| disease | Erythrodermic Psoriasis |
This disease is caused by improper treatment, especially when highly irritating drugs are applied during the acute progressive stage of psoriasis vulgaris, or when corticosteroids are used in large quantities over a long period for psoriasis vulgaris, followed by inappropriate withdrawal or dosage reduction. Additionally, erythroderma may also occur during the regression of pustules in pustular psoriasis. This condition accounts for approximately 1% of psoriasis cases.
bubble_chart Etiology
The exact cause remains unclear. Currently, it has not been possible to induce this disease in animals or humans through experimental methods. In recent years, it has been widely believed that genetic factors, metabolic disorders, infections, and immune dysfunction may be significant contributing factors to the onset of the disease. Seasonal changes, humidity, psychological trauma, or surgery may also trigger the condition.
**Genetics**: International reports suggest a family history in approximately 30% of cases, while domestic data indicate a range of 10–17%. Regarding the mode of inheritance, some propose autosomal dominant inheritance with incomplete penetrance, while others suggest autosomal recessive or X-linked inheritance. The incidence of psoriasis also appears to vary by ethnicity, with reports indicating a lower prevalence among Black populations.
Recent studies have identified a strong association between human leukocyte antigens (HLA) and psoriasis. International reports show significantly higher frequencies of HLA-B13 and HLA-B17 antigens in psoriasis patients, though some studies also report elevated levels of HLA-B3, HLA-CL7, and HLA-W6. In Chinese patients, besides the notable increase in HLA-B13 and HLA-B17, HLA-BW35 levels are significantly lower. It is now generally accepted that psoriasis is controlled by multiple genes and influenced by environmental factors.
**Infections**: Clinically, some cases of psoriasis are linked to upper respiratory infections and tonsillitis. The condition may improve after antibiotic treatment or tonsillectomy, particularly in acute guttate psoriasis. Some reports indicate rapid worsening of psoriasis following streptococcal infections, accompanied by elevated anti-streptolysin O (ASO) titers, suggesting a connection between psoriasis onset and streptococcal infections. Some propose a viral etiology, noting that antiviral therapy in patients with concurrent viral infections may lead to psoriasis remission. Eosinophilic inclusions have been observed in the nuclei of spinous cells.**Metabolic Disorders**: Past suspicions implicated metabolic disturbances—such as protein, sugar, vitamin deficiencies, or sulfur and/or inorganic salt imbalances—in psoriasis development, though none have been confirmed. Recent research demonstrates that cAMP (cyclic adenosine monophosphate) levels in psoriatic epidermis are significantly lower than in normal skin, while cGMP (cyclic guanosine monophosphate) levels are higher. The latter promotes cell proliferation, leading to uncontrolled epidermal cell growth in lesions.
**Immune Dysfunction**: Growing evidence highlights the critical role of immune factors in the pathogenesis of psoriasis. Key processes include activation of dermal vascular endothelial cells, aggregation of mononuclear cells, expression of cytokines and adhesion molecules, and induced hyperproliferation of keratinocytes. Consequently, some argue that psoriasis is fundamentally an immune cell-mediated disorder.
Beyond the aforementioned factors, other reported triggers include psychological trauma, physical injury or surgery, cold, humidity, hemorheological changes, as well as associations with menstruation, pregnancy, childbirth, and diet. These are currently regarded as potential precipitating factors.
Initially, erythema appears at the original psoriatic skin lesions and rapidly spreads into large patches, eventually presenting as diffuse erythematous infiltration over the entire body. Among this diffuse erythematous infiltration, patchy areas of normal "skin islands" are often observed, which is one of the characteristic features of this condition. During the course of the disease, a large amount of scale sheds daily, and the scalp accumulates thick, scaly crusts. In the late stage (third stage), the hands and feet may exhibit extensive skin peeling, resembling worn-out socks or gloves. The nails become cloudy, thickened, deformed, and may even fall off. The mouth, throat, nasal cavity, and conjunctiva are congested and red. It is often accompanied by fever, chills, headaches, general malaise, and other symptoms. Superficial lymph nodes may swell, and the white blood cell count increases. The nature of this disease is stubborn, with a tendency to relapse after recovery. Cases accompanied by arthritis have a more severe prognosis. Due to prolonged persistence and recurrent episodes, patients gradually weaken and are prone to secondary complications, leading to adverse outcomes. After treatment, the skin returns to normal, but the psoriatic lesions reappear.
The primary basis is generalized diffuse erythroderma with extensive bran-like scales and residual normal "skin islands," along with a history of psoriasis. It should be differentiated from erythroderma caused by other factors (such as drug rash, pityriasis rubra pilaris, etc.), as the latter lacks a history of psoriasis.
