Psoriasis is a chronic autoimmune-related skin disease, the causes of which involve various complex biological mechanisms. Recent studies have shown that the onset of this disease is closely related to genetics, environmental triggers, immune system abnormalities, and interactions with the neuroendocrine system. The excessive proliferation of keratinocytes in the patient's skin and the abnormal activation of T lymphocytes create a vicious cycle, leading to the typical symptoms of redness, swelling, and scaly patches.
The medical community generally considers psoriasis to be a "multifactorial disease," resulting from the combined effects of genetic predisposition and external triggering factors. Abnormal activation of the immune system is the core pathological mechanism, but the specific triggering mechanisms remain to be fully elucidated. Environmental factors such as infections, stress, and drug reactions are often seen as key to triggering or exacerbating the condition.
Genetic studies have confirmed that psoriasis has a significant familial clustering, with a co-occurrence rate of up to 70% in identical twins. More than 100 genetic loci associated with psoriasis have been identified, among which specific subtypes of the HLA-C gene (such as HLA-Cw6) are strongly associated with disease severity. These genetic variations may affect the signaling of immune cells, leading to abnormal activation of T cells.
The PSORS1 region on chromosome 6 is the most important genetic risk locus, containing several immune-related genes such as CTLA4 and TNFAIP3. A family history is a major risk indicator, with a 10% increased risk of disease onset in children if one parent is affected, and a 50% increase if both parents are affected. It is noteworthy that genetic predisposition is not a decisive factor, as most genetically susceptible individuals do not necessarily develop the disease, requiring the presence of environmental triggering factors.
Infectious events are often viewed as key triggers for the onset of psoriasis. Streptococcal pharyngitis has a clear association with the outbreak of acute arthritic psoriasis, particularly evident in pediatric patients. Viral infections such as HIV may also induce or exacerbate the disease course, indicating that immune responses induced by infections may disrupt disease balance.
Physical stimuli such as trauma, cuts, or severe sunburn can trigger the "Koebner phenomenon," forming new lesions at sites of skin damage. Extreme climatic conditions, such as dry and cold environments, can exacerbate keratin abnormalities, which is a common phenomenon in winter when the condition worsens. In terms of drug-induced factors, medications like beta-blockers and lithium may trigger the appearance of lesions.
Smoking has been confirmed as an important environmental factor for the onset and exacerbation of psoriasis. The tar components in tobacco can directly damage skin barrier function while inducing the release of pro-inflammatory cytokines, such as the overexpression of 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 the systemic release of inflammatory cytokines (such as TNF-α), while inflammatory states may also lead to metabolic abnormalities. In terms of diet, high-sugar diets may exacerbate chronic inflammation, while excessive intake of Omega-6 fatty acids is associated with the spread of skin lesions. Insufficient stress management can exacerbate immune system disorders through abnormalities in the HPA axis.
Age factors indicate that psoriasis has two peaks of onset: 20-30 years and 50-60 years, suggesting that age-related changes in immune regulation may affect disease expression. In terms of gender, the incidence is slightly higher in males, but female patients are more likely to experience severe forms with joint involvement. Certain chronic diseases, such as metabolic syndrome and cardiovascular diseases, share common pathogenic mechanisms with psoriasis.
Congenital defects in the immune system, such as abnormalities in the IL-23 signaling pathway, lead to excessive activation of Th17 cells, forming a persistent inflammatory cycle. Dysbiosis of the gut microbiome has also been suggested to potentially affect systemic inflammatory states, but this association is still under investigation. Vaccinations (such as the BCG vaccine) may occasionally trigger lesions, indicating that immune stimulation could become a trigger point.
The causes of psoriasis result from the interaction of genetic susceptibility and external triggering factors. Genomic studies have shown that interactions among over 30 key genes influence disease expression, while environmental triggers such as tobacco smoke play a critical role. The imbalance of the cytokine network in the immune system is at the core of the pathology, but the specific gene-environment interaction mechanisms require further exploration. Understanding these complex pathogenic mechanisms will aid in the development of targeted treatment strategies and personalized preventive measures.
Patients should avoid contact with irritating chemicals on the skin, such as fragrances or strong detergents. Keeping the skin moisturized, avoiding dryness, and reducing stress triggers, for example, by relieving physical and mental tension through meditation or regular exercise, can reduce the frequency of flare-ups.
Does dietary adjustment help improve the condition?Current research shows that reducing high-sugar and high-fat diets may help control inflammatory responses, while foods rich in Omega-3 from deep-sea fish or antioxidant-rich foods may alleviate symptoms. However, individual differences are significant, so it is recommended to work with a nutritionist or dermatologist to develop a personalized dietary plan.
Will long-term use of steroid ointments lead to resistance?Long-term use of high-dose topical steroids may lead to side effects such as skin thinning or vasodilation, but resistance is less common. Physicians typically recommend rotating the use of different medications (such as retinoids or immunomodulators) and controlling the duration of use to reduce risks.
What is the relationship between emotional stress and the exacerbation of psoriasis?Stress can trigger or exacerbate skin symptoms, creating a "stress-inflammation" vicious cycle. Over time, patients may experience social anxiety or depression due to changes in appearance, and it is advisable to combine cognitive behavioral therapy or support groups to improve quality of life through a dual approach.
What is the principle of phototherapy? Is it suitable for all patients?Phototherapy uses specific wavelengths of ultraviolet light to suppress abnormal immune responses, divided into narrowband UVB and PUVA therapies, effective for 70-80% of patients. However, excessive sun exposure may worsen the condition, and a professional physician should assess skin type, lesion location, and patient health status before formulating a plan.
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