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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Juvenile dermatitis herpetiformis occurred in a 20-month-old girl. She had granular lgA, C3, and fibrin bound to the basement membrane zone of the skin by direct immunofluorescence and negative serum antibodies against the skin on indirect immunofluorescence. The HLA typing of peripheral lymphocytes was A1, Aw30, B8, Bw51 without clinical evidence of malabsorption syndrome. A rapid improvement was observed on dapsone therapy. These findings strongly suggest that juvenile dermatitis hepetiformis is a disease entity different from chronic bullous dermatosis of childhood.
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PMID:Juvenile dermatitis herpetiformis. 37 40

Malabsorption (M) is characterized by absorption defect of one or several nutriments in small bowel. Its clinical expression is rarely obvious and biological signs are: anaemia, low serum protein, albumin and lipid rates, low serum calcium, phosphorus and potassium level, and hypoprothrombinaemia. But only 4 simple and reliable tests are needed for diagnosis: i. e.: daily faecal fat amount measurement, daily faecal nitrogen excretion, the xylose test and the Schilling's test. This syndrome is related to many conditions which can be divided into 2 groups with and without intestinal abnormalities. The relationships between M and skin diseases belong to 4 types (J. Marks and S. Shuster): 1) M is responsible for the cutaneous signs, 2) M is caused by a skin disease, 3) both M and skin disease are the result of a same cause, 4) M and skin disease are associated in an indirect way. Only the two first types are dealt with in this report. Skin manifestations occur as a complication in 10 p. 100 to 20 p. 100 of cases of M. They are mostly polymorphous or non-specific, as they are related to multiple vitamin or essential amino acid deficiencies and heal with the treatment of M. The main conditions encountered are diffuse pigmentation, acquired ichthyosis, follicular keratosis, nail brittleness and hair loss. Mucous membrane lesions, purpura and eczematoid or psoriasis-like dermatitis have also been described. More uncommon are clubbing of fingers, finger print abnormalities, kwashiorkor or acrodermatitis enteropathica-like eruptions. The dermatogenic enteropathy, i. e. a M syndrome due to a skin disease, occurs as a result of widespread involvement of the body for instance in psoriasis or eczema; its clinical expression is rarely obvious, the histological record of gut biopsy usually normal and the results of biological tests often dissociated, but steatorrhoea is frequently found. The pathogenesis of the condition is still unknown but its importance is related to the extent of the skin disease and it only improves with the treatment of the latter. All these features and others are discussed in the report with a comprehensive review of the literature.
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PMID:[Cutaneous manifestations of malabsorption diseases (author's transl)]. 38 Apr 45

A 2-week-old baby boy had a periorificial dermatitis that progressively worsened, as did his failure to thrive. Decreased serum zinc, proteins, and amino acids, as well as an increase in fecal fat, were noted. The child's dermatitis responded promptly to nutritional therapy. Sweat chloride levels were markedly elevated. The dermatitis, occasionally seen as a presenting feature of cystic fibrosis, is most likely the result of malabsorption caused by pancreatic exocrine dysfunction.
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PMID:Cystic fibrosis presenting with periorificial dermatitis. 176 67

Acrodermatitis enteropathica is an inborn error of metabolism resulting in zinc malabsorption and severe zinc deficiency. From personal experience and a literature review the following conclusions were drawn: 1. Symptoms other than dermatitis, vary with age. Diarrhoea, mood changes, anorexia, and neurological disturbance were reported most frequently in infancy. Growth retardation, alopecia, weight loss and recurrent infections were prevalent in toddlers and schoolchildren. Spontaneous remission may occur at adolescence. 2. The severity of symptoms also varies. Intermittent or mild cases of the disease and those presenting with uncommon features such as ophthalmic, cerebral or hepatic involvement, are easily overlooked. In the severe cases this may result in a fatal outcome. If untreated, the overall mortality rate is 20%, being higher in males. 3. The laboratory diagnosis is hazardous. In patients, mean zinc values in serum, urine and hair were ca. 50% of normal levels. There is a 15% overlap with healthy controls; moreover, low zinc levels in serum, urine or hair are also found in other diseases. A more specific test is required. 4. In cases of doubt, in vitro or in vivo zinc absorption tests using radioisotopes (65Zn or 69mZn) may be performed. These appear not to be influenced by other conditions and show less overlap with controls. If such tests are unavailable, the clinical response to 3-30 mumol zinc/kg per day for 5 days may be awaited. This is recommended in infants or children with one or more symptoms of acrodermatitis enteropathica.
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PMID:Clinical and laboratory diagnosis of acrodermatitis enteropathica. 269 Dec 54

The pervasive role of zinc in the metabolic function of the body results from its function as a cofactor of a multitude of enzymes. Zinc is found in every tissue in the body, and because zinc metalloenzymes are found in every known class of enzymes, the metal has a function in every conceivable type of biochemical pathway. Symptoms resulting from zinc deficiency are as diverse as the enzymes with which the metal is associated. If chronic, severe, and untreated, zinc deficiency can be fatal. Less drastic symptoms include infections, hypogonadism, weight loss, emotional disturbance, dermatitis, alopecia, impaired taste acuity, night blindness, poor appetite, delayed wound healing, and elevated blood ammonia levels. Many symptoms of zinc deficiency result from poor diet consumption, but often the most severe symptoms result from other factors including excessive alcohol use, liver diseases, malabsorption syndromes, renal disease, enteral or parenteral alimentation, administration of sulfhydryl-containing drugs, and sickle cell disease. The most severe symptoms of zinc deficiency occur in young children affected with the autosomal-recessive trait, acrodermatitis enteropathica. This disease results in decreased synthesis of picolinic acid which causes an impaired ability to utilize zinc from common food. Because simple laboratory analyses are often not reliable in determining zinc nutriture of a patient, those symptoms caused by suspected zinc deficiency are best verified by the oral administration of zinc dipicolinate. This zinc compound is efficacious and safe and would provide an accurate means of identifying symptoms that do result from zinc deficiency.
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PMID:Zinc and its deficiency diseases. 351 57

The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal diseases, following uses of certain drugs such as penicillamine for Wilson's disease and diuretics in some cases, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. In pregnancy and during periods of growth the requirement of zinc is increased. The clinical manifestations in severe cases of zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males; it is fatal if unrecognized and untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss, and hyperammonemia. Zinc is a growth factor. Its deficiency adversely affects growth in many animal species and humans. Inasmuch as zinc is needed for protein and DNA synthesis and for cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis. Whether or not zinc is required for the metabolism of somatomedin needs to be investigated in the future. Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level; the hypothalamic-pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in cell division, its deficiency may adversely affect testicular size and thus affect its functions. Zinc is required for the functions of several enzymes and whether or not it has an enzymatic role in steroidogenesis is not known at present. Thymopoeitin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent. Zinc deficiency affects T-cell functions and chemotaxis adversely. Disorders of cell-mediated immune functions are commonly observed in patients with zinc deficiency. Zinc is beneficial for wound healing in zinc-deficient subjects. In certain zinc-deficient subjects, abnormal taste and abnormal dark adaptation have been noted to reverse with zinc supplementation.
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PMID:Clinical manifestations of zinc deficiency. 389 71

The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal disease, certain diuretics, the use of chelating agents such as penicillamine for Wilson's disease, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during the growing age period. The clinical manifestations in severe cases of zinc deficiency included bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males and it is fatal if untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss and hyperammonaemia. Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and in man. Inasmuch as zinc is needed for protein and DNA synthesis and cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis. Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level and the hypothalamic--pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in a cell division, its deficiency may adversely affect testicular size and thus its function. In mice, the incidence of degenerate oocytes, and hypohaploidy and hyperhaploidy in metaphase II oocytes were increased due to zinc deficiency. Zinc at physiological concentrations reduced prolactin secretion from the pituitary in vitro and it has been suggested that this trace element may have a role in the in vivo regulation of prolactin release. Thymopoietin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent. It is clear that zinc may have several roles in biochemical and hormonal functions of various endocrine organs. Future research in this area is very much needed.
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PMID:Clinical, endocrinological and biochemical effects of zinc deficiency. 390 80

The requirement of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, and chronic renal diseases; use of certain drugs such as penicillamine and, in some cases, diuretics; and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during growth. The clinical manifestations of severe zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, and hypogonadism in males; zinc deficiency can be fatal if unrecognized and untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss, and hyperammonemia. Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and humans, probably because zinc is needed for protein and DNA synthesis and cell division. The effects of zinc and growth hormone on growth appear to be independent of each other in experimental animals. Whether zinc is required for the metabolism of somatomedin needs further investigation. Thyroid and adrenal functions do not appear to change as a result of zinc deficiency. Glucocorticoids may have an effect on zinc metabolism, although the clinical relevance of this effect is not known at present. In contrast, testicular function is affected adversely as a result of zinc deficiency in both humans and experimental animals. The effect appears to be a direct one since the hypothalamic-pituitary axis is intact, and may relate to the reduction in testicular size as a result of the need for zinc in cell division. In addition, zinc is required for the function of several testicular enzymes, although a specific role in steroidogenesis has not been identified. Zinc appears to have a role in the modulation of prolactin secretion, in the secretion and action of insulin, and in the production and biologic effects of thymic hormones. It is clear that the endocrine consequences of zinc deficiency are multiple, and that continued investigation should provide additional pathophysiologic and therapeutic insights.
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PMID:Clinical, endocrinologic, and biochemical effects of zinc deficiency. 391 98

Zinc is essential for many metabolic and enzymatic functions in man. Deficiency of zinc in man has now been recognized to occur not only as a result of nutritional factors, but also in various disease states, including malabsorption syndromes, acrodermatitis enteropathica, Crohn's disease, alcoholism and cirrhosis of the liver. The deficiency state in human subjects exists as a spectrum extending from mild to severe degree. The clinical manifestations of mild zinc deficiency include oligospermia, weight loss and hyperammonaemia. Moderate zinc deficiency is characterized clinically by growth retardation, hypogonadism in males, skin changes, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In severe zinc deficiency states, bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorders, weight loss, intercurrent infections, hypogonadism in males and, if unrecognized, death have been observed. Zinc is needed for the functions of over 100 enzymes. It is essential for DNA, RNA and protein synthesis and, as such, is important for cell division. Zinc is an inducer of mRNA of metallothionein, a protein which may have an important role in the regulation of intestinal zinc absorption. Zinc has a specific effect on testes in animals and man. Recent reports indicate that in human subjects thymopoietin may be zinc dependent and in animal studies somatomedin may be affected adversely due to dietary zinc restriction. Zinc plays an important role in the protection of cell membrane integrity and may be protective against free radical injury. Zinc is known to compete with cadmium, lead, copper, iron and calcium for similar binding sites. In the future, a potential use of zinc may be to alleviate toxic effects of cadmium and lead in human subjects. Recent evidence suggests that thymic-dependent lymphocytes (T cells are zinc dependent. T-helper and suppressor cells, T-effector cells and T-natural killer cells appear to be zinc dependent. Zinc is also essential for some of the neutrophil functions. Thus, it appears that zinc may play an important role in immunity. One may suggest that some of the clinical features of cirrhosis of the liver, such as testicular atrophy, loss of body hair, night blindness, poor wound healing, poor appetite, susceptibility to infections and enhanced sensitivity to drugs, may be related to conditioned deficiency of zinc, future studies are required to determine whether or not zinc supplementation is beneficial to these patients.
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PMID:The role of zinc in gastrointestinal and liver disease. 661 39

Essential fatty acid deficiency can develop in man as the consequence of an inadequate diet or fatty acid malabsorption. Daily requirements in childhood vary from 1 to 4 caloric percent. Many abnormalities are described following essential fatty acid deficiency, such as cessation of growth, dermatitis, loss of hair, increased susceptibility to bacterial infections, histological abnormalities and disturbances of biochemical and physiological processes. These disorders can be explained as the result of a disturbed membrane structure and function, due to an abnormal serum fatty acid composition. This is also important in diagnosis of essential fatty acid deficiency. Supplementation of essential fatty acids can be realised by oral and parenteral route or by cutaneous application. A patient is described with an essential fatty acid deficiency. Cutaneous application of a linoleic acid rich mixture resulted in an enhanced growth velocity.
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PMID:[Essential fatty acid deficiency in childhood]. 726 52


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