**2. Management of psoriasis**

*Healthcare Access - Regional Overviews*

of action, with psychologists, rheumatologists and dermatologists collaborating in

In the dawn of the nineteenth century, Willan expanded on Celsus's explanations of papulosquamous afflictions by describing characteristics we know considered compatible with psoriasis. Even so, he labelled modern psoriasis as 'lepra vulgaris', which maintained the confusion between these two distinct diseases [6, 7, 10]. Afterwards, there was an incongruity when referring to these pathologies, as authors could not properly agree on which term to use. Ultimately, Gibert corroborated Willan's description with the term psoriasis, putting an end to some of the perplexity and guiding to an improved awareness and understanding of psoriatic patients. Heinrich Auspitz (1835–1886) noticed the papillary bleeding that appeared after removing the scale of psoriatic lesions, currently referred to as the Auspitz sign (or bloody dew phenomenon) [6, 7, 11, 12]. In 1877, Heinrich Köbner (1838–1904) defined the sign that carries his name, specifically the occurrence of a psoriatic lesion within the location of a physical injury. After two more decades, in 1898, William Munro (1863–1908) described the microabscesses that appear in psoriasis, otherwise known as Munro's abscesses. The beginning of the twentieth century led to further advancements in the understanding of psoriatic lesions. In 1910, Leo von Zumbusch (1874–1940) was the first to note generalized pustular psoriasis, now called the von Zumbusch disease [6, 13]. Among other descriptions was also the one of the Russian dermatologist D.L. Woronoff in 1926 regarding a pale halo now known as the 'Woronoff ring' enclosing a plaque of psoriasis [7, 14]. The characterization of the Auspitz sign, Köbner's phenomenon, Munro's abscess, and pustular psoriasis, as well as the Woronoff ring made it possible for practitio-

The next discoveries furthered our understanding of pathophysiology, especially concerning epidermal hyperplasia and keratinocytes' cell cycle shortening by van Scott and Ekel in 1963, followed by the role of the immune system by Gubner in 1951 and Muller in 1979 [6, 7]. However, there is still much to be learned about this

The treatment of psoriasis also varied across the ages, from arsenic and ammoniated mercury in the nineteenth century (which both had a comparable toxic potential), to chrysarobin, anthralin and coal tars in the late nineteenth and early twentieth centuries, reaching to corticosteroids, methotrexate and PUVA in the middle of the last century [6, 7, 10, 15]. In what follows, we describe the modern forms of therapy which have been scientifically proven to ameliorate the symptoms in psoriasis.

To properly understand the breakthroughs of modern treatment of psoriasis, it might be worthwhile to glance over the history of this complicated disease. The first reported cases were identified in ancient Greece, many of the description written by Hippocrates (460–377 BC) himself [6, 7]. Portrayals of psoriasis can also be traced back to the times of the Old Testament, wherein people suffering from such skin disorders were publicly ostracized since they were considered punished by divinity. Numerous historians acknowledge Celsus (ca. 25 BC–45 AD) as documenting the first clinical description of papulosquamous diseases, whereas Galen (133–200 AD) first utilized the term psoriasis [6, 8, 9]. However, his depiction was inconsistent regarding the disorder that we now know as psoriasis. He described it as a pruritic, scaly skin illness of the eyelids and scrotum, probably referred to as today as seborrheic dermatitis. Nevertheless, the unselective grouping together of all inflammatory skin disorders contributed to the stigmatization of psoriasis patients. During the Middle Ages, when it was believed that psoriasis was as contagious as leprosy, these patients were mandated to carry a chime or clapper that would announce their approach. Furthermore, they had to wear a special garment and could only eat or

order to deliver the best possible care, with the most satisfactory outcome.

come into physical contact with others considered lepers.

ners to more easily identify patients with psoriasis.

complex disease and its intricate mechanisms.

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In the past few years, countless achievements have been made in grasping the intricate physiopathological contrivances of psoriasis. Studies repeatedly demonstrated that it is a chronic, systemic immune-mediated ailment, the dermatologic manifestation representing its most debilitating aspect, usually followed by joint involvement. However, the explicit mechanisms of this process have not been untangled. Even so, it appears that the myeloid dendritic cells begin producing interleukins such as IL-12, IL-23 and TNF-α prior to a minor traumatic injury that perform as chemoattractants for the T helper Th-1 and Th-17 cells [16, 17]. In the next step, these cells will raise the production of psoriatic cytokines such as IL-17 within the site of injury, hence increasing the keratinocytes' turnover and eventually piloting towards the cutaneous symptoms of psoriasis [18–21]. Also, the proinflammatory substances may extend into the bloodstream with a significant influence on insulin signalling, angiogenesis, lipogenesis or adipogenesis, which will ultimately lead to comorbidities such as obesity and dyslipidaemia, hypertension, depression and type 2 diabetes mellitus [3, 22]. Grasping the mechanisms of psoriasis is the utmost step in offering the best available therapy.

Topical therapy as the only form of treatment has demonstrated a mediocre rate of improvement, with patients often describing ongoing clinical symptoms, for instance, redness, pruritus or scales [23]. One survey targeted to such patients showed that 40% of cases with a mild disease, circa 50% of those with moderate psoriasis and well above 40% with the severe form were discontented with the recommended topical therapies. The lowermost treatment satisfaction quotients were found in the topical medications versus systemic and phototherapy group [24]. Should topical therapy in itself fail to achieve the expected outcome, practitioners have to be ready for alternative strategies, such as systemic and biological therapies.

## **2.1 Topical therapy**

Topical therapies are recommended in mild psoriasis, when the affected body surface area is below 10% [25].
