An autoimmune disorder known as linear immunoglobulin A (IgA) dermatosis (LAD) causes a linear deposition of IgA at the basement membrane zone (BMZ). Both children and adults are impacted by the illness. It could be drug-related or unrelated to drugs. The cause of the non-drug category is largely unknown. But numerous cases have been documented after an illness episode (such as typhoid, brucella, TB, varicella, herpes zoster, other gynecological diseases, and upper respiratory infections). The illness in kids has previously been referred to as childhood chronic bullous dermatosis.

Introduction:

A condition known as linear IgA bullous illness causes blisters to appear on the outermost layer of skin and mucous membranes, including the conjunctivae, vaginal mucosae, and mouth.  Its name derives from the distinctive immunofluorescent immunoglobulin A (IgA) linear deposition findings at the dermo-epidermal border (at the basement membrane zone). It is also known as linear IgA bullous dermatosis, and in children, it may also be referred to as chronic bullous illness of childhood or linear IgA dermatosis of childhood. It is unclear what causes linear IgA disease biologically.

Antibodies to BP180 (collagen XVII), whose extracellular section is continuously shed from the cell exterior by ADAMs (proteinases that include adhesive and metalloprotease domains), are at the core of the disease. By stabilizing the hemidesmosome complex, BP180 performs the role of a cell-matrix binding molecule normally. Similar to MMP, in vivo and in vitro studies show that BP180 plays a crucial pathogenic function, but they also show that the severity of the disease depends on the serum concentration and epitope specificity of these antibodies.

Causes:

The precise process of lesion formation is not fully understood, despite the fact that it has been determined to be an autoimmune illness. Numerous antigens from human leukocyte types have been associated with the occurrence of chronic bullous illness in childhood, which may be influenced by genetic factors. Vancomycin is one of the most well-known factors for drug-induced linear IgA, however many other drugs can also cause it. In many drug-induced situations, the linear IgA, illness course is acute and goes away if the offending substance is stopped right once.

Symptoms:

Vesicular or bullous skin lesions typically appear in a herpetiform pattern in linear IgA disease. When it affects younger children, the face and perineum are frequently affected, and it frequently spreads to the limbs, trunk, hands, feet, and scalp. In adults, the top of the head, face, and limbs are frequently involved, while the trunk is almost always affected. Lesions frequently itch and even burn. Both age groups frequently experience mucosal involvement, while milia are not typical. Vaginal or genital manifestations, which are less frequent, can also exist. Mucosal involvement is seen in 65% to 85% of people, including both adults and children. These lesions are characterized by urticated plaques and papules with vesicles and blisters. Vesicles or blisters may appear on healthy skin or on top of urticated plaques.

Diagnosis:

As symptoms and signs of the disease frequently match those of other blistering disorders, a history and physical examination alone are typically insufficient to make a conclusive diagnosis. Direct immunofluorescence of skin next to a blister, which shows a linear band of IgA at the dermo-epidermal interface, is the best method for diagnosing linear IgA disease. Additionally, a full medication history should be obtained to identify any potential drug aetiologies.

Complications:

Scarring frequently leads to complications. Desquamative gingivitis, which can occur from gum lesions, can harm the teeth. Blindness could result from ocular linear IgA, which resembles cicatricial pemphigoid. According to reports, the pharynx, larynx, nose, rectum, and esophagus are all affected. Most idiopathic instances in youngsters become better within two years. Adults may experience longer-lasting disease that, in some situations, is refractory. Pregnancy may ameliorate linear IgA disease. Dapsone, the medication used to treat the condition, has never been associated with fetal harm.

Homeopathic Treatment:

The high demand for natural therapies and aromatic chemicals is reflected in the rising prevalence of tea tree oil dermatitis. IgA deposition in the basement membrane zone is a hallmark of the uncommon acquired subepidermal blistering syndrome known as linear IgA disease. In this case study, we present a patient whose linear IgA illness seems to have been triggered by a contact response to tea tree oil. Topical corticosteroids can be used to treat minor illnesses. Children can utilize oral erythromycin. Alternatives for all ages include colchicine, dapsone, and sulfonamides (with dosages and precautions identical to those for dermatitis herpetiformis). The mucosal lesions frequently respond later than the cutaneous lesions.

After 3 to 6 years, the majority of patients experience spontaneous remission. While corticosteroids should normally not be used in children because of its long-term negative effects, some patients may require a modest dosage of prednisone to prevent blister development or when there is substantial mucosal involvement in order to achieve better disease control. Tetracyclines are not recommended for use in children under the age of eight due to the possibility of permanent tooth discoloration, but other antibiotics such oxacillin, erythromycin, sulfamethoxypyridazine, flucloxacillin, and cotrimoxazole have been used with varying degrees of success. Nicotinamide, which has been studied either alone or in conjunction with dapsone, is a different medication that has been shown to be effective in treating linear IgA disorder. Nicotinamide’s therapeutic effect is to prevent the local variables that lead to blister formation.

Precautions:

Making a few dietary changes could help you stop the progression of linear IgA disease. This involves consuming a diet low in cholesterol and saturated fats. Lowering your sodium intake by consuming fewer sources of omega-3 fats, such as flaxseeds, soybean oil, cod liver oil, walnuts as well, and fish oil supplements, but maintaining a diet low in protein. You can attempt to adhere to a diet similar to the DASH diet to lower your intake of sodium and cholesterol. Dietary methods to stop hypertension or DASH. With this diet, you should consume fewer sodium-containing foods such as fruits, vegetables, healthy grains, and lean meats.