Dermatitis herpetiformis (DH), or Duhring-Brocq disease, is a chronic blistering skin autoimmune condition, characterized by the presence of skin lesions that have an extensive and symmetrical distribution, predominating in areas of greater friction, and affecting mainly both elbows, knees, buttocks, ankles, and may also affect the scalp and other parts of the body, and non-symmetrical occasionally. The lesions are vesicular-crusted and when flake off, they evolve to pigmented areas or achromic an intense burning, itchy and blistering rash. Despite its name, DH is neither related to nor caused by herpes virus: the name means that it is a skin inflammation having an appearance similar to herpes.

The age of onset is variable starting in children and adolescence but can also affect individuals of both sexes indistinctly at any age of their lives.

A fact that difficults its diagnosis is the relatively common presentation with atypical manifestations. Some patients may show erythema or severe pruritus alone, wheals of chronic urticaria, purpuric lesions resembling petechiae on hands and feet, palmo-plantar keratosis, leukocytoclastic vasculitis-like appearance, and/or lesions mimicking prurigo pigmentosa. DH may be confused with many different cutaneous lesions, such as atopic dermatitis, eczema, urticaria, scabies, impetigo, polymorphic erythema and other autoimmune blistering diseases.

DH is considered to be as "the coeliac disease of the skin". For this reason, the new guidelines of the European Society for Pediatric Gastroenterology, Hepatology and Nutrition for the diagnosis of coeliac disease conclude that its proven presence, by itself, confirms the diagnosis of coeliac disease. Nevertheless, duodenal biopsy is recommended in doubtful DH cases, or if there are suspected gastrointestinal complications, including lymphoma. People with DH have different degrees of intestinal involvement, ranging from milder mucosal lesions to the presence of villous atrophy.

The main and more efficacious treatment for DH is following a lifelong gluten-free diet, which produces the improvement of skin and gut lesions. Nevertheless, the skin lesions may take several months or even years to disappear. To calm itching, dapsone is often recommended as a temporary treatment, during the time it takes for the diet to work, but it has no effect on the gastrointestinal changes and may have important side effects.

Oat sensitivity represents a sensitivity to the proteins found in oats, "Avena sativa". Sensitivity to oats can manifest as a result of allergy to oat seed storage proteins either inhaled or ingested. A more complex condition affects individuals who have gluten-sensitive enteropathy in which there is also a response to avenin, the glutinous protein in oats similar to the gluten within wheat. Sensitivity to oat foods can also result from their frequent contamination by wheat, barley, or rye particles.

Gastrointestinal symptoms may include any of the following: abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation), nausea, aerophagia, gastroesophageal reflux disease, and aphthous stomatitis.

Reported symptoms of NCGS are similar to those of celiac disease, with most patients reporting both gastrointestinal and non-gastrointestinal symptoms. In the "classical" presentation of NCGS, gastrointestinal symptoms are similar to those of irritable bowel syndrome, and are also not distinguishable from those of wheat allergy, but there is a different interval between exposure to wheat and onset of symptoms. Wheat allergy has a fast onset (from minutes to hours) after the consumption of food containing wheat and can be anaphylaxic.

More than 250 symptoms of gluten sensitivity have been reported, including bloating, abdominal discomfort or pain, constipation and diarrhea. Sensitivity may also present with extraintestinal symptoms, including headache, "brain fog", tingling and/or numbness in hands and feet, fatigue, as well as muscular disturbances and bone or joint pain; also neuropsychiatric manifestations ("gluten-sensitive idiopathic neuropathies") have been reported on.

The classic symptoms of coeliac disease include pale, loose, and greasy stool (steatorrhoea) and weight loss or failure to gain weight. More common symptoms are subtle or primarily occur in organs other than the bowel itself. It is also possible to have coeliac disease without any classic symptoms whatsoever. This represents at least 43% of the cases in children. Many adults with subtle disease only have fatigue or anaemia.

Studies on farmers with grain dust allergy and children with atopy dermatitis reveal that oat proteins can act as both respiratory and skin allergens. Oat dust sensitivity in farms found 53% showed reactivity to dust, second only to barley (70%), and almost double that of wheat dust. The 66 kDa protein in oats was visualized by 28 out of 33 sera (84%). However, there was evident non-specific binding to this region and thus it may also represent lectin-like binding. IgA and IgG responses, meanwhile, like those seen to anti-gliadin antibodies in celiac disease or dermatitis herpetiformis, are not seen in response to avenins in atopic dermatitis patients. Food allergies to oats can accompany atopy dermatitis. Oat avenins share similarities with γ and ω-gliadins of wheat — based on these similarities they could potentiate both enteropathic response and anaphylactic responses. Oat allergy in gluten-sensitive enteropathy can explain an avenin-sensitive individual with no histological abnormality, no T-cell reaction to avenin, bearing the rarer DQ2.5"trans" phenotype, and with anaphylactic reaction to avenin.

Coeliac disease, also spelled celiac disease, is a long-term autoimmune disorder primarily affecting the small intestine that occurs in people who are genetically predisposed. Classic symptoms include gastrointestinal problems such as chronic diarrhoea, abdominal distention, malabsorption, loss of appetite, and among children failure to grow normally. This often begins between six months and two years of age. Non-classic symptoms are more common, especially in people older than two years. There may be mild or absent gastrointestinal symptoms, a wide number of symptoms involving any part of the body, or no obvious symptoms. Coeliac disease was first described in childhood; however, it may develop at any age. It is associated with other autoimmune diseases, such as diabetes mellitus type 1 and thyroiditis, among others.

Coeliac disease is caused by a reaction to gluten, which are various proteins found in wheat and in other grains such as barley, and rye. Moderate quantities of oats, free of contamination with other gluten-containing grains, are usually tolerated. The occurrence of problems may depend on the variety of oat. Upon exposure to gluten, an abnormal immune response may lead to the production of several different autoantibodies that can affect a number of different organs. In the small-bowel this causes an inflammatory reaction and may produce shortening of the villi lining the small intestine (villous atrophy). This affects the absorption of nutrients, frequently leading to anaemia.

Diagnosis is typically made by a combination of blood antibody tests and intestinal biopsies, helped by specific genetic testing. Making the diagnosis is not always straightforward. Frequently, the autoantibodies in the blood are negative and many people have only minor intestinal changes with normal villi. People may have severe symptoms and be investigated for years before a diagnosis is achieved. Increasingly, the diagnosis is being made in people without symptoms as a result of screening. Evidence regarding the effects of screening, however, is not sufficient to determine its usefulness. While the disease is caused by a permanent intolerance to wheat proteins, it is not a form of wheat allergy.

The only known effective treatment is a strict lifelong gluten-free diet, which leads to recovery of the intestinal mucosa, improves symptoms, and reduces risk of developing complications in most people. If untreated, it may result in cancers such as intestinal lymphoma and a slight increased risk of early death. Rates vary between different regions of the world, from as few as 1 in 300 to as many as 1 in 40, with an average of between 1 in 100 and 1 in 170 people. In developed countries, it is estimated that 80% of cases remain undiagnosed, usually because of minimal or absent gastrointestinal complaints and poor awareness of the condition. Coeliac disease is slightly more common in women than in men. The term "coeliac" is from the Greek κοιλιακός ("koiliakós", "abdominal") and was introduced in the 19th century in a translation of what is generally regarded as an ancient Greek description of the disease by Aretaeus of Cappadocia.

Wheat allergy is an allergy which typically presents itself as a food allergy, but can also be a contact allergy resulting from occupational exposure to wheat. Like all allergies, wheat allergy involves immunoglobulin E and mast cell response. Typically the allergy is limited to the seed storage proteins of wheat, some reactions are restricted to wheat proteins, while others can react across many varieties of seeds and other plant tissues. Wheat allergy may be a misnomer since there are many allergenic components in wheat, for example serine protease inhibitors, glutelins and prolamins and different responses are often attributed to different proteins. Twenty-seven potential wheat allergens have been successfully identified. The most severe response is exercise/aspirin induced anaphylaxis attributed to one omega gliadin that is a relative of the protein that causes celiac disease. Other more common symptoms include nausea, urticaria, atopy. Gluten sensitivity is not usually classified as a wheat allergy.

Diagnoses of wheat allergy may deserve special consideration. Omega-5 gliadin, the most potent wheat allergen, cannot be detected in whole wheat preparations; it must be extracted and partially digested (similar to how it degrades in the intestine) to reach full activity. Other studies show that digestion of wheat proteins to about 10 amino acids can increase the allergic response 10 fold. Certain allergy tests may not be suitable to detect all wheat allergies, resulting in cryptic allergies. Because many of the symptoms associated with wheat allergies, such as sacroiliitis, eczema and asthma, may be related or unrelated to a wheat allergy, medical deduction can be an effective way of determining the cause. If symptoms are alleviated by immunosuppressant drugs, such as Prednisone, an allergy-related cause is likely. If multiple symptoms associated with wheat allergies are present in the absence of immunosuppressants then a wheat allergy is probable.

The most common symptoms of salicylate sensitivity are:

- Stomach pain/upset stomach

- Tinnitus ringing of the ears

- Itchy skin, hives or rashes

- Asthma and other breathing difficulties

- Angioedema

- Headaches

- Swelling of hands, feet, eyelids, face and/or lips

- Bed wetting or urgency to pass water

- Persistent cough

- Changes in skin color/skin discoloration

- Fatigue

- Sore, itchy, puffy or burning eyes

- Sinusitis/Nasal polyps

- Diarrhea

- Nausea

- Hyperactivity

- Memory loss and poor concentration

- Depression

- Pseudoanaphylaxis

Salicylate sensitivity, also known as salicylate intolerance, is any adverse effect that occurs when a usual amount of salicylate is ingested. People with salicylate intolerance are unable to consume a normal amount of salicylate without adverse effects.

Salicylate sensitivity differs from salicylism, which occurs when an individual takes an overdose of salicylates. Salicylate overdose can occur in people without salicylate sensitivity, and can be deadly if untreated. For more information, see aspirin poisoning.

Salicylates are derivatives of salicylic acid that occur naturally in plants and serve as a natural immune hormone and preservative, protecting the plants against diseases, insects, fungi, and harmful bacteria. Salicylates can also be found in many medications, perfumes and preservatives. Both natural and synthetic salicylates can cause health problems in anyone when consumed in large doses. But for those who are salicylate intolerant, even small doses of salicylate can cause adverse reactions.

The various non-allergic NSAID hypersensitivity syndromes affect 0.5–1.9% of the general population, with AERD affecting about 7% of all asthmatics and about 14% of patients with severe asthma. AERD, which is more prevalent in women, usually begins in young adulthood (twenties and thirties are the most common onset times although children are afflicted with it and present a diagnostic problem in pediatrics) and may not include any other allergies. Most commonly the first symptom is rhinitis (inflammation or irritation of the nasal mucosa), which can manifest as sneezing, runny nose, or congestion. The disorder typically progresses to asthma, then nasal polyposis, with aspirin sensitivity coming last. Anosmia (lack of smell) is also common, as inflammation within the nose and sinuses likely reaches the olfactory receptors.

The respiratory reactions to aspirin vary in severity, ranging from mild nasal congestion and eye watering to lower respiratory symptoms including wheezing, coughing, an asthma attack, and in rare cases, anaphylaxis. In addition to the typical respiratory reactions, about 10% of patients with AERD manifest skin symptoms like urticaria and/or gastrointestinal symptoms such as abdominal pain or vomiting during their reactions to aspirin.

In addition to aspirin, patients usually also react to other NSAIDs such as ibuprofen, and to any medication that inhibits the cyclooxygenase-1 (COX-1) enzyme, although paracetamol (acetaminophen) in low doses is generally considered safe. NSAID that are highly selective in blocking COX-2 and do not block its closely related paralog, COX-1, such as the COX-2 inhibitors celecoxib and rofecoxib, are also regarded as safe. Nonetheless, recent studies do find that these types of drugs, e.g. acetaminophen and celecoxib, may trigger adverse reactions in these patients; caution is recommended in using any COX inhibitors. In addition to aspirin and NSAIDs, consumption of even small amounts of alcohol also produces uncomfortable respiratory reactions in many patients.

Aspirin-induced asthma, also termed Samter's triad, Samter's syndrome, aspirin-exacerbated respiratory disease (AERD), and recently by an appointed task force of the European Academy of Allergy and Clinical Immunology/World Allergy Organization (EAACI/WAO) Nonsteroidal anti-inflammatory drugs-exacerbated respiratory disease (N-ERD). is a medical condition initially defined as consisting of three key features: asthma, respiratory symptoms exacerbated by aspirin, and nasal/ethmoidal polyposis; however, the syndrome's symptoms are exacerbated by a large variety of other nonsteroidal anti-inflammatory drugs (NSAIDs) besides aspirin. The symptoms of respiratory reactions in this syndrome are hypersensitivity reactions to NSAIDs rather than the typically described true allergic reactions that trigger other common allergen-induced asthma, rhinitis, or hives. The NSAID-induced reactions do not appear to involve the common mediators of true allergic reactions, immunoglobulin E or T cells. Rather, AERD is a type of NSAID-induced hypersensitivity syndrome. EAACI/WHO classifies the syndrome as one of 5 types of NSAID hypersensitivity or NSAID hypersensitivity reactions.

Symptoms depend on each person's allergies and each perfume's or fragrance's ingredients. Symptoms may include allergic contact dermatitis, asthma attacks, headaches, and others. The most common allergic reactions to perfume or fragrances added to products is contact dermatitis, though other symptoms may occur, including allergic conjunctivitis.

The diagnosis of the causal allergen is made by patch testing with a mixture of fragrance ingredients, the fragrance mix. This gives a positive patch-test reaction in about 10% of tested patients with eczema, and the most recent estimates show that 1.7–4.1% of the general population are sensitized to ingredients of the fragrance mix.

Two studies show that inhalant-like allergies and sensitivity/intolerances are experienced by a subset of the US population, in the form of asthma and chemical sensitivities. Results aggregated from both surveys found that 30.5% of the general population reported scented products on others irritating, 19% reported adverse health effects from air fresheners, and 10.9% reported irritation by scented laundry products vented outside.

Household products, such as soaps and detergents, perfume products, cosmetics, and other consumer goods, are estimated to use 2,500 different fragrance ingredients. Of those, approximately 100 different substances are known to elicit responses in at least some individuals. An estimated 1.7–4.1% of the general population shows a contact allergic response to a mix of common perfume ingredients.

The diagnosis is made by patch testing with a mixture of fragrance ingredients, the fragrance mix. This gives a positive patch-test reaction in about 10% of tested patients with eczema, and the most recent estimates show that 1.7–4.1% of the general population are sensitized to ingredients of the fragrance mix.

Although products can be labeled "fragrance-free", many still contain lesser-known fragrance chemicals that consumers may not recognize.

Cinnamaldehyde (cinnamic aldehyde) is a common fragrance allergen.

Perfume intolerance or perfume allergy is a condition wherein people exhibit sensitivity or allergic reactions to ingredients in some perfumes and some other fragrances.

Lactose intolerance is a condition in which people have symptoms due to the decreased ability to digest lactose, a sugar found in milk products. Those affected vary in the amount of lactose they can tolerate before symptoms develop. Symptoms may include abdominal pain, bloating, diarrhea, gas, and nausea. These symptoms typically start between half and two hours after drinking milk or eating milk products. Severity depends on the amount a person eats or drinks. It does not cause damage to the gastrointestinal tract.

Lactose intolerance is due to the lack of enzyme lactase in the small intestines to break lactose down into glucose and galactose. There are four types: primary, secondary, developmental, and congenital. Primary lactose intolerance is when the amount of lactase declines as people age. Secondary lactose intolerance is due to injury to the small intestine such as from infection, celiac disease, inflammatory bowel disease, or other diseases. Developmental lactose intolerance may occur in premature babies and usually improves over a short period of time. Congenital lactose intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth.

Diagnosis may be confirmed if symptoms resolve following eliminating lactose from the diet. Other supporting tests include a hydrogen breath test and a stool acidity test. Other conditions that may produce similar symptoms include irritable bowel syndrome, celiac disease, and inflammatory bowel disease. Lactose intolerance is different from a milk allergy. Management is typically by decreasing the amount of lactose in the diet, taking lactase supplements, or treating the underlying disease. People are usually able to drink at least one cup of milk per sitting without developing significant symptoms, with greater amounts tolerated if drunk with a meal or throughout the day.

The exact number of adults with lactose intolerance is unknown. One estimate puts the average at 65% of the global population. Rates of lactose intolerance vary between regions, from less than 10% in Northern Europe to as high as 95% in parts of Asia and Africa. Onset is typically in late childhood or early adulthood. The ability to digest lactose into adulthood evolved in several human populations independently probably as an adaptation to domestication of dairy animals 10,000 years ago.

Lactose intolerance primarily refers to a syndrome having one or more symptoms upon the consumption of food substances containing lactose. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms. "Lactose malabsorption" refers to the physiological concomitant of lactase deficiency (i.e., the body does not have sufficient lactase capacity to digest the amount of lactose ingested). Hypolactasia (lactase deficiency) is distinguished from alactasia (total lack of lactase), a rare congenital defect.

Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy caused by lactase deficiency. Milk allergy, occurring in only 4% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction.

Photodermatitis may result in swelling, difficulty breathing, a burning sensation, a red itchy rash sometimes resembling small blisters, and peeling of the skin. Nausea may also occur. There may also be blotches where the itching may persist for long periods of time. In these areas an unsightly orange to brown tint may form, usually near or on the face.

Symptoms range in severity from mild to disabling.

Symptoms are common, but vague and non-specific for the condition. The most common are feeling tired, "brain fog" (short-term memory problems, difficulty concentrating), gastrointestinal problems, headaches, and muscle pain.

A partial list of other symptoms patients have attributed to MCS include: difficulty breathing, pains in the throat, chest, or abdominal region, skin irritation, headaches, neurological symptoms (nerve pain, pins and needles feelings, weakness, trembling, restless leg syndrome), tendonitis, seizures, visual disturbances (blurring, halo effect, inability to focus), anxiety, panic and/or anger, sleep disturbance, suppression of immune system, digestive difficulties, nausea, indigestion/heartburn, vomiting, diarrhea, joint pains, vertigo/dizziness, abnormally acute sense of smell (hyperosmia), sensitivity to natural plant fragrance or natural pine terpenes, dry mouth, dry eyes, and an overactive bladder.

Photodermatitis, sometimes referred to as sun poisoning or photoallergy, is a form of allergic contact dermatitis in which the allergen must be activated by light to sensitize the allergic response, and to cause a rash or other systemic effects on subsequent exposure. The second and subsequent exposures produce photoallergic skin conditions which are often eczematous.

Multiple chemical sensitivity (MCS), also known as idiopathic environmental intolerances (IEI), is a disputed chronic condition characterized by symptoms that the affected person attributes to low-level exposures to commonly used chemicals. Symptoms are typically vague and non-specific. They may include fatigue, headaches, nausea, and dizziness.

Commonly attributed substances include scented products, pesticides, plastics, synthetic fabrics, smoke, petroleum products, and paint fumes.

Although the symptoms themselves are real, and can be disabling, MCS is not recognized as an organic, chemical-caused illness by the World Health Organization, American Medical Association, or any of several other professional medical organizations. Blinded clinical trials show that people with MCS react as often and as strongly to placebos as they do to chemical stimuli; the existence and severity of symptoms is related to perception that a chemical stimulus is present. Some attribute the symptoms to depression, somatoform disorders, or anxiety disorders.

With single or prolonged exposure by inhalation the lungs may become sensitized to beryllium. Berylliosis has an insidious onset and runs an indolent course. Some people who are sensitized to beryllium may not have symptoms. Continued exposure causes the development of small inflammatory nodules, called granulomas. Of note, the authors of a 2006 study suggested that beryllium inhalation was not the only form of exposure and perhaps skin exposure was also a cause, as they found that a reduction in beryllium inhalation did not result in a reduction in CBD or beryllium sensitization.

Granulomas are seen in other chronic diseases, such as tuberculosis and sarcoidosis, and it can occasionally be hard to distinguish berylliosis from these disorders. However, granulomas of CBD will typically be non-caseating, i.e. not characterized by necrosis and therefore not exhibiting a cheese-like appearance grossly.

Ultimately, this process leads to restrictive lung disease (a decrease in diffusion capacity).

The earliest symptoms are typically cough and shortness of breath. Other symptoms include chest pain, joint aches, weight loss, and fever.

Rarely, one can get granulomas in other organs including the liver.

The onset of symptoms can range from weeks up to tens of years from the initial exposure. In some individuals, a single exposure to beryllium can cause berylliosis.

These conditions are sometimes considered together with the small vessel vasculitides.

Polyarteritis nodosa (PAN). Systemic necrotizing vasculitis and aneurysm formation affecting both medium and small arteries. If only small vessels are affected, it is called microscopic polyangiitis, although it is more associated with granulomatosis with polyangiitis than to classic PAN. At least 3 out of 10 criteria yields sensitivity and specificity of 82 and 87%:

- unexplained weight loss > 4 kg

- livedo reticularis

- testicular pain

- myalgias, weakness

- Abdominal pain, diarrhea, and GI bleeding

- mononeuropathy or polyneuropathy

- new onset diastolic blood pressure > 90 mmHg

- elevated serum BUN (> 40 mg/dL) or serum creatinine (> 1.5 mg/dL)

- hepatitis B infection

- arteriographic abnormalities

- arterial biopsy showing polymorphonuclear cells

Kawasaki disease. Usually in children(age<4), it affects large, medium, and small vessels, prominently the coronary arteries. Associated with a mucocutaneous lymph node syndrome. Diagnosis requires fever lasting five days or more with at least 4 out of 5 criteria:

- bilateral conjunctival injection

- injected or fissured lips, injected pharynx, or strawberry tongue

- erythema of palms/soles, edema of hands/feet, periungual desquamation

- polymorphous rash

- cervical lymphadenopathy (at least one node > 1.5 cm)

Isolated cerebral vasculitis. Affects medium and small arteries over a diffuse CNS area, without symptomatic extracranial vessel involvement. Patients have CNS symptoms as well as cerebral vasculitis by angiography and leptomeningeal biopsy.

Granulomatosis with polyangiitis (GPA; formerly known as Wegener's granulomatosis). Systemic vasculitis of medium and small arteries, including venules and arterioles. Produces granulomatous inflammation of the respiratory tracts and necrotizing, pauci-immune glomerulonephritis. Most common cause of saddle nose deformity in USA (nose flattened due to destruction of nasal septum by granulomatous inflammation). Almost all patients with WG have c-ANCA, but not vice versa. Current treatment of choice is cyclophosphamide. At least 2 out of 4 criteria yields sensitivity and specificity of 88 and 92%.

- nasal or oral inflammation (oral ulcers or purulent/bloody nasal discharge, may be painful)

- abnormal CXR showing nodules, infiltrates, cavities

- microscopic hematuria or RBC casts

- vessel biopsy shows granulomatous inflammation

- Peak incidence: ages 40–60, males > females

Eosinophilic granulomatosis with polyangiitis (EGPA; formerly known as Churg-Strauss syndrome). Affects medium and small vessels with vascular and extravascular granulomatosis. Classically involves arteries of lungs and skin, but may be generalized. At least 4 criteria yields sensitivity and specificity of 85 and 99.7%.

- asthma (history of wheezeing or presently wheezing)

- eosinophilia > 10% on CBC

- mononeuropathy or polyneuropathy

- migratory or transient pulmonary opacities on chest x-ray (CXR)

- paranasal sinus abnormalities

- vessel biopsy showing eosinophils in extravascular areas

Microscopic polyarteritis/polyangiitis. Affects capillaries, venules, or arterioles. Thought to be part of a group that includes granulomatosis with polyangiitis since both are associated with ANCA and similar extrapulmonary manifestations. Patients do not usually have symptomatic or histologic respiratory involvement.