Clinical Features of Patients with Psoriasis Vulgaris

CHAPTER 1 OVERVIEW

1.1. Common psoriasis

1.1.1. Medical history

Psoriasis has been known for a long time. Hippocrates (460-375 BC) described psoriasis as a scaly skin condition and named it

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―Lopoi‖. Galen (133-140 AD) was the first to use the term psoriasis (derived from the Greek word psora meaning itch) [13]. At the end of the 18th century, psoriasis and leprosy were considered to be one group. By the 19th century, Willan described the characteristics of the disease and psoriasis was separated from leprosy in 1841 by Hebra. In Vietnam, Professor Dang Vu Hy was the first to name the disease psoriasis [4],[13] , [14].

1.1.2. Psoriasis situation

Psoriasis is one of the most common skin diseases, accounting for 2 to 3% of the world's population [4], [13], [14]. The highest incidence rate in European countries is Denmark (2.9%), in the US it ranges from 2.2% to 2.6% and the lowest in Asia is 0.4% [4], [14]. In Vietnam, according to Nguyen Xuan Hien and colleagues, psoriasis accounts for 6.44% of dermatological patients at Military Hospital 108 [13]. Tran Van Tien's study at the Central Dermatology Institute had 134 psoriasis patients treated between March 1999 and August 2000, accounting for 12.04% of inpatients [15].

The incidence of the disease is equal in men and women [14]. Psoriasis can appear at any age [14].

1.1.3. Pathogenesis of psoriasis vulgaris

Nowadays, it is recognized that psoriasis is a chronic disease. Although the pathogenesis is not really clear, psoriatic lesions are formed due to a combination of genetic, environmental and immune factors.

1.1.3.1. Genetic factors

Genetic factors

The genes in psoriasis have been known for nearly 100 years. After many years, based on extensive population studies and pedigree studies, many authors support the hypothesis that psoriasis is a disease related to many genes. Recently, many studies have focused on finding specific genes for the disease, and a number of locations called PSORS psoriasis susceptibility sites have been confirmed, including PSORS1, PSORS2, PSORS3, PSORS4, PSORS5, PSORS6, PSORS7, PSORS8, PSORS9 [16].

It is estimated that the risk of psoriasis in children is 41% if both parents are affected, 14% if only one parent is affected, 6% if one sibling is affected, and 2% if no parent, sibling, or sibling is affected [16].

The prevalence of psoriasis in identical twins varies from 35-73% depending on the study but is <100%. This demonstrates the role of environmental factors in the onset of the disease. The effectiveness of UV treatment of psoriasis also suggests that UV may be a major environmental factor interacting with genes to cause psoriasis [14].

Human leucocyte antigen (HLA)

As we know, PSORS1 located on the HLA coding gene segment is a strong influencing factor in psoriasis. HLA has many alleles associated with psoriasis such as HLA-Cw6, HLA-B13, HLA-B37, HLA-B46, HLA-B57, HLA-Cw1, HLA-DR7, HLA-DQ9. Of which, HLA-Cw6 is proven to be the highest risk factor for psoriasis in white people. People with HLA-Cw6 have psoriasis 9-15 times higher than normal people. However, HLA-Cw6 has different associations in type I and type II psoriasis: in the early onset group, 85% have HLA-Cw6, but in the late onset group, this rate is only 15% [14],[16].

Family history in psoriasis

Family history in psoriasis has been of interest to many scientists and is considered a risk factor. The familial nature of psoriasis has been known for a long time and family history is known in about 30% of cases [6]. According to a large study in Germany, if both parents have psoriasis, the risk for the child is 41%; while if only 1 parent has psoriasis, the risk for the child is 14%; this risk is 6% if only 1 sibling has the disease [17].

Age of onset and type of psoriasis

Psoriasis can start at any age but is rare under 10 years old, most common between 15-30 years old [4]. Christophers based on the presence of HLA-Cw6, HLA-DR7, age of disease onset, family history to divide psoriasis into 2 types [18].

Age of onset of psoriasis in both men and women if before 40 years old is called early onset, has genetic background, is called type I psoriasis. If the disease starts after 40 years old is called late onset, has no genetic background, is not related to HLA, is called type II psoriasis [4],[9]. Onset of the disease after 40 years old, perhaps during life, under the influence of many environmental factors causing gene mutations, so there is no genetic background [9].

Through some studies, it has been found that type I psoriasis has a low threshold for disease onset and is more easily triggered by environmental factors than type II psoriasis and thus, in addition to family history, age of onset is an important risk factor for psoriasis [6]. According to Mroweitz (2009), half of psoriasis patients have their first symptoms before the age of 21, the disease progresses over many years, long-term treatment is necessary, especially when the disease is severe and chronic [9].

Thus, most authors agree that psoriasis is a genetic disease.

1.1.3.2. Factors that promote disease

Psoriasis is considered a disease caused by the interaction between genetic, immune and environmental factors. Many factors that trigger the disease have been mentioned by researchers such as stress, infection, trauma, weather, drugs, food, etc.

Stress factors have been confirmed to be related to the onset and progression of the disease, including psychological stress, mental stress and emotional stress. The prevalence of stress in psoriasis patients ranges from 35-70% according to each author.

Foci of localized infection, especially upper respiratory tract infections, especially caused by group A β-hemolytic streptococci, can trigger guttate psoriasis or aggravate existing psoriasis. Psoriatic lesions can appear at sites of epidermal trauma (Koebner phenomenon): surgical incisions, burns, scratches and abrasions.

According to Nograles et al., the progression of psoriasis is clearly related to season and weather. Most of the time, the disease is severe in winter and mild in summer (winter form); but there are also cases with the opposite (summer form) [19].

Some drugs can trigger or worsen psoriasis: β-blockers, lithium, antimalarials, nonsteroidal anti-inflammatory drugs... Abruptly stopping systemic corticosteroids can also cause the disease to appear or become severe, so it is recommended not to use systemic corticosteroids for all forms of psoriasis.

The role of food: Recently, there has been a proven link between psoriasis and alcohol consumption and smoking. Many authors advise psoriasis patients to eat more fish oil, fruit, and reduce sugar, fat, and salt.

1.1.3.3. Immune factors

The role of several immune factors is increasingly being elucidated in the pathogenesis of psoriasis. The formation of psoriatic lesions is explained in the following stages: First is the activation of the presenting cells

antigen (APC-Antigen presenting cell) in the skin is Langerhans cell. Then there is interaction between antigen presenting cell and T lymphocytes in the skin, T lymphocytes are activated and migrate to the neighboring lymph nodes. Skin-directed lymphocytes will migrate back to the skin tissue. T-CD4 and T-CD8 lymphocytes are reactivated in the dermis and produce cell-mediated chemicals such as IL-2, IL-17, IL-6, IL-22, TNF-  ... These substances will stimulate epithelial cell proliferation and form psoriatic lesions.

Currently, people mention three main pathways in the immune mechanism of psoriasis: Th1, Th17 and Th22 activation pathways. Of which, recently it is believed that Th17 and its products play a leading role in the pathogenesis of psoriasis [19], [20], [21].

1.1.4. Clinical characteristics of patients with psoriasis vulgaris

1.1.4.1. Characteristics of skin lesions and classification of psoriasis vulgaris

Psoriasis vulgaris is the most common form, accounting for about 90% of psoriasis patients. Skin lesions of this form are:

 The basic damage is red patches: initially red patches appear, bright red, congested, discolored when pressed, clearly demarcated from healthy skin, size and quantity vary, can be red dots or red skin patches. On the red skin, white, thick, easily peeling scales gradually appear, peeling off layer by layer in many stages, making the red skin area thick and raised above the skin surface.

 Location: most of the disease starts in the scalp, hairline or localized in the skin contact area, pressure: elbow, knee, sacrum, buttocks, greater trochanter of femur, then the lesion spreads to the whole body, symmetrical on both sides. Based on the location of the lesion, common psoriasis can be divided into the following types [13], [14], [22]:

+ Inverse psoriasis: lesions are mainly concentrated in folds and intertriginous areas such as armpits, groin, breast folds...

+ Scalp psoriasis: the main lesions are red, scaly patches on the scalp without lesions on the body. This may be an early manifestation of psoriasis, which is often misdiagnosed as seborrheic dermatitis of the scalp.

+ Psoriasis localized to the palms and soles: lesions are only localized to the palms and soles. This form is easily confused with atopic dermatitis.

 The size of the lesions varies greatly, from a few millimeters to large patches. Depending on the size of the lesions, psoriasis can be divided into different types such as [16]:

+ Guttate psoriasis: many small lesions less than 1cm in diameter, scattered all over the body, often found in young children [23].

+ Nummular psoriasis: lesions are 1-4cm in size, tend to be round like coins, and can number up to several dozen.

+ Plaque psoriasis: large lesions 5-10 cm in diameter or larger, localized in pressure areas (back, chest, sacrum, elbows, knees, front of lower legs) with clear boundaries.

Psoriasis is classified mainly by size, number of lesions, clinical morphology and anatomical location. Previously, in some classifications of psoriasis, the term "nummular psoriasis" appeared. According to Otto Braun-Falco, author of Dermatology published in 2000, nummular psoriasis is one of the forms classified by size and distribution of lesions, in which nummular psoriasis is the most common type, the basic lesions are patches of several centimeters in size, mainly on the knees, elbows, buttocks, back and head; in addition, there are also guttate, follicular, geographic, and erythrodermic types [24]. "Nummular psoriasis" also appeared in the study of Bergstedt C et al. in 1992 on the treatment of this disease with topical clobetasol propionate [25]. According to the study of C Beylot et al.

In 1979, guttate and nummular psoriasis were the early stages of psoriasis in children [26]. In general, the literature using the classification ― nummular psoriasis” was found to be limited and mostly old.

Currently, we find that most authors agree on the classification of psoriasis without the “nummular form” as in the above documents. Specifically, according to Langley RGB et al., psoriasis is divided into plaque psoriasis, guttate psoriasis, inverse psoriasis, erythrodermic psoriasis, pustular psoriasis, palmoplantar pustular psoriasis, and nail psoriasis. Langley RGB describes coin-sized or nummular plaque lesions belonging to plaque psoriasis [27]. “Nummular” or “nummular” is used by Van de Kerkhof in the Texbook of Psoriasis (2003) to describe the size of psoriatic lesions; this author classifies small lesions as guttate psoriasis and larger lesions, from coin-sized (nummular) to palm-sized, are generally classified as chronic plaque psoriasis [28]. In the 2020 American treatment guidelines, psoriasis is classified into plaque, inverse, erythrodermic, pustular, guttate, onychomycosis, and arthrosis, of which plaque includes well-demarcated plaque-like lesions ranging in size from 1 to several centimeters. “Nummular” is not used in this guideline, either to classify or describe the lesions [29]. Thus, it can be seen that “nummular psoriasis” is no longer a type of psoriasis, and can only be used to describe the characteristics of lesion size.

For consistency in classification and terminology, we use the Fitzpatrick classification of psoriasis [4], which includes:

+ Chronic plaque psoriasis, also known as psoriasis vulgaris;

+ Guttate psoriasis, small plaque psoriasis;

+ Inverse psoriasis;

+ Erythrodermic psoriasis;

+ Pustular psoriasis includes localized and systemic forms.

1.1.4.2. Lesions accompanying skin lesions in patients with psoriasis vulgaris

Nail damage

Approximately 30% - 40% of psoriasis patients have fingernail and toenail lesions [4], [14]. Nail lesions can appear alone or accompanied by skin lesions. Nail lesions in psoriasis include:

+ Nail plate damage: pitted nails; thick, brittle nails; nails with horizontal lines; red nail crescent.

+ Nail bed lesions: nail separation, subungual keratosis, oil drop sign, hemorrhage.

+ Damage around the nail: paronychia.

Joint damage

The rate of joint damage in psoriasis depends on the type. In mild cases, skin damage is localized, only about 2% of patients have joint damage. Meanwhile, in severe, persistent cases, up to 20% of patients have joint damage. The most common symptoms are chronic arthritis, joint deformities, joint stiffness, joint dislocation, and patients have difficulty moving around... Some patients have little skin damage but very severe joint damage, especially in the knee and spine [4], [14].

Mucosal damage

Mucosal lesions in psoriasis are quite rare. The most commonly damaged mucosa is the glans mucosa. In addition, there may be lesions on the tongue with the image of geographic glossitis or hypertrophic desquamative glossitis. In addition, there may be lesions on the eye mucosa including: conjunctivitis, keratitis or blepharitis [4], [14].