## 4 Discussion  
Psoriasis is known as a heterogamous condition with no genetic homogeneity, which comprises multiple distinct disease phenotypes that are linked to various genetic variations. The prevalence of psoriasis differs, being reported between 0.27% and 11.4% depending on sex, age, geographical area, ethnicity, genetic and environmental factors. The lower prevalence of disease is found in East Asia (0.04% to 0.30%), and it is more common in Australia (0.50% to 5.73%) and Western Europe (0.87% to 2.74%) [17]. It was observed that the risk of psoriasis is 2-3 times higher in monozygotic twins compared to dizygotic twins, concluding that discordance between familial disease aggregations and lack of disease is based on the multifactorial pathogenesis of psoriasis [18]. Studies on family aggregations have revealed a high prevalence of the disease in relatives, the risk of relapse being between 4 and 18.75% in first-degree relatives affected by psoriasis [19]. A study published in 2014 on family aggregation of moderate-to-severe psoriasis showed a family history of disease in 59.37%, with 27.18% having at least one affected parent, 16.56% second-degree relatives and 5.31% third-degree relatives [20]. Soriasis is not a disease with 100% genetic determinism, so various favorable factors lead to the onset of the disease or its aggravation. Soriasis plaques are characterized by chronic inflammation, accelerated keratinocyte proliferation, and exaggerated inflammatory responses generated by a multicellular influx that produces a complex cytokine cascade. Injuries compromise epithelial barriers, leaving them vulnerable to external threats. Thus, the survival of the body depends on the rapid restoration of the barrier after damage. Immunocompromised individuals and immunodeficient animals have profound defects in epithelial repair. During the wound healing process, stem cell offspring are not limited to their niche, but rather migrate to the affected area when tissue damage occurs. Throughout the wound repair process, groups of different cells participate. Given the amplified inflammatory reactions in psoriatic skin, healing of the skin after injury is considered a persistent and aberrant reaction [21; 22; 23; 24]. Also, studies have shown \begin{table}
\begin{tabular}{c c c c c c c c c c} \hline \hline  & \multicolumn{2}{c}{**Plaque**} & \multicolumn{2}{c}{**Arthropathic**} & \multicolumn{2}{c}{**Palmoplantar**} & \multicolumn{2}{c}{**Plaque**} & \multicolumn{2}{c}{**Floriasis**} & \multicolumn{2}{c}{**Arthropathic Fsoiasis**} & \multicolumn{2}{c}{**Palmoplantar Posoriasis**} \\  & \multicolumn{2}{c}{**Psoriasis**} & \multicolumn{2}{c}{**Psoriasis**} & \multicolumn{2}{c}{**Psoriasis**} & \multicolumn{2}{c}{**Psoriasis**} & \multicolumn{2}{c}{**Psoriasis**} & \multicolumn{2}{c}{**Arthropathic Fsoiasis**} & \multicolumn{2}{c}{**Plamoplantar Posoriasis**} \\ \cline{2-10}  & **Mild** & **Severe** & **Mild** & **Severe** & **Mild** & **Severe** & **_p-Value_ & _p-Value_ & _p-Value_ \\ \hline
**GG** & 7 & 14 & 2 & 3 & 6 & 3 & GG/GA & 0.5692 & 0.8231 & 0.3173 \\ \hline
**GA** & 1 & 4 & 1 & 1 & 0 & 0 & GG/AA & 0.1266 & 0.6547 & 0.5127 \\ \hline
**AA** & 0 & 0 & 0 & 0 & 1 & 0 & GA/AA & 0.1797 & 1 & - \\ \hline
**G** & 15 & 32 & 5 & 7 & 12 & 6 & & 0.5868 & 0.8317 & 0.3415 \\ \hline
**A** & 1 & 4 & 1 & 1 & 2 & 0 & & 0.5868 & 0.8317 & 0.3415 \\ \hline  & Mild & Severe & Mild & Severe & Mild & Severe & & & & \\ \hline
**CC** & 0 & 6 & 0 & 1 & 5 & 2 & CC/CT & 0.0246 & 0.3865 & 0.8864 \\ \hline
**CT** & 10 & 9 & 3 & 3 & 2 & 1 & CC/TT & 0.0070 & - & 0.2568 \\ \hline
**TT** & 2 & 1 & 0 & 0 & 0 & 0 & CT/TT & 0.4096 & 1 & 0.5637 \\ \hline
**C** & 6 & 29 & 3 & 5 & 12 & 5 & & 0.0154 & 0.6522 & 0.4431 \\ \hline
**T** & 10 & 11 & 3 & 3 & 2 & 2 & & & \\ \hline \hline \end{tabular}
\end{table} 
Table 8: Comparative tests for each type of psoriasis depending on the severity of the disease.