Pemphigus is a group of chronic autoimmune maculopathies caused by antibodies against bridging granule core proteins (pemphigus antibodies) in the serum. Patients with pemphigus antibodies in the serum combine with autoantigens in the skin and mucous membranes to stimulate an immune response, resulting in the development of loose blisters and vesicles on normal skin or mucous membranes, often secondary to infection, which can be life-threatening, with a mortality rate of approximately 5-15% reported in the literature. Most patients first develop blisters on the oral mucosa, followed by batches of blisters on the skin throughout the body, with thin, flaccid walls that break down easily and form vesicles that do not heal easily. Patients often have symptoms of itching, pain and fever. As the vesicular surface exudes more fluid and protein, coupled with the difficulty of eating due to oral mucosal lesions, the patient’s nutritional status deteriorates and resistance decreases rapidly, making him prone to complications such as bacterial infections, which can be life-threatening in severe cases. Several other types of aspergillosis have relatively mild skin mucosal damage. The etiology and pathogenesis of pemphigus are unknown. Certain medications Pemphigus and herpetiform aspergillosis are autoimmune skin diseases that commonly affect middle-aged and elderly people and are characterized by erythema, blistering, erosion, infection with itching and pain throughout the body, and in severe and even life-threatening cases. The cause of the disease is not clear in most patients, but after careful questioning by the doctor, it may be found that the onset of the disease in some patients is related to certain drugs. In terms of chemical structure, drugs that can cause aspergillosis are divided into three main categories: drugs containing sulfhydryl radicals (such as captopril, penicillamine, sodium thiosulfate gold, etc.), phenols (such as rifampin, methyldopa, etc.), and non-mercapto-nonylphenols (angiotensin-converting enzyme inhibitors, calcium channel blockers, glibenclamide, etc.), which cause aspergillosis through different mechanisms of action. The drugs reported to cause aspergillosis in China include: amoxicillin, cephalosporins, captopril, rifampin, penicillamine, and also antiepileptic drugs have been reported to cause aspergillosis. There are many drugs that can induce pemphigus vulgaris, and the common ones include the following categories: diuretics, antibiotics (including β-lactams, quinolones, and sulfonamides), nonsteroidal anti-inflammatory drugs, antimetabolites, and angiotensin-converting enzyme inhibitors. The induction of herpetiform aspergillosis has also been reported with photochemotherapy for certain skin conditions. Other drugs that have been reported in the literature, although less common in causing herpetiform aspergillosis, include the calcium channel blockers nifedipine and amlodipine. They have also been seen to cause pemphigus vulgaris in some infants and children who have received vaccinations. These drugs containing sulfur groups, especially thiol compounds, and sulfonamide derivatives, are more common. In general, penicillamine, furosemide, and photochemotherapy are the most common causes. Therefore, patients with autoimmune herpetic diseases such as aspergillosis and herpetiform aspergillosis should inform their physicians of the medications they are taking, and the physicians should carefully question such patients about the medications they have taken prior to the onset of the disease, and the physicians should analyze the possibility of drug triggers with the patient. Since aspergillosis and herpetiform aspergillosis occur mostly in middle-aged and elderly people, the combination of other diseases is more common, and a variety of medications may be taken. Therefore, in most cases, it is difficult to determine whether the two diseases are drug-induced or what kind of drugs are used to induce them. If it is clear that the pemphigus or herpetiform aspergillosis is caused by a specific medication, the first step is to discontinue these medications and follow up with systematic treatment under medical supervision. Drugs such as penicillamine and captopril can induce aspergillosis, and those with tumors are called paraneoplastic aspergillosis. Most patients with pemphigus are in serious condition, and certain conditions are needed to confirm the diagnosis. The diagnosis should be confirmed by dermatopathology, immunopathology, enzyme-linked immunosorbent assay and other tests at a hospital of comparable standard, and the concentration of antibodies to pemphigus should be tested to guide treatment. The principles of treatment are early diagnosis, early treatment, regular medication, and long-term follow-up, with most patients requiring 3-4 years or more of continuous medication. Most patients with pemphigus need to take glucocorticoids and immunosuppressive drugs, and the dosage should be gradually reduced under the guidance of a doctor after the disease is controlled. Glucocorticoids can cause side effects such as peptic ulcers, high blood pressure, and high blood sugar, so patients with pemphigus need a low-salt, low-sugar, high-protein diet and avoid foods that irritate the gastrointestinal tract, such as foods that are too hard, salty, spicy, and indigestible. Blindly avoiding food is not good for the recovery of aspergillosis. Changes in blood sugar, blood pressure, electrolytes, and bone density need to be closely monitored while using hormones. When using immunosuppressants such as cyclophosphamide, it is especially important to regularly check the blood routine, liver and kidney functions and other items.