Nutritional skin changes

Introduction Human nutrition and normal metabolism are important material guarantees for the health of the body. Once nutrition and metabolic disorders, not only the various systems of the body will be damaged to varying degrees, but also a series of skin changes and damages. With the improvement of social and economic conditions, some Nutrition-deficient skin diseases are less common than in the past, but due to certain diseases, changes in living environment, adverse lifestyle habits or drug treatment factors such as chronic diarrhea or long-term use of isoniazid cause secondary nutritional deficiency and metabolism Obstacles still occur from time to time, a variety of nutritional metabolic disorders, including vitamin B2 deficiency, vitamin A deficiency, niacin deficiency and other metabolic abnormalities leading to nutritional skin changes. Different nutrients and metabolic disorders, The reason is different from the performance.

Cause

The cause of nutritional skin changes:

Causes of vitamin B2 deficiency: The main cause of vitamin B2 deficiency is insufficient dietary supply, limited food supply, improper storage and processing, such as unreasonable cooking (such as excessive rice, soaking vegetables after chopping, etc.), food is heated, Destroyed in the process of exposure to sunlight, consumption of dehydrated vegetables or milk boiled by infants can cause vitamin B2 deficiency. But there are other reasons for concurrency such as:

1. Absorption disorder: Gastrointestinal dysfunction such as diarrhea, infectious enteritis, digestive tract or biliary obstruction, limited bile secretion, and limited gastric acid secretion can cause vitamin B2 deficiency. In addition, alcoholics may also be deficient in vitamin B2 due to decreased intestinal absorption and decreased bioavailability.

2. The need for increased or excessive consumption: such as pregnancy, breastfeeding, physical labor, mental stress, etc., the body's vitamin B2 needs increased in the process of Beijing disease, such as high fever, pneumonia due to accelerated metabolism, increased consumption, patients The demand for vitamin B2 increases; on the other hand, it is often caused by poor appetite, nausea, vomiting, etc., and vitamin B2 deficiency such as keratitis.

3. Drug effects, such as drugs for the treatment of psychosis, imipramine and amitriptyline, cloprazine. There are also some drugs such as doxorubicin and arsenic that inhibit the absorption of vitamin B2.

4. In addition, protein energy malnutrition is accompanied by a decrease in the absorption and utilization of vitamin B2.

5. Others such as caffeine, copper, zinc, iron ions, etc. also affect the absorption of vitamin B2.

The cause of vitamin A deficiency

1 improper diet: the vitamin A stored in the liver when the baby is born is rarely consumed quickly, but the content of colostrum is extremely high. Human milk and milk are the main sources of vitamin A required by the baby. Other foods such as vegetables, fruits, eggs and liver. Can supply enough vitamin A, so proper diet can provide enough vitamin A not to cause deficiency, but the food in infants is simply as insufficient milk and does not replenish food supplements. It is easy to cause subclinical vitamin A deficiency. If the baby is weaned after long-term use alone Rice cake batter porridge to fat milk and other food feeding without the addition of protein and fat-rich food supplements can cause deficiency.

2 digestive system diseases: chronic diseases of the digestive system such as long-term diarrhea, chronic diarrhea, intestinal tuberculosis, pancreatic diseases, etc. can affect the absorption of vitamin A. The liver is the main organ of vitamin A metabolism and storage. Cholate in the bile can emulsifie lipids to promote vitamin A. Absorbs and strengthens the activity of -carotene-1515-oxygenase to promote its conversion to retinol. Therefore, hepatobiliary diseases such as congenital biliary atresia and chronic hepatitis are prone to vitamin A deficiency caused by various viruses. Hepatitis or toxic hepatitis complicated by infectious diseases can also cause vitamin A deficiency should be vigilant

3 wasting diseases: such as chronic respiratory infections, persistent pneumonia, measles, etc., due to insufficient intake of vitamin A, symptoms due to increased consumption of vitamin A, and long-term intake of mineral oil (such as liquid paraffin, etc.) and Methotrexate and other drugs can also affect the absorption of vitamin A. The urinary system disease can increase the excretion protein deficiency of vitamin A. The synthesis of retinol transporter causes vitamin A to try to reduce it in plasma and cause symptoms.

4 hypothyroidism and diabetes: can make the blood and skin accumulate a large amount of carotene is very similar to jaundice but the bulbar conjunctiva is not yellow.

5 Zinc deficiency: Pre-albumin and vitamin A reductase combined with vitamin A are reduced, vitamin A can not be used and excreted. Vitamin A deficiency can also occur. In recent years, changes in nutritional status have also affected the use of vitamin A.

Causes of niacin deficiency:

The dietary supply of niacin in adults is 6.6 mg for each intake of 4.1868 MJ. Niacin is found in animal and plant foods such as meat, liver, milk, beans, cereals and vegetables. The human body can convert the tryptophan in the animal food protein into niacin, 60mg of tryptophan can be converted to produce 1mg of niacin, and bacteria in the intestine can also synthesize niacin. The cause of this disease is the lack of niacin in the diet; malabsorption; the liver is not fully utilized during chronic alcoholism; the amount of infection is increased when the disease is affected; the disease has been prevalent in people who eat corn without supplements, because The combination of niacin in corn can not be used, and the content of tryptophan is low. Patients with carcinoid syndrome can turn a large amount of tryptophan into serotonin, resulting in reduced niacin synthesis and pathogenesis; genetic metabolic defects such as Hartnup disease, Due to intestinal absorption and renal tubular reabsorption of tryptophan and other amino acids, plus the lack of tryptophan peroxidase, causing metabolism of tryptophan; the conversion of tryptophan to niacin in vivo requires pyridoxine (vitamin B6), when vitamin B6 is severely deficient or taking vitamin B6 antagonist isoniazid, this transformation is hindered by metabolic enzymes, which inhibit the conversion of a tryptophan-nicotinic acid metabolizing enzyme, which causes niacin Lack of factors.

The severe deficiency of niacin and its precursor tryptophan (the body's ability to synthesize niacin from tryptophan) is a major cause of pellagra. The primary deficiency usually occurs in areas where corn is the staple food. The bound niacin present in corn cannot be absorbed in the intestine unless it is first treated with a base, such as a tortilla. Zein is also deficient in tryptophan. Amino acid imbalances may also contribute to the lack of psoriasis, which is common among people in India who eat millet with high levels of leucine.

an examination

Related inspection

Body organ function and nutrient detection in human body

Examination and diagnosis of nutritional skin changes:

Symptoms of vitamin B2 deficiency: If the body does not supply vitamin B2 for 3-4 months, symptoms of vitamin B2-deficient deficiency can be observed, presenting special epithelial damage, seborrheic dermatitis, mild diffuse epithelial keratosis There are seborrheic alopecia and neurological disorders.

Symptoms of vitamin A deficiency: skin symptoms are more common in older children, dry and desquamation at the beginning, after the keratinized hyperkeratosis is stuffed in the hair follicle and protrudes from the leather surface, resembling "chicken skin", which has a rough feeling; The damage is first seen on the upper and lower limbs, and then the other parts are involved; the hair is dry and easy to fall off, and the nail is easy to break.

Symptoms of niacin deficiency: lesions are mostly located at the exposed site, often symmetrically distributed, such as the back of the hand, the back of the finger, the wrist, the lateral side of the forearm, the face, the neck, the upper chest, the back of the foot, the ankle and the extension of the calf, can also occur in the easy Rubbed parts such as shoulders, elbows, knees and buttocks.

In the early exposure, bright red or purple erythema appeared in the exposed area. The boundary was clear, slightly elevated, itching or burning, resembling sunburn, and then the skin lesion turned reddish brown, with obvious edema, severe blister on the erythema. Secondary infection forms pustules, or blister rupture, exfoliation of the epidermis forms a large erosion, accompanied by oozing out of the slurry, or ulceration, crusting after drying, after 2 to 3 weeks, the damage is reddish brown or brownish black, rough and scaly It can also have cleft palate and follicular keratinization, and its edge can be seen as a 1-2mm wide red part, like a rim. In acute attacks, there may be symptoms such as high fever, phlegm and exhaustion. Chronic cases of recurrent episodes, edema of skin lesions is not obvious, but skin thickening and skin lines are obvious, the color turns dark brown, rough and lacks elasticity, with hyperkeratosis, dry scales, chapped, bleeding or bloody . Older patients have dry skin, scaly flaky, and ichthyosis-like changes on the calf extension.

Occasionally, the skin lesions affect the nasal passages, presenting with seborrheic dermatitis with blackheads, similar to those with riboflavin deficiency. Skin lesions often occur or worsen in the summer, and the winter is reduced or subsided. There is a large amount of desquamation during healing, leaving atrophy, pigmentation, depression or hypopigmentation.

The keratitis is mainly wet and white in the mouth, and it can also be seen in the mouth and lips, dry and chapped, and desquamation. Early glossitis is redness of the tip of the tongue and tongue, redness of the papillary nipple, severe tongue rupture, tongue erosion or shallow ulceration. After a long time, the tongue nipple is atrophied, dry, smooth and red like beef. Inflammation can affect the oral mucosa, gums, throat and esophagus, conscious pain, increased saliva, affecting eating, and often secondary infections.

Perineal, genital, perianal and mucosal lesions can occur simultaneously with stomatitis. There are inflammations or ulcers in the rectum and vaginal mucosa, and vaginal secretions increase, so that nearby skin is impregnated or infected.

Differential diagnosis

Nutritional skin changes are confusing symptoms:

Identification with other skin diseases:

1. The rash is a wheal, a tidal plaque, varying in size and shape. Often happen suddenly, appear in batches, and quickly disappear after a few hours, leaving no trace after disappearing, but often repeated.

2. Conscious pruritus, may be associated with abdominal pain, nausea, vomiting and chest tightness, palpitations, difficulty breathing, a few have fever, joint swelling, hypotension, shock, throat edema and asphyxia symptoms.

3. The length of the disease varies, the course of acute urticaria is within 1 month; more than 1 month is chronic.

4. Some cases of skin scratch test showed a positive reaction.

5. Special types of clinical: A. Protein? Urticaria is an antigen-antibody reaction caused by protein absorption directly through the intestinal mucosa; B. Cold urticaria can be divided into familial cold urticaria and acquired cold sputum Measles is a physical urticaria caused by cold; C. Thermal urticaria can be divided into two types: acquired and hereditary. After contact with hot water, wheal is present at the contact site; D. Cholinergic urticaria Induced by heat, mental stress and exercise, more common in the trunk and proximal extremities, skin lesions mainly 1-2mm size wheal, surrounded by red halo; E. solar urticaria, more women, after exposure to sunlight Onset, rash is confined to the exposed site; F. Compressive urticaria, after 4-6 hours of heavier and longer compression, diffuse, edematous, painful plaques appear in the compression site; G. Waterborne urticaria In contact with water and sweat, it causes small itchy wheal around the pores; H. Serum urticaria, which is caused by exposure to allogeneic serum, vaccines, drugs, etc., and the clinical manifestations are fever. Rash, arthritis and lymphadenopathy; I. Of progesterone urticaria, occurred in the early and mid menstruation, is caused by progesterone.

Symptoms of vitamin B2 deficiency: If the body does not supply vitamin B2 for 3-4 months, symptoms of vitamin B2-deficient deficiency can be observed, presenting special epithelial damage, seborrheic dermatitis, mild diffuse epithelial keratosis There are seborrheic alopecia and neurological disorders.

Symptoms of vitamin A deficiency: skin symptoms are more common in older children, dry and desquamation at the beginning, after the keratinized hyperkeratosis is stuffed in the hair follicle and protrudes from the leather surface, resembling "chicken skin", which has a rough feeling; The damage is first seen on the upper and lower limbs, and then the other parts are involved; the hair is dry and easy to fall off, and the nail is easy to break.

Symptoms of niacin deficiency: lesions are mostly located at the exposed site, often symmetrically distributed, such as the back of the hand, the back of the finger, the wrist, the lateral side of the forearm, the face, the neck, the upper chest, the back of the foot, the ankle and the extension of the calf, can also occur in the easy Rubbed parts such as shoulders, elbows, knees and buttocks.

In the early exposure, bright red or purple erythema appeared in the exposed area. The boundary was clear, slightly elevated, itching or burning, resembling sunburn, and then the skin lesion turned reddish brown, with obvious edema, severe blister on the erythema. Secondary infection forms pustules, or blister rupture, exfoliation of the epidermis forms a large erosion, accompanied by oozing out of the slurry, or ulceration, crusting after drying, after 2 to 3 weeks, the damage is reddish brown or brownish black, rough and scaly It can also have cleft palate and follicular keratinization, and its edge can be seen as a 1-2mm wide red part, like a rim. In acute attacks, there may be symptoms such as high fever, phlegm and exhaustion. Chronic cases of recurrent episodes, edema of skin lesions is not obvious, but skin thickening and skin lines are obvious, the color turns dark brown, rough and lacks elasticity, with hyperkeratosis, dry scales, chapped, bleeding or bloody . Older patients have dry skin, scaly flaky, and ichthyosis-like changes on the calf extension.

Occasionally, the skin lesions affect the nasal passages, presenting with seborrheic dermatitis with blackheads, similar to those with riboflavin deficiency. Skin lesions often occur or worsen in the summer, and the winter is reduced or subsided. There is a large amount of desquamation during healing, leaving atrophy, pigmentation, depression or hypopigmentation.

The keratitis is mainly wet and white in the mouth, and it can also be seen in the mouth and lips, dry and chapped, and desquamation. Early glossitis is redness of the tip of the tongue and tongue, redness of the papillary nipple, severe tongue rupture, tongue erosion or shallow ulceration. After a long time, the tongue nipple is atrophied, dry, smooth and red like beef. Inflammation can affect the oral mucosa, gums, throat and esophagus, conscious pain, increased saliva, affecting eating, and often secondary infections.

Perineal, genital, perianal and mucosal lesions can occur simultaneously with the stomatitis cavity. There are inflammations or ulcers in the rectum and vaginal mucosa, and vaginal secretions increase, so that nearby skin is impregnated or infected.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.