner, yielding the melanocyte-stimulating hormones (MSHs), corticotrophin (ACTH) and beta-endorphin. The gene for alpha-MSH is encoded for by the POMC gene, but alpha-MSH cannot be produced from POMC gene transcription and translation without these specific post-translational proteolytic steps taking place. The MSHs and ACTH bind to the extracellular G-protein-coupled melanocortin receptors (MCR), of which there are five subtypes. Two (MC1R and MC5R) show widespread cutaneous expression. ACTH and alpha-MSH bind to MC1R to influence both pigmentation and the immune system. MC5R regulates the sebaceous glands. Mutations in the MC1R gene lead to fair skin and red hair in humans, which is also seen with inactivating human POMC gene mutations. MC1R mutant receptor expression can also correlate with an increased incidence of the three commonest forms of skin cancer. Other mutations can occur in the POMC system or parallel interacting pathways, such as in prohormone convertase 1 and agouti signalling protein, a human homologue of murine agouti protein. However, they do not necessarily affect skin colour or function in humans, and further studies are needed to clarify these observations.

Perimenstrual exacerbations of dermatoses are commonly recognized, yet our knowledge of the underlying pathophysiological mechanisms remains imperfect. Research into the effects of oestrogen on the skin has provided evidence to suggest that oestrogen is associated with increases in skin thickness and dermal water content, improved barrier function, and enhanced wound healing. Research into the effects of progesterone suggests that the presence of various dermatoses correlates with peak levels of progesterone. Dermatoses that are exacerbated perimenstrually include acne, psoriasis, atopic eczema and irritant dermatitis, and possibly also erythema multiforme. Exacerbations occur at the peak levels of progesterone in the menstrual cycle. Underlying mechanisms include reduced immune and barrier functions as a result of cyclical fluctuations in oestrogen and/or progesterone. Autoimmune progesterone and oestrogen dermatitis are the best-characterized examples of perimenstrual cutaneous reactions to hormones produced during the menstrual cycle. In this review, we describe the current understanding of the menstrual cycle, and its effect on the skin and cutaneous disorders.

Since at least biblical times, humans have pondered on why there might be variation in skin color and what might constitute the nature of that difference. In this article, two historical trails are followed, one beginning with the Ancient Greeks, the other with the Ancient Chinese. These two paths converge to provide us with some historical evidence to back recent scientific discoveries in the dynamic regulation of skin pigmentation, focusing on melanocyte-stimulating hormone and its natural antagonist agouti-signaling protein.

We report a case of dermatitis herpetiformis co-localised with segmental vitiligo in a 37-year-old woman with a background history of autoimmune polyglandular syndrome type 2. We propose genetic mosaicism as a possible mechanism. There has only been one previous case report in which dermatitis hepetiformis co-localised in close proximity but not exclusively within vilitigo in a patient with autoimmune thyroiditis. To our knowledge, this is the first case report of dermatitis herpetiformis co-localised exclusively to segmental vitiligo in the presence of autoimmune polyglandular syndrome.

The increasing problem of obesity in childhood is recognized as both a short-term and long-term serious public-health concern. Excess body weight may contribute to psychological morbidity; cancers; metabolic, cardiovascular and musculoskeletal disorders; and dermatological conditions. There is increasing recognition of the role of genetic factors in the aetiology of obesity. Although in the vast majority of cases these influences are polygenic, some obese children suffer from monogenic disorders, which may present with obesity alone. However, more often than not, they generally display other syndromic features. Some of these syndromes have a clear cutaneous phenotype, and these conditions will be the focus of this review.

Obesity is a serious global health problem, perhaps the biggest public health issue of our times. Excess body weight may be a factor in carcinogenesis in general, as well as contributing to the pathogenesis of metabolic, cardiovascular and musculoskeletal disorders. Obesity also has many cutaneous features, which form the basis for this review article. Many of these clinical entities are common to the majority of obese patients, e.g. striae distensae, plantar hyperkeratosis and an increased risk of skin infections. However, it may also be associated with poor wound healing, malignant melanoma and an increased risk of inflammatory dermatoses, such as psoriasis, as well as some rarer disorders. Therapeutic interventions for obesity, whether over-the-counter, prescription medicines or surgical interventions, are increasingly commonplace. All of these treatment modalities potentially have dermatological side-effects too.

Many syndromes predisposing to cancer have dermatological features, which, although often subtle, will alert the clinician to the possibility of systemic malignancy. Many of these conditions are hereditary and are therefore also of relevance to the families of these patients. Early detection and appropriate genetic counselling is vital, as this will allow the patient and their relatives to be screened appropriately. This review will provide an overview of dermatological features of several cancer-predisposing syndromes divided according to organ system, describing the main clinical features and presentation of the selected syndromes.

Sudden hair whitening (canities) was first reported centuries ago. Although a rare event, it has affected well-known historical figures, including Sir Thomas Moore and Queen Marie Antoinette of France. Early reports are substantiated by more recent cases in the scientific literature. Often, there is association with psychological stress; in the two historical cases above, the condition is thought to have been a reaction to the sentence of execution. In this paper, we examine some case histories of those afflicted throughout history and discuss hypotheses to explain the phenomenon.

Vitiligo has been mentioned in the tomes of every major religion, with its first description dating back more than 3000 years, to the earliest Vedic and Egyptian texts. Despite this ancient recognition, confusion with disorders such as leprosy has been a problem throughout the ages. This has lead to the stigmatization of vitiligo sufferers. This is a social problem that is still widespread in some, but not all, parts of the world. The ancients also practiced phototherapy for vitiligo. This practice only became common in the Western world with development of psoralen plus ultraviolet A and later ultraviolet B phototherapy in the latter half of the 20th century. In this article, the history of vitiligo up until the end of the 20th century is outlined, covering medical, scientific, and social aspects.

Since the dawn of time, Beelzebub has been showering fire and brimstone (sulphur) on tortured souls, but the cutaneous effects of this have been poorly described. Sulphur has also been used for centuries as a treatment for many skin conditions, such as fungal infections, scabies, psoriasis, eczema and acne. It has also been used extensively in cosmetic preparations and by cosmetic dermatologists treating conditions such as seborrhoeic eczema. Many natural bathing spas have high levels of sulphur; such balneology has been advocated by medical and cosmetic dermatologists as an effective treatment for cutaneous disorders for more than 500 years. Sulphur was often the active agent in many of the so-called 'patent medicines' that became popular in the mid-nineteenth century. Time has not withered medical practitioners' enthusiasm for sulphur. There are various reports in the medical literature of its current use. However sulphur treatment is not without its risks; a sulphur spring dermatitis has been described from a spa bath in Taiwan. With the satanic threat of bio-terrorism, some dermatologists may be treating the effects of contact with sulphur mustard all too soon.

The precursor protein, proopiomelanocortin (POMC), produces many biologically active peptides via a series of enzymatic steps in a tissue-specific manner, yielding the melanocyte-stimulating hormones (MSHs), corticotrophin (ACTH) and β-endorphin. The MSHs and ACTH bind to the extracellular G-protein coupled melanocortin receptors (MCRs) of which there are five subtypes. The MC3R and MC4R show widespread expression in the central nervous system (CNS), whilst there is low level expression of MC1R and MC5R. In the CNS, cell bodies for POMC are mainly located in the arcuate nucleus of the hypothalamus and the nucleus tractus solitarius of the brainstem. Both of these areas have well defined functions relating to appetite and food intake. Mouse knockouts (ko) for pomc, mc4r and mc3r all show an obese phenotype, as do humans expressing mutations of POMC and MC4R. Recently, human subjects with specific mutations in β-MSH have been found to be obese too, as have mice with engineered β-endorphin deficiency. The CNS POMC system has other functions, including regulation of sexual behaviour, lactation, the reproductive cycle and possibly central cardiovascular control. However, this review will focus on feeding behaviour and link it in with the neuroanatomy of the POMC neurones in the hypothalamus and brainstem.