Psoriasis is a chronic autoimmune-related skin disease, involving complex biological mechanisms. Recent studies indicate that its pathogenesis is closely related to interactions among genetics, environmental triggers, immune system abnormalities, and neuroendocrine system. Excessive proliferation of keratinocytes and abnormal activation of T lymphocytes create a vicious cycle, leading to the characteristic symptoms of redness, swelling, and scaly plaques.
The medical community generally considers psoriasis a "multifactorial disease," resulting from the combined effects of genetic predisposition and external triggers. Abnormal immune activation is the core pathological mechanism, but the specific triggering processes are still not fully understood. Environmental factors such as infections, stress, and drug reactions are often viewed as key factors in initiating or exacerbating the condition.
Genetic studies confirm that psoriasis exhibits significant familial aggregation, with a concordance rate of up to 70% in monozygotic twins. Over 100 genetic loci associated with psoriasis have been identified, with specific alleles of the HLA-C gene (such as HLA-Cw6) strongly correlated with disease severity. These genetic variations may influence immune cell signaling, leading to abnormal T cell activation.
The PSORS1 region on chromosome 6 is the most important genetic risk locus, containing several immune-related genes such as CTLA4 and TNFAIP3. Family history is a major risk indicator; children with affected parents have a 10% increased risk of developing the disease, and if both parents are affected, the risk rises to 50%. It is important to note that genetic predisposition is not deterministic; most genetically susceptible individuals do not develop the disease without environmental triggers.
Infections are often considered key triggers for psoriasis flare-ups. There is a clear association between streptococcal pharyngitis and outbreaks of acute guttate psoriasis, especially in children. Viral infections such as HIV may also induce or worsen the disease, indicating that infection-induced immune responses can disrupt disease balance.
Physical stimuli such as trauma, cuts, or severe sunburns can trigger the "Koebner phenomenon," leading to new lesions at damaged skin sites. Extreme weather conditions like cold and dryness can exacerbate keratinocyte abnormalities, which is also common during winter. Certain medications, such as beta-blockers and lithium, may induce lesion development.
Smoking has been confirmed as an important environmental factor in the onset and worsening of psoriasis. Components like tar in tobacco can directly damage the skin barrier and induce the release of pro-inflammatory cytokines such as IL-17 and IL-22. Quitting smoking can significantly reduce disease severity, demonstrating the reversibility of this behavioral factor.
Obesity has a bidirectional relationship with psoriasis: excess body fat increases systemic release of inflammatory cytokines like TNF-α, and the inflammatory state can lead to metabolic abnormalities. Diet-wise, high sugar intake may exacerbate chronic inflammation, and excessive omega-6 fatty acids are associated with the spread of skin lesions. Poor stress management can worsen immune dysregulation through hypothalamic-pituitary-adrenal (HPA) axis abnormalities.
Age shows two peaks in psoriasis onset: 20-30 years and 50-60 years, suggesting age-related immune regulation changes may influence disease presentation. Males have a slightly higher incidence, but females are more prone to severe joint involvement. Certain chronic diseases like metabolic syndrome and cardiovascular disease share common pathogenic mechanisms with psoriasis.
Innate immune deficiencies, such as abnormalities in the IL-23 signaling pathway, lead to overactivation of Th17 cells, creating a persistent inflammatory cycle. Dysbiosis of the gut microbiota has also been proposed to influence systemic inflammation, though this relationship is still under investigation. Vaccinations (e.g., BCG vaccine) can occasionally trigger lesions, indicating immune stimulation as a potential trigger.
The etiology of psoriasis results from the interaction of genetic susceptibility and external triggers. Genomic studies show that interactions among over 30 key genes influence disease expression, while environmental stimuli such as tobacco smoke play a critical triggering role. The imbalance in cytokine networks within the immune system is central to the pathology, but the specific gene-environment interaction mechanisms require further research. Understanding these complex pathogenic mechanisms can aid in developing targeted therapies and personalized preventive strategies.
Patients should avoid contact with irritating chemicals such as fragrances or strong cleaning agents. Keeping the skin moist, avoiding dryness, and reducing stress triggers—such as through meditation or regular exercise—can decrease the frequency of flare-ups.
Does dietary adjustment help improve the condition?Current research suggests that reducing high-sugar and high-fat diets may help control inflammatory responses, while consuming omega-3-rich deep-sea fish or antioxidant foods may alleviate symptoms. However, individual differences are significant, and it is recommended to work with a nutritionist or dermatologist to develop a personalized diet plan.
Will long-term use of corticosteroid ointments lead to drug resistance?Prolonged use of high-dose topical corticosteroids may cause side effects such as skin thinning or vascular dilation, but resistance is rare. Doctors usually recommend rotating different medications (such as retinoids or immunomodulators) and controlling the duration of use to reduce risks.
What is the relationship between emotional stress and psoriasis exacerbation?Stress can trigger or worsen skin symptoms, creating a "stress-inflammation" vicious cycle. Long-term, patients may develop social anxiety or depression due to appearance changes. It is advisable to combine cognitive-behavioral therapy or support groups to improve quality of life.
How does phototherapy work, and is it suitable for all patients?Phototherapy uses specific wavelengths of ultraviolet light to suppress abnormal immune responses, including narrowband UVB and PUVA therapy, which are effective in 70-80% of patients. Excessive sun exposure can worsen the condition; therefore, treatment should be carefully evaluated by a professional based on skin type, lesion location, and overall health status.
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