Ascher (Ascher)’s syndrome, also known as bilabial syndrome, goiter and bilabial syndrome; and eyelid laxity syndrome. in 1909, Laffer first reported a patient with bilabial and eyelid laxity, and in 1920, Ascher, an ophthalmologist in Prague, discovered a third symptom – nontoxic Therefore, some scholars also call the above triad the Laffer-Ascher syndrome, the Ascher syndrome, or the triad of bilabial, ptosis, and nontoxic goiter. If all three syndromes are present, the syndrome is called Ascher syndrome complete. Those without an enlarged thyroid gland are called incomplete Ascher syndrome. 1. Etiology: Ascher syndrome is a rare benign disease, and a review of the literature shows that only a few hundred cases have been reported in the global literature. In 2007, Kamran et al. suggested that the disease may be an autosomal dominant disorder. Since many of the reported cases occurred during adolescence, some scholars have speculated that this group of patients may be caused by endocrine dysfunction. However, Papanayotou has reported a case in which the measured 17-OH and 17-KS values were within the normal range. Meanwhile, Lili Guo et al. reported that some patients had normal free T3 and T4, ultrasensitive TSH, thyroid microsomal antibody TM, estradiol E2, and testosterone. Fuehs et al. also reported a case of a patient who developed the disease after swimming in a river under hot sky and concluded that the etiology of the disease was a vascular neural mechanism reaction. He hypothesized that inappropriate hot and cold stimuli induced the endocrine system or neurovascular abnormal response, leading to the occurrence of the syndrome. 2. Clinical features Ascher syndrome occurs mostly in adolescence. Recurrent eyelid edema is the main feature and is often the first clinical symptom or occurs in conjunction with lipomegaly. 80% of cases develop progressive eyelid edema before the age of 20, followed by eyelid atrophy and thinning and drooping, mainly involving the upper lid, with capillary dilatation, and in severe cases affecting the lower lid, rarely with monocular onset. Many patients have a history of mental or physical trauma. Some cases present with progressive edema without acute deterioration. The number of episodes decreases with age and most are in a relatively stationary phase. Repeated edema can damage the eyelid tissue, manifesting as hypertrophy or atrophy, with weakening of the orbital septum allowing fat to prolapse and the eyelid to appear full, and in atrophic cases (flaccid) the eye appears sunken, secondary to significant fat atrophy, resulting in a pseudo-inferior canthus. In chronic cases, the upper lid skin is light red and thin, and dilated capillaries may be present under the epidermis. The upper lid laxity is often combined with hypertrophy or prolapse of the lacrimal gland, a hard, flat oval mass that can be palpated on the upper upper lid and can be retracted into the orbit, which is more obvious when the eye is turned down. The main cause of prolapse is hypertrophy of the lacrimal gland. As the volume of the orbital fossa remains the same and the volume of the other tissues in the orbit remains the same, the hypertrophied lacrimal gland is displaced downward by the crowding of other tissues and gravity, while the hemolymphatic circulation of the eyelid skin is impaired, resulting in degenerative changes over time that lead to relaxation of the orbital septum and lacrimal gland support ligaments and gradual thinning and downward prolapse. The clinical manifestation is a rough, uneven mass that can be palpated over the upper upper eyelid. In individual cases, the canthus is narrowed due to secondary rupture of the medial canthal ligament, and in advanced cases, the ligament and eyelid tissue become unanchored, the canthus becomes horizontally shortened, the outer canthus becomes circumferentially deformed, and the upper lid skin appears excessive, which can affect vision. The second typical clinical manifestation of the disease is bilabialism: it may be recurrent at first and then turn into persistent upper lip enlargement, occasionally involving the lower lip or both upper and lower lips at the same time. As the mucous membrane of the upper lip bulges out in excess, the mucous membrane of the migrating part sags, forming a double arch in the horizontal direction, which is called bilabial syndrome. The specific manifestations are obvious bloating of the upper or lower lip, dry and chapped lip mucosa, mostly occurring in the upper lip, and when eating, speaking and laughing, another lip red appears on the inner side near the lip red, so it is also called heavy lip. When the mouth is closed, the heavy lip part first contacts with the lower lip, and the upper and lower lips cannot contact each other normally, and it is necessary to force the mouth to close in order to make the heavy lip deformity disappear. The third typical clinical feature is a thyroid lesion, which appears late or not at all. It presents only as a mild enlargement, the eyes do not protrude, and there are usually no toxic symptoms of hyperthyroidism or goiter. This symptom usually appears a few years after the onset of the eyelid lesion, with normal basal metabolism and occasional mild elevation, and occurs mostly in the 20s and 30s. Some patients may have clinical manifestations such as facial skin with hyperpigmentation or mild hemifacial atrophy. The biopsy was performed with various tissue stains: the epidermis of the eyelid skin was found to be normal in thickness or moderately atrophic, with basal hyperpigmentation and various degrees of vacuole-like changes, loose collagen fibers in the skin area, not in bundles, capillary dilation, increased number, vascular endothelial hyperplasia, fragmented elastic fibers, and significantly reduced or absent, as evidenced by colloidal iron staining, mucopolysaccharidic acid visible in the epidermis of the lesion increased, inflammatory cell infiltration. Slight or moderate melanin was common in the histiocytes and reticular dermis. Lip mucosal epithelium was hyperkeratotic or underkeratotic, with proliferation of fibrovascular tissue. Abnormal hyperplasia and enlargement of the small salivary glands of the lip. Inflammatory edema of lip mucous glandular tissue, perivascular inflammatory cell infiltration, and focal vasodilatation and congestion between a large number of salivary glands. 4. Diagnosis and differential diagnosis: 4.1 Diagnosis: Ascher syndrome is diagnosed mainly on the basis of clinical symptoms, mostly in adolescence. Recurrent edema of the eyelids is often the first symptom or occurs concurrently with orofacial hypertrophy, and the edema of the eyelids may develop progressively. Non-toxic goiter can also be combined, but is less common. It has been suggested that the third symptom, goiter, is not necessary for the diagnosis of the disease. 4.2 Differential diagnosis: 4.2.1 Ptosis should be differentiated from ptosis and laxity of the eyelid, in which the skin is normal without laxity or folds; laxity of the eyelid is a congenital developmental defect or degenerative change in old age, with no thickening of the upper lip mucosa. The erythema of the upper lid skin should be differentiated from hemangiomas and lymphangioleiomas of the upper lid; the lacrimal gland hyperplasia or prolapse of the upper lid should be differentiated from a displaced salivary gland: the former is located posterior to the orbital septum fat, is dark red, consists of multiple lobules, and can be returned to the orbit: the latter is located anterior to the orbital septum fat and cannot be returned to the orbit; pathologic diagnosis is the basis for its differentiation. 4.2 Mucosal malformations of both lips need to be differentiated from chronic labyrinthitis, lip sarcoidosis, lymphadenopathy, angioneurotic edema, neurofibromatosis, rubbery disease, recurrent dermatitis, syphilis, tuberculosis, leishmaniasis, amyloidosis, and other diseases causing similar thickening of the lip tissue. 5. Glucocorticoids can be used when edema is present before treatment of eyelid laxity, and plastic surgery is feasible when eyelid laxity and upper lip hypertrophy cause dysfunction. The upper eyelid is mainly treated with conventional upper lid laxity correction, and there are no special requirements for the procedure. If there is a combination of lacrimal gland hyperplasia and prolapse, the key to surgery is to shorten the orbital septum and strengthen it. The lacrimal gland is treated in two ways: one is to return the prolapsed lacrimal gland; the other is to remove part of the lacrimal gland. The orbital lacrimal gland is generally easier to separate and return to the lacrimal fossa above the orbit. The lacrimal gland of the lid is located below the lateral ligament of restraint and can be appropriately separated and returned to the lacrimal fossa as far as possible. For lacrimal glands with significant edema or where the lacrimal gland has been dislocated near the lid plate and cannot be completely retracted, partial lacrimal resection is feasible. The excision should not exceed 1/3 of the lacrimal tissue of the lid, and care should be taken not to damage the main branch of the lacrimal duct, which may affect tear secretion. To avoid this, the lacrimal gland should be removed in its lowermost part, lobe by lobe, not in its entirety. Heavy lip surgery is also treated according to the principles of plastic surgery. The enlarged thyroid gland can be treated with iodine.