Gut health issues cause many different adverse skin conditions. From acne, psoriasis, to eczema many people who suffer from poor gut health also have skin problems. What if I told you there is a skin condition that is strongly linked to celiac disease, gluten ingestion, and upper gut pathogens including H.pylori. An autoimmune condition, dermatitis herpetiformis, is overlooked and misdiagnosed by most doctors and sadly goes untreated. So how can you make sure your doctor accurately diagnoses dermatitis herpetiformis and what can be done to overcome the condition?

What Is Dermatitis Herpetiformis and How Is It Diagnosed?

Dermatitis herpetiformis is a chronic skin condition that causes an intensely itchy small red rash that resembles a widespread herpes outbreak. The rash is distributed systemically externally on the skin, and the blisters can vary in size from being very small to a couple of centimeters across. The outbreak is mainly found on the buttocks, back of the neck, scalp, knees, elbows, back, trunk, abdomen, and face. The first signs of the skin condition are strong burning or itching and reddening of the skin then small vesicles appear that look like tiny red bumps. The rash, unlike a herpes outbreak, rarely appears on mucous membranes including the mouth, vagina, nasal cavity, or the lips. The rash can even blister if the inflammation is severe or the person inflicted with the condition scratches the rash intensely. Finally, during the healing phase of the disease, the rash fades, and the blister heals leaving pigment skin changes and occasionally scarring.

Dermatitis herpetiformis is usually diagnosed by a dermatologist or a gastroenterologist, but it can be easily misdiagnosed as well as other conditions including medication-induced skin lesions (linear IgA bullous dermatosis for example caused by vancomycin), contact dermatitis, scabies, herpes outbreak, or dyshidrosis. The diagnosis of dermatitis herpetiformis can be achieved through a tissue transglutaminase IgA serum antibody test. For a correct antibody test result, you would have had to ingest gluten recently to test positive, or a false negative may occur on those who have given up gluten months beforehand. Skin eruptions may occur in people who are only gluten sensitive and do not suffer from celiac disease; you can even have negative tissue transglutaminase IgA serum antibody test results as well. The only way you would know for sure if gluten is the cause of your skin eruptions is by going on a strict gluten-free diet for a few months to see if the outbreaks heal and remain in remission.1 2

Skin tissue biopsies may be needed to diagnose dermatitis herpetiformis. However, biopsies may still be sometimes confused with other skin issues, so it is essential to still run blood antibody tests to tissue transglutaminase for an accurate diagnosis. “Classically, in dermatitis herpetiformis there is granular IgA deposition along the dermoepidermal junction with concentration at the papillary tips. In contrast, linear IgA bullous dermatosis has linear IgA deposition along the cutaneous basement membrane zone. However, DIF alone offers little guidance in ambiguous cases, particularly when IgA deposition appears both granular and linear at the same time. In our experience, DH does not always have the classic granular deposition of IgA, but can be more linear, like LABD.“ Finally, increased neutrophils are usually found on the lesions where the dermis meets the epidermis.3 4 5

What Are the Causes of Dermatitis Herpetiformis?

Dermatitis herpetiformis symptoms generally appear around young adulthood between the ages of twenty and thirty. The condition seems to be triggered from the ingestion of gluten proteins (glutenin and gliadin mostly) over time in people with undiagnosed celiac disease. Genetic polymorphisms and dysbiosis might contribute to the disease as well. HLA-DQ2 and HLA-DQ8 are two out of many genes that regulate the human leukocyte antigen system which is responsible for the regulation of our immune system. The HLA-DQ proteins that our immune system produce function as cell surface receptors for peptide antigens (gluten proteins concerning these genes) and antigen-presenting cells, presenting them to T helper cells. When we produce HLA-DQ2 and DQ8 our T helper cells do not react when exposed to gluten and little to no inflammatory processes are generated. So, if you are trying to determine if you are suffering from gluten intolerance or celiac disease, I would get these genes tested by your medical professional for a proper diagnosis. Finally, other genes can contribute to dermatitis herpetiformis and celiac disease including MYO9B, MAGI2, and PARD3, which are tight intestinal junction pathway-related genes. People with polymorphisms in these genes might have a higher chance in developing “leaky gut.” Therefore, if gluten proteins are not broken down somewhat by a healthy microbiome, they might cross the intestinal barrier more often in people with these gene mutations and enter the bloodstream. Once those proteins enter the bloodstream where they do not belong they trigger the immune system causing the symptoms of gluten insensitivity, dermatitis herpetiformis, or celiac disease.6 7 8

Our skin just like our digestive tract contains the enzyme transglutaminase which is a cytosolic enzyme involved in skin cell envelope formation during the differentiation of keratinocytes within the epidermis. “The cornified cell envelope (CE) is a critical structure for barrier function at the outermost layer of the skin epidermis. For CE formation in terminal keratinocyte differentiation, covalent cross-linking of constituting proteins such as involucrin, loricrin, small proline-rich protein is essential. This reaction requires transglutaminase (TGase), which is a calcium-dependent enzyme catalyzing an intermolecular isopeptide bond formation between proteins.” Epidermal transglutaminase (transglutaminase three) has been found in precipitates of skin-bound IgA from the affected skin. Dermatitis herpetiformis may be caused by deposition of both IgA and epidermal transglutaminase within the dermis. IgA antibodies cross-react with epidermal transglutaminase, and form complexes that deposit within the papillary dermis and cause skin lesions. The body may eventually metabolize these complexes after long-term gluten avoidance and make take up to ten years for severe cases.9 10

Gluten proteins can pass through open gut junctions (leaky gut) into the lamina propria where they are deamidated by tissue transglutaminase (transglutaminase two). Tissue transglutaminase deamidates the gluten proteins including gliadin into immunogenic gluten peptides and glutamic acid. Dendritic cells absorb the peptides and if they recognize them as foreign substances begin to secrete IL-8 in the lamina propria. The IL-8 signals neutrophil’s (the most abundant type of human white blood cell which is known as the first responders of our immune system) to the area because the immune system believes there is a potential foreign body that needs to be eliminated, triggering inflammation. Th1 cell (t helper cells are lymphocytes that can change their subtype and secrete different cytokines depending on their immunity need) differentiation occurs because of the release of IL-8 and starts reacting to the gliadin immunogenic peptides by producing more interleukins further triggering inflammatory responses. However, T helper cells do not produce anti-transglutaminase antibodies (which are cross-reactive with epidermal transglutaminase) which our B cells (another type of lymphocyte that are usually activated with T helper cells accumulate) do, and both cells work together as a team on antigen-specific matters. B cells then begin to differentiate into plasma cells which start to produce IgA deposits which both bind to macrophages in the area activating them to a potential foreign body and cross-react with transglutaminase to form reactive complexes. The reactive complexes, IgA, and tissue transglutaminase antibodies may enter the bloodstream if the gut junctions are dilated enough, triggering systemic immune reactions. Finally, macrophages secrete more IL-8, continuing the neutrophil-mediated inflammatory response.11 12 13 14

One last topic I wanted to cover is that there is a strong correlation between the developing and worsening of celiac disease and dermatitis herpetiformis in people with upper gut H. pylori dysbiosis suffering from gastritis “The frequency of CAG in the corpus was significantly more common in the DH patients than in the control subjects suffering from dyspepsia. No such a difference was seen in the antrum of the stomach. Previously, Primignani et al. conducted a study in 57 Italian patients with DH and found a prevalence of CAG of 30%, compared to 15% in non-DH control subjects with dyspepsia. Patients with DH do not usually suffer from dyspepsia, and therefore the control group was not analogous to the study group. Storskrubb et al. carried out esophago-gastroduodenoscopy at random for 1000 Swedish adults. The overall frequency of corpus atrophy was 5% and antrum atrophy 2%. Our data thus indicate that atrophic corpus gastritis is more common in patients with DH than in the population in general. H. pylori infection is common in CAG. In line with this, the present DH patients with CAG had H. pylori significantly more often than those without CAG. The age difference may partly explain this; H. pylori are more common in older people, and our patients with GAG were older than those without. However, the presence of H. pylori in all DH patients (18.3%) was significantly higher than among dyspeptic control subjects with a similar age distribution (9.1%. By comparison, Crabtree et al. examined 58 DH patients in Britain and by serological methods found H. pylori IgG antibodies in 63% of patients, this frequency being however only slightly higher than in other dermatological patients.” I did not have any noticeable symptoms of celiac disease till I developed H. pylori dysbiosis and gastritis almost ten years ago.15

So If You Have Dermatitis Herpetiformis What Can Be Done About It?

First, you must go on a gluten-free diet, and for most, it might be for their whole life to achieve remission. You need to avoid ingesting gluten at all possible. For some people, you may be fine eating labeled gluten-free meals at restaurants with dedicated kitchen space and consuming foods that are either naturally gluten-free or if processed certified gluten-free. You may need to have separate dishes and cookware (including microwaves or toasters, for example) from the rest of your family if they consume gluten, and you may not be able to use the same sponge, place them in the same sink as dishes containing gluten until they are cleaned, and the sink is cleaned, dried on the same rack, or using the family dishwasher to wash your dishes. You also might need to store your food in a particular separate area of the cabinets, refrigerator, or freezer. If your disease is severe enough, you sadly must eat all home cooked meals, consume foods that are either naturally gluten-free or if processed certified gluten-free, and you must maintain a gluten-free household, which may be an inconvenience for the rest of your family, but it is for your health. The length that one must go to avoid even the tiniest molecule of gluten depends on the severity of their reaction to it.16

There are many different supplements and lifestyle changes that you can do to help reduce any Th1 dominance, heal the lesions, and improve the integrity of your gut junctions. Here are some supplements that may help minimize Th1 dominance, I recommend curcumin, boswellia, CBD oil, and black cumin seed oil. I would suggest applying a thieves oil or allicin cream on the lesions if they are infected to help them heal. If they are not an excellent natural moisturizing lotion that contains retinol may help. Finally, to improve the integrity of your gut junctions I recommend that you consume enough omega 3 fatty acids in your diet, follow the Perfect Health Diet, consume collagen and bone broth a few times weekly, consume pastured animal liver once or twice weekly for vitamin A, get proper sunlight exposure, and use a Squatty Potty or squat when you use the bathroom. You should also avoid iron-fortified food and iron supplements if possible, practice correct SIBO) or upper gut dysbiosis, you need to relieve it as well to help the gut junctions close properly.

Dermatitis herpetiformis and celiac disease are both severe conditions that can easily be misdiagnosed. If you are breaking out in lesions and have the symptoms of either condition, it might be best that you ask your doctor to perform the tests necessary to see if you are suffering from the disease or give up gluten for a few months and see if you get better. Though both conditions can be scary, they can be overcome from lifelong abstain of gluten, and most people can still ingest delicious and healthy foods without gluten and feel great. If you are suffering from dermatitis herpetiformis or celiac disease or believe that you do, contact me for coaching, and we will get you better!