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PubMed1987

[Zinc deficiency in artificial nutrition].

A 35-year-old patient was parenterally fed for a total of 170 days because of a twice reoperated gastric ulcer followed by a gastric-antrum small intestinal fistula. This lead to a complete acute zinc deficiency syndrome with pronounced acrodermatitis enteropathica-like skin changes in the face and the genital region, paronychia, flat blistering on the hands and feet, loss of hair, fingernail ridging (Beau's) and serious physical changes. A dramatic improvement and healing of all these skin changes, the antrum and small intestinal fistula as well as physical disorders occurred after intravenous and subsequent oral intake of zinc.

Adult↗
PubMed1988

[Clinical aspects of erythema migrans (Lyme) borreliosis].

Erythema migrans or Lyme borreliosis may be classified according to 3 stages. Erythema migrans is the typical initial lesion of the disease, often associated with general symptoms. Carditis, meningitis, musculoskeletal symptoms including arthralgia may develop in stage 2; arthritis (arthralgia), acrodermatitis chronica atrophicans (ACA), and encephalomyelitis may occur in stage 3. Borrelial lymphocytoma may be seen either in the early phase of the disease or along with the ACA. However, there is no definite therapeutical concept, so far. We recommend tetracyclines during the first stage, and high doses of penicillin G during stages 2 and 3 as well as for pregnant women.

Humans↗
PubMed1987

Zinc and the central nervous system.

The effect of zinc nutriture and metabolism on brain function has been reviewed. Zinc nutriture and its effect on the concentration and metabolism of essential elements (e.g. zinc, copper, manganese, magnesium, sodium, potassium and calcium) and on the concentration and metabolism of toxic elements (e.g. aluminum and lead) are discussed in relationship to brain function. In addition, possible interrelationships between zinc nutriture and metabolism and its effect on a number of diseases including acrodermatitis enteropathica, Pick's disease, Alzheimer's disease, schizophrenia, fifth day fits, and epilepsy are discussed. Descriptions and comparisons of methods to measure brain zinc are presented. Behavioral changes and the altered brain morphology which have been associated with zinc deficiency are reviewed. Some possible mechanisms for the association of anorexia with zinc deficiency are outlined. Perinatal brain damage produced by early zinc deficiency followed by rehabilitation with adequate zinc appears to be long term, maybe permanent. Interrelationships between zinc nutriture and aspects of neurochemistry are outlined. Some of the neurochemistries discussed include nucleic acid and protein synthesis, cytoskeletal proteins, neurotransmitters (e.g. catecholamines, indoleamines, glutamate, gamma-aminobutyric acid, and neuropeptides), neurotransmitter receptors, 7S nerve growth factor and zinc-binding proteins. Recent evidence linking zinc and neurotransmission is discussed.

Animals↗
PubMed1987

Inborn errors of biotin metabolism.

The important role of biotin in human physiology has been highlighted by the recognition of two newly discovered human inborn errors of the metabolism of biotin. The molecular defect in the neonatal-onset disease is in the enzyme holocarboxylase synthetase. The defect in the later infantile-onset disease is in the enzyme biotinidase. Both disorders present with impressive clinical manifestations involving the skin and hair. In the neonatal disease, alopecia totalis is associated with a bright red scaly total body eruption. In biotinidase deficiency, the alopecia is more patchy and the skin lesions resemble acrodermatitis enteropathica. Both disorders are complicated by recurrent episodes of life-threatening acidosis and massive ketosis.

Amidohydrolases↗
PubMed1987

[Psoriasis pustulosa generalisata--classification, clinical aspects and therapy. Review and experiences with 18 patients].

On the basis of clinico-morphological criteria we suggest the following classification of various pustular forms of psoriasis into four subtypes: generalized pustular psoriasis (von Zumbusch) and its atypical forms, erythema anulare centrifugum-like psoriasis with and without pustulation (EACP); psoriasis vulgaris with pustulation; palmo-plantar pustular psoriasis (Königsbeck-Barber) and its acral variant; acrodermatitis continua suppurativa (Hallopeau), and transitional forms. This classification takes into consideration both clinical aspects and response to treatment, and allows a prognosis of the various types of pustular psoriasis. Owing to its mild course and good treatment results, EACP represents a special form of psoriasis pustulosa generalisata. In our group of patients, systemic glucocorticosteroid therapy has proved deleterious, whereas oral photochemotherapy and etretinate have been found to be highly effective modes of therapy with only mild side effects and have been able to induce even permanent remission in EACP.

Adult↗
PubMed1988

[Immunochemical analysis of the immune response in late manifestations of Lyme borreliosis].

Compared to American strains, European Borrelia burgdorferi strains revealed considerable heterogeneity of major proteins. Four strains isolated from ticks, human skin and human CSF were selected from our 23 Borrelia burgdorferi isolates. These strains and the American type strain B31 were characterized by SDS-PAGE (Coomassie Blue staining) and Western blots (using rabbit immune sera against two of the strains and two monoclonal antibodies (H5323 and H3TS) against a major outer surface protein (OspA]. The strains showed considerable differences in SDS-PAGE pattern. Corroborating the results of a previous study, we could demonstrate that the OspA (31/32K) can change from a minor to a major protein and in reverse the pC (21/22K) from a major to a minor protein during subculturing. Moreover, European strains can antigenically differ in OspA, pC and also in a further low molecular weight protein of 17/18K. To examine whether the antigenic heterogeneity of European isolates is reflected in the immune response of European patients we examined sera from patients with late manifestations of Lyme Borreliosis by Western blot using the five strains as antigens. Sera from seven patients with acrodermatitis chronica atrophicans (ACA) showed a surprisingly strong reactivity with the skin isolate. All sera had antibodies against the 17/18K protein of the skin isolate, but none was reactive with the analogous 17/18K of the other strains. On the other hand a comparable predominance of one strain was not found testing sera from patients with Lyme arthritis. One patient even had antibodies against OspA and OspB proteins of strain B31. Contrary to findings in American Lyme Disease antibodies against the OspA were rarely observed in the sera of our patients (only one patient had such antibodies) although we tested the patients sera with five different strains. Only two patients had stronger reactions with the skin isolate. These findings suggest that ACA is caused by antigenically closely related Borreliae. This could explain the finding that ACA is rarely observed in the US (US strains are antigenically closely related to strain B31). Our findings in patients with Lyme Arthritis--on the other hand--suggest that "different serotypes" can cause Lyme Arthritis. This does not exclude the possibility that Borrelia proteins are an important factor in the pathogenesis of Lyme arthritis. Finally the differences in reactivity of sera with different strains in the Western blot led us to examine whether such differences are also found in serodiagnostic tests using different strains as antigens.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Zinc and its deficiency diseases.

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.

Humans↗
PubMed1986

[Lyme borreliosis].

Lyme borreliosis has in common features with another spirochetosis, syphilis, e.g. the development in three stages and the occurrence of reinfection and congenital infection. The European variant (erythema migrans disease in the broader sense) initially more often seems to have a mild course than in the United States, but lymphocytoma, Bannwarth syndrome and acrodermatitis chronica atrophicans seem to be more common in Europe. Administration of tetracycline for stage 1 and of parenteral penicillin G in high doses for stages 2 and 3 and during pregnancy is recommended.

Anti-Bacterial Agents↗
PubMed1987

[Lyme arthritis].

Infection by spirochete Borrelia burgdorferi is mainly observed in the United States where it has taken the name of Lyme's disease, and in Europe. Its evolution may be very extended, in several phases. A few weeks after a tick-bite, the primary lesion appears, which is a chronic migrating erythema. In the following weeks or months, in the secondary phase, nerve lesions may appear, quite similar in Europe and in the United States, and cardiac lesions, mostly seen in the United States. In the following weeks, months, or years, during the tertiary phase, articular lesions may appear, frequent in the United States, much more unusual in Europe. Several years later, chronic lesions of the central nervous system may appear, described in the United States, and chronic skin lesions such as chronic atrophying acrodermatitis sometimes associated with destructive lesions of the joints underlying the skin lesion, which are only recognized in Europe. The discovery of the spirochete in a small number of these lesions, including the latest in the evolution, permits to think that, throughout this evolution, this disease is secondary to the persistence of the germ within the body; this explains the efficacy of the penicillin treatment, including in the oldest forms of the disease. Serology is quite reliable; but it becomes positive only 2 to 4 weeks after the onset of the chronic migrating erythema: needless to say the importance of this single cutaneous lesion which enables to make the diagnosis and requires the use of a tetracycline or penicillin treatment.

Arthritis, Infectious↗
PubMed1987

[Cutaneous manifestations of zinc deficiency in ethylic cirrhosis].

Thirty-three patients with alcoholic cirrhosis (AC), selected on widely recognized criteria (16, 57), were investigated prospectively for cutaneous manifestations of zinc deficiency. The patients were divided into 3 groups: group A (n = 12): AC without skin lesions; group B (n = 12): AC with skin lesions responsive to a zinc-free topical treatment or resistant to enteral zinc sulfate intake; group C (n = 9): AC with skin lesions cured by oral zinc replacement therapy alone. The lesions observed in group C were studied microscopically. Data concerning zinc metabolism (Zn concentrations in plasma, red cells, urine and hair; alkaline phosphatase values), biochemical criteria of AC (plasma serum-albumin concentration, IgA/transferrin ratio) and a malabsorption test (xylosemia 120 min after oral absorption of D-xylose 25 g) were compared by the variance analysis method. A control group (D, n = 12) was used as reference. Few cases of cutaneous manifestations of zinc deficiency in AC patients have been published. In more than one half of the 15 or so we found in the literature, an aggravating factor (total parenteral nutrition, digestive tract surgery) had to be taken into account. In this prospective study 9 new cases in which AC was the only cause of zinc deficiency are reported. A clinical picture similar to acrodermatitis enteropathica with peribuccal bullous lesions was observed in only one patient. In all other cases the patients presented with a cracked and reticulated eczema on the extensor aspect of the limbs and (often erosive) in the perianal and genital regions. The eczema was associated with cheilitis, glossitis, stomatitis, alopecia and, seldom, ungual Beau's lines. Disorders of behaviour, diarrhoea and bouts of lever regressing under zinc replacement therapy were frequent. Histology was not very specific, except for the presence of necrotic areas in the stratum germinativum, sometimes associated with small subcorneal pustules containing altered polymorphonuclears. In every case, it was the rapid regression of symptoms under zinc sulfate treatment that confirmed the diagnosis. Plasma zinc concentrations were most significantly decreased in all AC groups as compared to controls (61.2 +/- 19.4 vs 97.8 +/- 10.4 micrograms/100 ml) and also in AC patients with skin manifestations of zinc deficiency as compared to the other AC patients (44.4 +/- 9.2 vs 66.5 +/- 18.8 micrograms/100 ml) table V). Changes in serum-albumin levels and in hepatocellular function were parallel to changes in plasma zinc concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1986

[Disease (Lyme disease) in pediatric patients in Switzerland caused by spirochetes (Borrelia burgdorferi) of Ixodes ricinus].

Lyme disease in children is studied in the light of questionnaires sent out twice to departments and divisions of pediatrics in Switzerland. Thirty-six serologically proven cases were collected. The 48 clinical signs attributed to Lyme disease involved the skin in 40%, the nervous system in 40%, and the joints in 20%. They were erythema chronicum migrans (13), lymphocytoma (4), acrodermatitis chronica atrophicans (2), peripheral facial palsy (14), sensomotor radiculoneuritis (2), meningoencephalitis (3) and arthritis (10, 7 of which were monoarthritic). Only half the patients had a history of tick-bite. Antibiotic therapy, usually with penicillin, reduced both the duration of symptoms and frequency of secondary disease. Cardiac involvement and chronic stages with residua were not observed in this series.

Adolescent↗
PubMed1978

[Cutaneous manifestations of malabsorption diseases (author's transl)].

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.

Alopecia↗
PubMed1985

Clinical, endocrinologic, and biochemical effects of zinc deficiency.

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.

Burns↗
PubMed1985

Netherton's syndrome. Report of a case and review of the literature.

A patient with Netherton's syndrome who was followed since birth had previously been diagnosed as having Leiner's disease and acrodermatitis enteropathica; the disorder was recognized clinically when the patient was 20 years of age. Therapy with 13-cis-retinoic acid significantly aggravated the ichthyosis and induced increased fragility of the skin. This patient also had an intermittent aminoaciduria with clinical investigations that showed normal renal function. Furthermore, the aminoaciduria resolved spontaneously after the discontinuance of topically applied corticosteroids. The normal results of clinical studies and a review of the literature suggest that the aminoaciduria may have been artifactual because excess absorption of topically applied corticosteroids directly affects the renal tubules and impairs renal reabsorption or enhances the free excretion of amino acids. We review forty-two other cases of Netherton's syndrome in the literature and reaffirm the significance of associated ichthyosis, atopy, trichorrhexis invaginata, and other findings in this unique syndrome.

Adult↗
PubMed1979

Zinc deficiency syndrome versus glucagonoma syndrome.

In this paper two patients with uncommon syndromes, viz. acrodermatitis enteropathica-like eruption due to acute zinc deficiency, when on long-term intravenous hyperalimentation for Crohn's disease, and necrolytic migratory erythema as a consequence of a malignant glucagon secreting alpha-cell tumour of the pancreas (glucagonoma syndrome) are reported. Attention is paid to the many common features of the skin lesions in both syndromes. This is discussed in detail. Both patients passed through a catabolic stage. Laboratory investigations, however, failed to demonstrate a common biochemical mechanism which might be responsible for the skin lesions. Administration of zinc in the first patient and surgical treatment of the second patient results in rapid clearing of the skin lesions and other symptoms.

Acute Disease↗
PubMedDate not supplied

[Zinc and chronic enteropathies].

In recent years the nutritional importance of zinc has been well established; its deficiency and its symptoms have also been recognized in humans. Furthermore, Acrodermatitis Enteropathica has been isolated, a rare but severe disease, of which skin lesions, chronic diarrhoea and recurring infections are the main symptoms. The disease is related to the malfunctioning of intestinal absorption of zinc and can be treated by administering pharmacological doses of zinc orally. Good dietary sources of zinc are meat, fish and, to a less extent, human milk. The amount of zinc absorbed in the small intestine is influenced by other nutrients: some compounds inhibit this process (dietary fiber, phytate) while others (picolinic acid, citric acid), referred to as Zn-binding ligands (ZnBL) facilitate it. Citric acid is thought to be the ligand which accounts for the high level of bioavailability of zinc in human milk. zinc absorption occurs throughout the small intestine, not only in the prossimal tract (duodenum and jejunum) but also in the distal tract (ileum). Diarrhoea is one of the clinical manifestations of zinc deficiency, thus many illnesses distinguished by chronic diarrhoea entail a bad absorption of zinc. In fact, in some cases of chronic enteropathies in infants, like coeliac disease and seldom cystic fibrosis, a deficiency of zinc has been isolated. Some of the symptoms of Crohn's disease, like retarded growth and hypogonadism, have been related to hypozinchemia which is present in this illness. Finally, it is possible that some of the dietary treatments frequently used for persistent post-enteritis diarrhoea (i.e. cow's milk exclusion, abuse and misuse of dietary fiber like carrot and carub powder, use of soy formula) can constitute a scarce supply of zinc and therefore could promote the persistency of diarrhoea itself.

Biological Availability↗
PubMed1981

Hair changes due to zinc deficiency in a case of sucrose malabsorption.

A 7-year-old girl suffering from chronic diarrhoea due to sucrase deficiency was referred because of poor hair growth. Her scalp hair had a poor, colourless appearance and was much thinned in the occipital region. Her skin was dry, but otherwise normal. P-zinc was low (7.9 mumol/l), whereas P-albumin was normal. Oral zinc therapy, 40 mg daily, had a marked beneficial effect on her scalp hair, eyebrows and eyelashes, which became thicker and pigmented. Beau lines appeared on thumb-nails and 4th left finger-nail. A rise in P-zinc and S-alkaline phosphatase levels was observed during the zinc supplementation. Microscopic examination of her poor scalp hair, using polarized light, revealed well-defined abnormalities of the hair shafts, as reported by others in a case of acrodermatitis enteropathica: 1) a marked individual variation in diameter, 2) narrowing often associated with waving or sharp bending and broken ends, 3) striation with a tendency to trichonodosis. Such changes were absent in the pigmented hair appearing after the start of zinc therapy.

Alkaline Phosphatase↗
PubMed1984

Primary and secondary sites of occupational contact dermatitis.

Patterns of distribution of allergic contact dermatitis follow a certain order in time. The disease starts at a given site, most often as a unilateral acrodermatitis and, should it become chronic, spreads locally. The subsequent pattern of distribution varies depending on the primary site and the type--occupational or otherwise--of the disease. In this study data collected two decades ago are confronted with the more recent ones relating to 1055 cases of occupational allergic contact dermatitis. Examination of this material brought to light no essential difference between the older and more recent patterns of distribution of secondary sites. The incidence, however, of certain multiple localizations and of the primary or secondary involvement of the face has diminished.

Dermatitis, Atopic↗