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A novel zinc-regulated human zinc transporter, hZTL1, is localized to the enterocyte apical membrane.

Zinc is essential to a wide range of cellular processes; therefore, it is important to elucidate the molecular mechanisms of zinc homeostasis. To date, no zinc transporters expressed at the enterocyte apical membrane, and so essential to mammalian zinc homeostasis, have been discovered. We identified hZTL1 as a human expressed sequence tag with homology to the basolateral enterocyte zinc transporter ZnT1 and deduced the full-length cDNA sequence by PCR. The protein of 523 amino acids belongs to the cation diffusion facilitator family of membrane transporters. Unusually, the predicted topology comprises 12 rather than 6 transmembrane domains. ZTL1 mRNA was detected by reverse transcription-PCR in a range of mouse tissues. A Myc-tagged hZTL1 clone was expressed in transiently transfected polarized human intestinal Caco-2 cells at the apical membrane. Expression of hZTL1 mRNA in Caco-2 cells increased with zinc supplementation of the nutrient medium; however, in the placental cell line JAR hZTL1 appeared not to be regulated by zinc. Heterologous expression of hZTL1 in Xenopus laevis oocytes increased zinc uptake across the plasma membrane. The localization, regulatory properties, and function of hZTL1 indicate a role in regulating the absorption of dietary zinc across the apical enterocyte membrane.

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Long-term serological follow-up of patients treated for chronic cutaneous borreliosis or culture-positive erythema migrans.

The kinetics of antibodies to Borrelia burgdorferi following successful treatment of early and late cutaneous borreliosis were analysed in consecutive serum samples by an enzyme-linked immunosorbent assay (ELISA) technique. Twenty-three patients with culture positive erythema migrans were followed for 23+/-14 months: 41% stayed seronegative, 35% showed an isolated immunoglobulin M (IgM) response, 8% an isolated IgG response and 16% a combined IgM and IgG responses. In general, antibody levels peaked within the first 3 months of symptom onset, whereafter a gradual decline was observed within 1 year. Twenty-two patients with chronic cutaneous borreliosis were followed for 23+/-11 months and all patients stayed IgG positive. Nearly three-quarters showed a clear decline in IgG levels over the years, while the rest did not. After 9+/-1 years 88% of 16 patients examined were still IgG positive. In conclusion, treatment of erythema migrans should be initiated on clinical appearance as a substantial number of patients stayed seronegative. Treatment success may in part be monitored serologically for both seropositive erythema migrans and chronic cutaneous borreliosis as most patients show declining titres after successful treatment. However, continuously high titres do not necessarily indicate treatment failure.

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Gianotti-Crosti syndrome and allergic background.

The aim of the study was to verify whether there is a relationship between Gianotti-Crosti syndrome and an allergic background in children. Twenty-nine children affected by Gianotti-Crosti syndrome were first screened for a large panel of microbiological examinations, including serological and cultural tests for viruses and bacteria. A causative agent was identified in only 10 cases (34.4%). In five cases a diagnosis of Epstein-Barr virus infection was made on the basis of significant titres of anti-Epstein-Barr virus antibodies (IgM) associated with constitutional symptoms (fever, pharyngitis-tonsillitis). Our data concur with several clinical studies demonstrating that Epstein-Barr virus is now the most common viral agent associated with Gianotti-Crosti syndrome. For allergic evaluation, a group of 59 age- and sex-matched children investigated for recurrent infections were used as controls. The presence of atopic dermatitis (24.1%) in those with Gianotti-Crosti syndrome was significantly higher (p < 0.005) than in the control group (6.8%). In addition, a more common family history for atopy was 51.7% vs. 31% (p < 0.027) and the percentage of patients with total IgE greater than +2 SD for age higher than in controls (27.6% vs. 13.7%), as was the percentage of specific IgE present (31% vs. 17.2%). These results indicate that atopy is significantly associated with Gianotti-Crosti syndrome.

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Acute exanthems in children. Clues to differential diagnosis of viral disease.

The numerous viral skin diseases that affect children present a diagnostic challenge to the clinician. Most of these diseases may be conveniently grouped according to the clinical appearance of the exanthem as maculopapular, petechial, papular, or vesicular. In some situations, viral infection may be difficult to differentiate clinically from nonviral disease; thus, extensive laboratory evaluation is sometimes necessary to pinpoint the virus involved. Nonviral disease should be considered in the differential diagnosis of a patient with skin eruptions, especially of the maculopapular type. Common nonviral causes include Kawasaki disease, toxic shock syndrome, and drug reactions.

Acrodermatitis↗

Zinc and spinal cord injury: a review.

Everything that is living needs zinc. Because of its multiple cellular functions, many symptoms and signs have been associated with zinc deficiency in humans including poor wound healing, rashes, diarrhea, decreased sexual function, and growth retardation. These problems are usually caused by other factors and indiscriminate use of zinc supplements is associated with some risk. Because inaccurate diagnosis can prevent alternative appropriate therapy and evidence is lacking that zinc supplementation beyond normal levels is generally beneficial, zinc status should be assayed prior to its administration; serum-zinc levels are the easiest method obtainable. A normal value is strong evidence against zinc deficiency (unless zinc replenishment has just been initiated); a single depressed value, however, may reflect the body's response to stress and not true zinc deficiency. A single low value in an acutely stressed patient should be interpreted with caution and repeated in several days. Symptoms and signs caused by zinc deficiency usually respond to zinc supplementation.

Acrodermatitis↗

Zinc metabolism in malabsorption syndromes.

Zinc deficiency may complicate many gastrointestinal malabsorptive states. Zinc deficiency may manifest itself in a myriad of ways, ranging from skin lesions to immune dysfunction. This paper reports many of the ways in which zinc deficiency may appear in malabsorption syndromes and possible mechanisms for the development of this zinc deficiency.

Acrodermatitis↗

Control of polyunsaturated acids in tissue lipids.

Since the discovery in 1929 that certain polyunsaturated fatty acids (PUFA) are essential for life and health, intense investigation has revealed the multiplicity of members in each of several families of PUFA, no two of which are equivalent. The quantified nutrient requirements for the essential dietary precursors of the two dominant families of PUFA have been estimated, and the general functions of these families are slowly becoming known. The PUFA are essential components of structural membrane lipids. The functions of the individual members are not yet differentiated, except as they act as precursors of synthesis of unique octadecanoid, eicosanoid, and docosanoid products of oxidation that have potent biological properties. The PUFA occur in animals and higher plants as ubiquitous and essential components of structural lipid that are in a dynamic equilibrium with the pool of dietary acyl groups. Many human diseases have been found to involve unique essential fatty acid (EFA) deficiencies or distortions of the normal equilibrium pattern. The equilibrium is influenced by the level of dietary intake or precursors, by the presence of competing essential and nonessential acyl groups, by nonoptimum intake of other essential nutrients, by hormonal effects, by drug therapy, and by other effects upon physiological condition. With the many variables already known to modulate or control the equilibrium, it should be possible with more precise understanding of each variable to shift abnormal equilibria in the direction of normalcy. This perhaps will be the next area of intensive investigation in this field of nutrition and metabolism.

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Acro-angiodermatitis. A simulant of Kaposi's sarcoma.

Acro-angiodermatitis, usually related to venous insufficiency of the lower limbs, may simulate some of the features of Kaposi's sarcoma, both to the clinician and the dermatopathologist. With the increasing incidence of Kaposi's sarcoma related to the acquired immune deficiency syndrome (AIDS), there is a greater awareness of Kaposi's sarcoma than the benign simulant. Against this background, there is a danger that acro-angiodermatitis will be misdiagnosed as Kaposi's sarcoma.

Acrodermatitis↗

Basal cell carcinomas arising over arteriovenous malformations: some speculations on the theme.

The modulating effects of mesoderm on ectoderm during the embryonic period have been well documented. Some cutaneous conditions such as dermatofibroma with basaloid proliferation are examples of such a relationship. Seven cases of basal cell carcinoma (BCC) developing in port-wine stains and one case developing over an arteriovenous (AV) malformation have been reported. We report 3 elderly patients with BCC developing over AV malformations of the lower extremities. The association between BCC and AV malformation range from a chance association to a complex interaction between mesenchyme and epithelium, in which mesenchyme induces and modulates epithelial growth through the elaboration of specific growth factors (GF).

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Acroangiodermatitis (pseudo-Kaposi's sarcoma) associated with Klippel-Trénaunay syndrome.

Acroangiodermatitis is an unusual cutaneous sequela of chronic venous insufficiency and congenital vascular malformations of the lower extremities. It typically manifests as purple-colored plaques on the extensor surfaces of the toes of the affected limb. Histologically, it closely resembles Kaposi's sarcoma and had thus been named "pseudo-Kaposi's sarcoma." This is a report of acroangiodermatitis in a patient with Klippel-Trénaunay syndrome.

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