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PubMed1985

Clinical, endocrinological and biochemical effects of zinc deficiency.

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.

Adrenal Gland Diseases↗
PubMed2003

[Acquired zinc deficiency in a breast-fed premature infant].

UNLABELLED: Symptomatic zinc deficiency can occur in exclusively breast-fed infants. We report a case in a preterm infant. CASE REPORT: A 3-months-old exclusively breast-fed premature infant presented with peri-orificial and acral eczematoid lesions. Laboratory investigations revealed lowered zinc levels in the infant's serum and in her mother's milk. A rapid healing occurred after oral zinc supplementation. DISCUSSION: Zinc deficiency in breast-fed infants is a rare disease caused by a low level of zinc in mother's milk. The clinical features resemble those of acrodermatitis enteropathica. Oral zinc supplementation is required until weaning.

Breast Feeding↗
PubMed1998

Scleroderma-like disorders.

Scleroderma-like disorders are widely disparate conditions mimicking either systemic sclerosis or cutaneous localized scleroderma, not infrequently displaying features of both. Some are exclusively sclerotic, some scleroatrophic with prevailing sclerosis or atrophies. The recognition of scleroderma-like disorders is of practical importance because by establishing the cause of the disease, it is possible to introduce an effective therapy, as in scleredema Buschke or scleredema diabeticorum, sclerodermiform porphyria, Borrelia burgdorferi-induced sclerodermiform acrodermatitis atrophicans, sclerodermiform phenylketonuria, drug-induced conditions, and so on. Scleroderma-like disorders strongly suggest that the pathogenesis of skin sclerosis and internal involvement may be divergent, and of various causes. Some of them, such as atrophoderma Pasini-Pierini or progressive facial hemiatrophy, frequently overlapping with scleroderma, make the differentiation very difficult, if at all possible, and the diagnosis is often arbitrary. Some, as sclerodermiform graft-versus-host reaction, point to the autoimmune origin of scleroderma. The amply-covered congenital sclerodermiform conditions present a large spectrum of still not widely known and extremely heterogeneous syndromes, associated with numerous anomalies and/or malignancies.

Adolescent↗
PubMed2003

Lyme borreliosis.

Lyme borreliosis is a multi-organ infection caused by spirochetes of the Borrelia burgdorferi sensu lato group with its species B burgdorferi sensu stricto, Borrelia garinii, and Borrelia afzelii, which are transmitted by ticks of the species Ixodes. Laboratory testing of Lyme borreliosis includes culture, antibody detection using ELISA with whole extracts or recombinant chimeric borrelia proteins, immunoblot, and PCR with different levels of sensitivity and specificity for each test. Common skin manifestations of Lyme borreliosis include erythema migrans, lymphocytoma, and acrodermatitis chronica atrophicans. The last two conditions are usually caused by B garinii and B afzelii, respectively, which are seen more frequently in Europe than in America. Late extracutaneous manifestations of Lyme borreliosis are characterised by carditis, neuroborreliosis, and arthritis. We present evidence-based treatment recommendations for Lyme borreliosis and review the prevention of Lyme borreliosis, including the Lyme vaccines.

Adolescent↗
PubMed2001

Detection and molecular typing of Borrelia burgdorferi sensu lato in Ixodes ricinus ticks and in different patient samples from southwest Germany.

The prevalence of different genospecies of Borrelia burgdorferi sensu lato in infected ticks could be a determinant for the risk of acquiring Lyme borreliosis (LB) and its clinical presentation. A total of 7373 ticks and 2761 samples from LB patients from the same area in southwest Germany were analyzed by PCR to assess the frequency of the occurrence of LB-associated genospecies. Fifteen percent of the tick samples and 19% of the human samples were found positive for the presence of B. burgdorferi sensu lato. Further identification of 1106 B. burgdorferi sensu lato positive tick samples by reverse line blotting and 125 positive patient samples by nested PCR using species-specific primers revealed the occurrence of B. afzelii, B. burgdorferi sensu stricto, B. garinii and B. valaisiana. Both single-species and mixed infections were noted and a similar distribution of the different genospecies was found in ticks compared with human samples. It was also the purpose of this study to obtain more information about a possible correlation between the distribution of Borrelia species and clinical syndromes of LB. Skin biopsies of 59 patients with acrodermatitis chronica atrophicans and cerebrospinal fluid samples from 78 patients with possible neuroborreliosis were analyzed. In conclusion, the distribution of the different genospecies in ticks is the decisive factor for the occurrence of the different Borrelia genospecies in samples from LB patients. Borrelia afzelii is the predominant genospecies in all kind of samples from the observed area and there seems to be no association of particular Borrelia genospecies with distinct clinical manifestations of LB.

Animals↗
PubMed2000

Morphoea is neither associated with features of Borrelia burgdorferi infection, nor is this agent detectable in lesional skin by polymerase chain reaction.

BACKGROUND: The aetiology of morphoea is still unknown. Borrelia burgdorferi as a causative agent of morphoea has been discussed since 1985, but the relationship remains uncertain. OBJECTIVES: We aimed to find evidence for infection with B. burgdorferi by combined evaluation of different clinical and laboratory data in a group of 54 patients with morphoea. METHODS: In each patient, an evaluation of the case history was performed with regard to infection with B. burgdorferi, using a standardized questionnaire. Questions focused on previous tick bites and skin changes suspicious for erythema migrans (EM). The case history data of 52 patients were compared with those of 104 matched control subjects and of 25 patients with acrodermatitis chronica atrophicans (ACA). Serological examinations were performed in 53 patients with morphoea. Furthermore, lesional skin was examined for borrelial DNA in 33 patients, using nested polymerase chain reaction (PCR) for the ospA and the borrelial rRNA gene. RESULTS: Results of the questionnaire showed no differences between patients with morphoea and matched controls. In contrast, patients with ACA showed a much higher prevalence of tick bites and skin changes suspicious for EM as compared with patients with morphoea. Serological examination was positive in only one patient with morphoea alone and in two additional patients with coexistent ACA. No borrelial DNA was detected by PCR in lesional skin of 33 patients with morphoea. CONCLUSIONS: No evidence was found for B. burgdorferi infection in patients with morphoea.

Adolescent↗
PubMed1999

Enhanced expression of human metalloelastase (MMP-12) in cutaneous granulomas and macrophage migration.

Accumulation of inflammatory cells such as macrophages may lead to degeneration of connective tissue matrix in various skin diseases. Macrophage metalloelastase, is a matrix metalloproteinase (MMP-12) capable of degrading elastin as well as various basement membrane components. To investigate the role of human macrophage metalloelastase in skin, we assessed by in situ hybridization and immunohistochemistry 66 specimens representing skin diseases characterized either by changes in elastic fibers or by pronounced infiltrations of extravasating and migrating macrophages. CD68 immunostaining was performed to identify the human macrophage metalloelastase-positive cells and Weigert's Resorcin-Fuchsin staining to reveal the status of elastic fibers. We found abundant expression of human macrophage metalloelastase mRNA in macrophages in areas devoid of normal elastic fibers in granulomatous skin diseases sarcoidosis, necrobiosis lipoidica diabeticorum, and granuloma annulare. Positive cells for human macrophage metalloelastase protein could be detected in the same regions as well as positive immunostaining for urokinase plasminogen activator. Of the other matrix metalloproteinases capable of degrading elastin, 92 kDa gelatinase colocalized with human macrophage metalloelastase, while 72 kDa gelatinase was produced by surrounding fibroblast-like cells. Furthermore, human macrophage metalloelastase was expressed by macrophages in areas with disrupted basement membrane, as assessed by type IV collagen staining, in pityriasis lichenoides and dermatitis herpetiformis. Specimens of anetoderma, acrodermatitis chronica atrophicans and pseudoxanthoma elasticum showed no signal for human macrophage metalloelastase. Matrilysin was not detected in any of the samples investigated. Our study suggests that human macrophage metalloelastase may contribute to elastin degradation occurring in granulomatous skin diseases and may aid macrophage migration through the epidermal and vascular basement membranes in inflammatory disorders.

Cell Movement↗
PubMed2000

Lyme borreliosis.

Lyme borreliosis is a worldwide, multistage, and multi-system disease caused by borrelia spirochetes, which are transmitted by ixodes ticks. It is focally endemic in temperature climates of the northern hemisphere. Primary erythema migrans occurs at the site of inoculation. Secondary erythema migrans occurs at sites of hematogenous dissemination. Variations in genospecies account for variations in presentation, including borrelial lymphocytoma. Disseminated disease includes constitutional signs and symptoms, intermittent oligoarticular arthritis, meningitis, cranial neuritis, radiculoneuropathy, encephalopathy, atrioventricular block, and myopericarditis. Late persistent disease includes acrodermatitis chronica atrophicans, chronic arthritis, neurological impairment, and fatigue. There can be difficulties with both clinical and laboratory diagnosis. First-line oral therapies for early uncomplicated disease are doxycycline and amoxicillin. First-line intravenous therapy for complicated or resistant disease is ceftriaxone. Prevention includes avoiding tick habitats, dressing sensibly, judicious use of repellants, and early removal of imbedded ticks. Vaccination is indicated only for frequent or prolonged exposure to tick-infested habitat.

Anti-Bacterial Agents↗
PubMed1985

[Erythema migrans borreliosis in the Federal Republic of Germany. Epidemiology and clinical aspects].

A positive antibody titre against Ixodes-ricinus-Borrelia (burgdorferi), using indirect immunofluorescence or ELISA, could be detected in serum and (or) liquor of 935 (32%) out of a total of 2955 patients between January 1984 and July 1985. In 289 of these cases the typical clinical manifestations were lacking whereas a characteristic disease picture enabled a diagnosis to be made in 171 patients with negative or borderline antibody titres. The 1106 cases of infection observed covered all regions of the country. A typical clinical syndrome was seen in 817 (74%) of these. Most common were erythema chronicum migrans (n = 458) and meningopolyneuritis Garin-Bujadoux-Bannwarth (n = 404); in 42% of the cases meningopolyneuritis was preceded by an erythema. Arthritis (n = 63), acrodermatitis chronica atrophicans (n = 72), carditis (n = 13) and lymphadenosis benigna cutis (n = 5) were much less common. Chronic Borrelian encephalomyelitis (n = 45) appeared surprisingly often (n = 45). The fact that in 73% of cases the various syndromes appeared alone, were double in 24% and combined only in 3%, illustrates the polymorphic nature of this disease.

Adolescent↗
PubMed2003

Anetoderma: another facet of Lyme disease?

Lyme disease has been suspected to be one cause of secondary anetoderma. We present a 25-year-old male patient with multiple lesions of anetoderma with a diameter of up to 2 cm that developed within the last 4 weeks without subjective symptoms. The histopathologic pattern was similar to the inflammatory stage of acrodermatitis chronica atrophicans. Polymerase chain reaction analysis out of the paraffin-embedded tissue, confirmed by sequencing of the obtained nucleotide product, revealed a part of the 23 S ribosomal RNA gene of Borrelia burgdorferi sensu lato. Enzyme-linked immunosorbent assay showed an increased serum IgG titer against B burgdorferi corroborated by Western blot analysis. After a treatment with oral doxycycline (100 mg twice a day) for 30 days the anti-B burgdorferi titer decreased significantly and no new lesions appeared. Some cases of anetoderma might be caused by Borrelia and patients with anetoderma should be examined for borreliosis including serology and polymerase chain reaction of lesional skin. In cases of Borrelia-induced anetoderma, early antibiotic treatment could prevent further progression of the disfiguring skin lesions and the underlying disease.

Adult↗
PubMed1979

Impairment of cell-mediated immunity functions by dietary zinc deficiency in mice.

Several immunologic features were analyzed in mice on a zinc-deficient diet [Zn(-)], in mice pair-fed a diet containing zinc [Zn(+)], in mice fed a Zn(+) diet ad lib, and in mice fed laboratory chow ad lib. When placed on a Zn(-) diet, 6- to 8-week-old A/Jax, C57BL/Ks, and CBA/H mice showed loss of body weight, low lymphoid tissue weight, and profound involution of the thymus within 4-8 weeks after initiation of the regimen. Approximately 50% of the mice on the Zn(-) diet developed severe acrodermatitis enteropathica (lesions on tail and paws) and diarrhea. Pair-fed mice on the Zn(+) diet did not show any of these symptoms. Mice on the Zn(-) diet showed the following immune deficiencies: (i) depressed plaque-forming cells against sheep erythrocytes after in vivo immunization; (ii) depressed T killer cell activity against EL-4 tumor cells after in vivo immunization; and (iii) low natural killer cell activity. However, antibody-dependent cell-mediated cytotoxicity against chicken erythrocytes was normal in the mice on the Zn(-) diet. Deficiency of T killer cell activity was not observed when immunization with EL-4 allogeneic lymphoma cells was carried out in vitro. Progressive loss of relative and absolute number of Thy 1.2+ cells and a proportionate relative increase in cells bearing Fc receptors was seen in spleen and lymph nodes of Zn(-) animals. It appears that zinc is an essential element for maintenance of normal T cell and other immune functions in vivo.

Animals↗
PubMed1999

The neutral cysteine protease bleomycin hydrolase is essential for epidermal integrity and bleomycin resistance.

The papain superfamily member bleomycin hydrolase (Blmh) is a neutral cysteine protease with structural similarity to a 20S proteasome. Bleomycin (BLM), a clinically used glycopeptide anticancer agent, is deaminated in vitro by Blmh. We used gene targeting to generate mice that lack Blmh and demonstrated that Blmh is the sole enzyme required for BLM deamination. Although some Blmh null mice were viable and reproduced, only about 65% of the expected number survived the neonatal period, revealing an important role for Blmh in neonatal survival. Mice lacking Blmh exhibited variably penetrant tail dermatitis that resembled rodent ringtail. The histopathology of the tail dermatitis was similar to skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Compared with controls, Blmh null mice were more sensitive to acute BLM lethality and developed pulmonary fibrosis more readily following BLM treatment. Thus, we have established that Blmh is an essential protectant against BLM-induced death and has an important role in neonatal survival and in maintaining epidermal integrity.

Aging↗
PubMed2003

Zn2+-stimulated endocytosis of the mZIP4 zinc transporter regulates its location at the plasma membrane.

Zinc is an essential nutrient for all organisms. Its requirement in humans is illustrated dramatically by the genetic disorder acrodermatitis enteropathica (AE). AE is caused by the reduced uptake of dietary zinc by enterocytes, and the ensuing systemic zinc deficiency leads to dermatological lesions and immune and reproductive dysfunction. The gene responsible for AE, SLC39A4, encodes a member of the ZIP family of metal transporters, hZIP4. The mouse ZIP4 protein, mZIP4, stimulates zinc uptake in cultured cells, and studies in mice have demonstrated that zinc treatment decreases mZIP4 mRNA levels in the gut. In this study, we demonstrated using transfected cultured cells that the mZIP4 protein is also regulated at a post-translational level in response to zinc availability. Zinc deficiency increased mZIP4 protein levels at the plasma membrane, and this was associated with increased zinc uptake. Significantly, treating cells with low micromolar zinc concentrations stimulated the rapid endocytosis of the transporter. Zinc-regulated localization of the human ZIP4 protein was also demonstrated in cultured cells. These findings suggest that zinc-regulated trafficking of human and mouse ZIP4 is a key mechanism controlling dietary zinc absorption and cellular zinc homeostasis.

Animals↗
PubMed2004

The adaptive response to dietary zinc in mice involves the differential cellular localization and zinc regulation of the zinc transporters ZIP4 and ZIP5.

The ZIP5 gene encodes a protein closely related to ZIP4, a zinc transporter mutated in the human genetic disorder acrodermatitis enteropathica. Herein, we demonstrate that mouse ZIP5 and ZIP4 genes are co-expressed in several tissues involved in zinc homeostasis (intestine, pancreas, embryonic yolk sac). However, unlike expression of the ZIP4 gene, which is induced during periods of zinc deficiency, ZIP5 gene expression is unaltered by dietary zinc. Immunohistochemistry localizes ZIP5 to the basolateral surfaces of enterocytes, acinar cells, and visceral endoderm cells in mice fed a zinc-adequate diet. However, this protein is removed from these cell surfaces and internalized during dietary zinc deficiency. In contrast, ZIP4 is induced and recruited to the apical surface of enterocytes and endoderm cells during zinc deficiency. In the pancreas, ZIP4 is expressed in beta-cells, whereas ZIP5 is expressed in acinar cells. These results suggest that the function of ZIP5 is antagonistic to that of ZIP4 in the control of zinc homeostasis; rather than functioning in the acquisition of dietary zinc, as does ZIP4, ZIP5 may function in the removal of zinc from the body. Thus, during periods when dietary zinc is replete, ZIP5 may function to remove zinc from the blood via the pancreas and intestine, the major sites of zinc excretion in mammals, whereas the acquisition of dietary zinc by intestinal ZIP4 would be minimal. In contrast, during periods of dietary zinc deficiency when secretion of zinc by the pancreas and intestine is minimized, ZIP5 is removed from the cell surface, and the intestinal uptake of zinc is augmented by induction of ZIP4.

Amino Acid Sequence↗
PubMed2007

A histidine-rich cluster mediates the ubiquitination and degradation of the human zinc transporter, hZIP4, and protects against zinc cytotoxicity.

Zinc is an essential nutrient. Genetic evidence for this nutritional requirement in humans is the zinc deficiency disease, acrodermatitis enteropathica. This disorder is caused by mutations in hZIP4 (SLC39A4), a zinc importer required for zinc uptake in enterocytes and other cell types. Studies in mice have demonstrated that levels of the mZIP4 mRNA are reduced by elevated dietary zinc, resulting in a decreased abundance of the ZIP4 protein at the plasma membrane. Moreover, studies in cultured cells have demonstrated that low micromolar concentrations of zinc stimulate the endocytosis of the mZIP4 protein resulting in a reduction in cellular zinc uptake. In this study, we demonstrate an additional level of hZIP4 regulation involving ubiquitination and degradation of this transporter in elevated zinc concentrations. Mutational analysis identified a cytoplasmic histidine-rich domain that was essential for ubiquitin-dependent degradation of ZIP4 and protection against zinc toxicity. However, this motif was dispensable for zinc-induced endocytosis. These findings indicate that ubiquitin-mediated degradation of the ZIP4 protein is critical for regulating zinc homeostasis in response to the upper tier of physiological zinc concentrations, via a process that is distinct from zinc-stimulated endocytosis.

Cation Transport Proteins↗
PubMed2004

Intestinal and placental zinc transport pathways.

Mammalian members of the cation diffusion facilitator (CDF) and zrt-, irt-like protein (ZIP) families of Zn transporters, initially identified in Saccharomyces cerevisiae and Arabidopsis thalania spp., have been cloned during the last 8 years and have been classified as families SLC30 and SLC39 respectively. The cloning of human Zn transporters ZnT-like transporter 1 (hZTL1)/ZnT5 (SLC30A5) and hZIP4 (SLC39A4) were major advances in the understanding of the molecular mechanisms of dietary Zn absorption. Both transporters are localised at the enterocyte apical membrane and are, therefore, potentially of fundamental importance in dietary Zn uptake. hZTL1 mediates Zn uptake when expressed in Xenopus laevis oocytes and hZIP4 is mutated in most cases of the inherited Zn deficiency disease acrodermatitis enteropathica. Localisation of hZTL1/ZnT5 at the apical membrane of the placental syncytiotrophoblast indicates a fundamental role in the transfer of Slc30 Zn to the foetus. Observations in rodent models indicate that in the intestine increased Zn availability increases expression of Zn transporters. Human intestinal Caco-2 cells show a similar response to increasing the Zn2+ concentration of the nutrient medium in relation to the expression of mRNA corresponding to several Zn transporters and that of ZnT1 (SLC30A1) and hZTL1/ZnT5 proteins. In the human placental cell line JAR, however, expression at the mRNA level of a number of Zn transporters is not modified by Zn availability, whilst ZnT1 and hZTL1/ZnT5 proteins are reduced under Zn-supplemented conditions. These differences between Caco-2 and JAR cells in Zn transporter gene responses to Zn supply may reflect the different extracellular Zn concentrations encountered by the corresponding cell types in vitro.

Amino Acid Sequence↗
PubMed2001

Avidity determination of Borrelia burgdorferi-specific IgG antibodies in Lyme disease.

The avidity indices of Borrelia burgdorferi-specific IgG antibodies were estimated using ELISA in sera from patients with different stages of Lyme disease. In addition, sera from healthy students with proof of borrelial-specific IgG antibodies from standard serology were tested. Low avidity indices were detected predominantly in sera from patients with early-stage Lyme disease [erythema migrans (EM); n = 25]. High avidity indices were found in healthy students (n = 72) and in most of the patients with neuroborreliosis (NB; n = 44) and chronic late-stage Lyme disease [acrodermatitis chronica atrophicans (ACA); n = 36]. In conclusion, early-stage Lyme disease (EM) could be differentiated from advanced and chronic stages (NB, ACA) and from "seropositive" healthy persons using avidity determination in the majority of patients in this study.

Antibody Affinity↗
PubMed1994

Aetiology of chronic diarrhoea in children: experience at King Khalid University Hospital, Riyadh, Saudi Arabia.

Forty-eight cases of chronic diarrhoea in children seen at King Khalid University Hospital over a 5-year period were analysed. The mean age at presentation was 1.8 years (range 0.08-10 years); 34 were boys and 14 girls. Forty-four patients were Saudi and four were non-Saudi Arabs. Most children presented with failure to thrive and pallor. The aetiological factors identified were: the post-gastro-enteritis syndrome with or without lactose intolerance in 16 (33%); coeliac disease in ten (21%); congenital chloride diarrhoea in five (10%); glucose-galactose malabsorption and acrodermatitis enteropathica, each in three (6%); ulcerative colitis, intestinal lymphangiectasia, cow's milk protein intolerance and ataxia telangiectasia, each in two (4%); and giardiasis, immune deficiency and cystic fibrosis, each in one (2%). Five children died.

Child↗