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PubMed1984

[Pseudoscleroderma and sclerodermiform states].

Pseudo-scleroderma should not be confused with true scleroderma, the prognosis of which is unpredictable and often serious. Progressive acrosclerosis must be differentiated from Raynaud's disease, congenital or hereditary disorders of unknown aetiology: Werner's syndrome, acrogeria and progeria; Rothmund-Thomson's syndrome, Steinert's disease, phenylketonuria, disorders of glycogen metabolism; metabolic disorders: mutilating acropathies, scleromyxoedema, porphyria cutanea tarda; occupational and iatrogenic disorders: acroosteolysis, toxic epidermic syndrome (Spain), scleroderma-like change induced by bleomycin, chronic graft-versus-host disease; and leprosy. Acute diffuse scleroderma should not be confused with Buschke's scleroedema, sclerema neonatorum, systemic amyloidosis and scleroderma-like changes in hypothyroidism. Linear pseudo-scleroderma is suggested by the following scleroderma-like conditions: facial hemiatrophy, acrodermatitis atrophicans, melorheostosis, pseudo-scleroderma after corticosteroid injection, and cutaneous lesions in carcinoid syndrome. Scleroderma in plaque must be differentiated from hypodermitis sclerotisans, panatrophy and localized lipoatrophies, hypodermitis after vitamin K injection, basal cell carcinoma, necrobiosis lipoidica, vitiligo, chronic radiodermatitis, cutaneous lymphatic invasion. Scleroderma-like changes after drug injection (vitamin B12, progestin), anetoderma barely resemble morphea guttata.

Adipose Tissue↗
PubMed1983

[Genodermatosis in man and animal. Comparative overview].

Fourteen monogenic cutaneous disorders of man are compared to similar gene defects in animals. The traits are classified into two groups. In the first group, an identity (homology) of the underlying gene defects is likely. This group includes oculo-cutaneous albinism, Chédiak-Higashi syndrome, aplasia cutis congenita, Ehlers-Danlos syndrome (type I), hypohidrotic ectodermal dysplasia of the Christ-Siemens-Touraine type, X-linked dominant chondrodysplasia punctata, ichthyosis congenita gravis, Menkes syndrome, erythropoetic porphyria, porphyria cutanea tarda, and acrodermatitis enteropathica. In the second group, the traits are similar but the question of their homology cannot be settled. It includes alopecia congenita, hidrotic ectodermal dysplasia of the Clouston type, and hereditary lymphedema. The existence of identical mutations in man and animals provides evidence for the close relationship between the various mammalian species. Homologous traits affecting the skin are of practical importance since the use of these animal models may help to answer those questions which cannot be answered by performing research in human patients.

Animals↗
PubMed1984

Discovery and importance of zinc in human nutrition.

The present explosion in knowledge of zinc has been the result of several factors, the major ones being the recognition of the important role of zinc in human health and diseases, its vital functions in biochemical reactions, and the technological advances that make it feasible to quantitate this essential trace element in biological fluids. Deficiency of zinc in humans due to nutritional factors and several disease states has now been recognized. The high phytate content of cereal proteins is known to decrease the availability of zinc; thus, the prevalence of zinc deficiency is likely to be high in a population consuming large quantities of proteins. Alcoholism, malabsorption, sickle cell anemia, chronic renal disease, and chronically debilitating diseases are now known to be predisposing factors for zinc deficiency. A severe deficiency of zinc such as that seen in patients with acrodermatitis enteropathica may be life-threatening. A spectrum of clinical manifestations ranging from mild to severe degrees has now been recognized in human zinc deficiency states. Zinc appears to be involved in many biological functions including DNA synthesis. Roles for zinc in enzymatic functions, cell membranes, and immunity are now well established.

Calmodulin↗
PubMed1984

[Cutaneous manifestations of the malabsorption syndrome].

A review of the skin changes in malabsorption syndrome, is presented; dividing the symptoms in skin, mucous membranes and adnexal involvement. In this way, acquired ichtyosis, hiperpigmentation changes, purpura and echimosis and eczematoid or psoriatic-like with generalized pruritus are described. The mucous membranes alterations are the most frequent ones, the angular cheilitis, glositis, ulcerations and aphthaes are pointed out, as well as the changes in the shape and colour of hair and nail abnormalities. Special mention deserve the particular cases of malabsorption syndromes that appears in: acrodermatitis enteropathica, dermatitis herpetiformis, Whipple disease, Cronkhite-Canada syndrome, dermatogenic enteropathy and abnormalities that occur as complication from the surgery treatment for obesity improvement.

Arthritis↗
PubMedDate not supplied

Ixodes ricinus spirochete and European erythema chronicum migrans disease.

From three endemic locations of erythema chronicum migrans disease in North Rhine-Westphalia, Germany, we recovered 19 isolates of a spirochete from Ixodes ricinus ticks. The infection rate in adult ticks was 16 percent. The isolated spirochete is immunologically related to the Ixodes dammini spirochete, Borrelia duttoni, and Treponema pallidum. Using indirect immunofluorescence, the sera of 90 patients with erythema chronicum migrans disease showed antibody titers against the isolated spirochete, which correlated with the clinical course. Similarly, antibodies were demonstrated in the sera of 21 patients with acrodermatitis chronica atrophicans. These results suggest an etiologic role for the Ixodes ricinus spriochete in European erythema chronicum migrans disease.

Antibodies, Bacterial↗
PubMed1984

[Acquired zinc deficiency mimicking glucagonoma dermatitis. Histology and electron microscopy].

A 47-year-old man suffering from colitis ulcerosa developed serious anaemia, oedema, stomatitis with burning tongue, dry skin and erosive lesions with peripheral spreading on the ankles. Histology and electron microscopy showed characteristic signs for necrolytic migratory erythema, zinc deficiency acrodermatitis, or pellagra. Decreased serum zinc level and response to oral zinc substitution finally proved the diagnosis of acquired zinc deficiency.

Dermatitis↗
PubMed1983

[Therapeutic possibilities of hereditary diseases in dermatology].

Several years ago the therapeutic possibilities for the treatment of inherited skin disorders were rather restricted; recently new possibilities have been developed and successfully applied. The author discusses the indications for a surgical procedure in basal cell nevus syndrome and the satisfying results revealed by dermabrasion in sebaceous adenoma of Pringle. The use of a low phenylalanine and tyrosine diet in case of palmoplantar keratosis with tyrosinemia is of theoretical as well as practical interest. However, a most striking therapeutic success is obtained by the treatment with drugs. The substitution of zinc in acrodermatitis enteropathica is very effective and not expensive! The positive effect of phenytoin in epidermolysis bullosa cicatricans is based on the partial inhibition of collagenase activity by this drug. Finally the author discusses the advantages of a treatment with retinoids in different hereditary keratinization disorders.

Dermatologic Agents↗
PubMed1984

[Skin changes in paraproteinemias (monoclonal gammopathies)].

Numerous skin disorders or skin lesions are associated with a monoclonal gammopathy (formerly: paraproteinemia). These skin diseases can be differentiated in the following way: specific skin lesions caused by monoclonal immunoglobulin producing cells in the skin, in generalized plasmocytoma or morbus Waldenström. In another group of disorders the monoclonal immunoglobulins induce functional disturbances, e.g. Raynaud syndrome (if the monoclonal immunoglobulins are cryoglobulins), xanthomatosis through interactions between these immunoglobulins and lipoproteins, purpura in immunoglobulin induced stasis and hyperviscosity. The unlimited spreading of the plasmocytoma cells replaces normal immunoglobulin producing plasma cells followed by a disturbance of the humoral immune response, which is frequently accompanied by atypical infections of skin or other organs. Furthermore, an almost obligatory association with monoclonal gammopathies has been demonstrated in a few skin diseases, e.g. scleromyxedema. However, the role of the immunoglobulins in these disorders is unknown. In some other skin diseases, such as pyoderma gangrenosum, acrodermatitis atrophicans Herxheimer, scleredema Buschke etc., a monoclonal gammopathy is only detectable in some patients.

Amyloidosis↗
PubMed1980

Zinc deficiency: a complication of Crohn's disease.

Twenty-one of 52 patients with regional enteritis had low serum zinc concentrations on initial testing. Fourteen of 31 patients followed longitudinally had low serum zinc concentrations. Two patients are presented as case reports who developed acrodermatitis skin lesions that responded to zinc therapy. Hypogonadism, growth retardation, and abnormalities in taste were frequent complications in Crohn's patients with low serum zinc levels. Certain complications of regional enteritis may be due, in part, to zinc deficiency.

Adult↗
PubMedDate not supplied

Zinc and immune function.

Zinc and immune function relationship has been extensively studied. Both in experimentally induced mineral deficit and in genetically determined deficit observable in acrodermatitis enteropathica and in enteropathy of Danish A-46 cattle, a B and T dependent antibody response decrease, a T dependent cytolytic response decrease and a natural killer cytotoxic activity decrease are present noteviously. Serious reduction of the immune function is present, in proportion to the value of low zinc plasmatic level, in elderly patients, in malnourished and seriously zinc deficient children, in patients subjected to total parenteral supply, in HIV infections and especially in evident AIDS: in this condition the plasmatic zinc level can be considered, together with the CD4+ lymphocytes amount and the B2-microglobulin value, a disease progression marker. Zinc immunostimulating action mechanisms are complex, although thymic hormone (of which zinc is essential cofactor) stimulation seems to be most important. Zinc supplementation, also parenterally, can be useful in immunodeficiency (in the elderly, in the post-surgical patients, in genetically determined or alimentary induced deficit, in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1995

[Diagnosis of Lyme borreliosis].

Lyme borreliosis is an infectious disease, caused by the spirochaete Borrelia burgdorferi and transmitted by ticks, in our regions by the tick Ixodes ricinus. The disease mainly affects skin, nervous system, joints and heart. Lyme borreliosis develops in three stages, and the various clinical manifestations may assigned to the respective stages. As far as skin is concerned, in stage I typically appears erythema chronicum migrans, very often accompanied by flu-like symptoms; in stage III, months to years after the manifestations of the early phase, acrodermatitis chronica atrophicans, may be encountered. Among the neurological manifestations, in stage II, meningoradiculoneuritis (Bannwarth's syndrome) develops as the most frequent disease, characterized by pheripheral paresis at the lower extremities and bilateral facial nerve palsy. Lyme arthritis mainly affects the knee. To assure the diagnosis of Lyme borreliosis, a number of serological tests is performed as the direct detection of the causative agent is rather difficult and time consuming. Possibly, the use of the polymerase chain reaction to detect B. burgdorferi DNA may improve the diagnostic tools.

Animals↗
PubMedDate not supplied

Zinc: an overview.

Zn deficiency in humans is widespread throughout the world. It is more prevalent in areas where the population subsists on cereal proteins. Conditioned Zn deficiency is seen in many disease states. Its deficiency during growth periods results in growth failure and lack of gonadal development in males. Other effects of Zn deficiency include skin changes, poor appetite, mental lethargy, delayed wound healing, neurosensory disorders, and cell-mediated immune disorders. Severe Zn deficiency, as seen in acrodermatitis enteropathica (a genetic disorder), is fatal if Zn is not administered to these patients. A clinical diagnosis of marginal Zn deficiency in humans remains problematic. Assays of Zn in granulocytes and lymphocytes provide better diagnostic criteria for marginal Zn deficiency than plasma Zn. Approximately 300 enzymes are known to require Zn for their activities. Zn is required for DNA synthesis, cell division, and protein synthesis. Recently, we learned that Zn-finger proteins are involved in genetic expression of various growth factors and steroid receptors. We suspect that several hundred Zn-containing nucleoproteins are probably involved in gene expression of various proteins. Zn deficiency adversely affects lymphocyte proliferation. This may be related to the enzymatic role of Zn in DNA synthesis and cell division. Thymulin, a thymic hormone involved in T-lymphocyte maturation, is known to be Zn dependent and is adversely affected by Zn deficiency. Thus, an adverse effect of Zn deficiency may also be in lymphocyte differentiation and maturity. Zn deficiency is known to decrease interleukin 2 production by helper T lymphocytes, and abnormalities in T-lymphocyte subpopulations have been observed in Zn-deficient humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Detection of Borrelia burgdorferi DNA in human skin biopsies and dog synovial fluid by the polymerase chain reaction.

The polymerase chain reaction was used to amplify DNA sequences of the etiologic agent of Lyme disease, Borrelia burgdorferi, and was applied to the detection of the spirochete in humans and dogs. Oligonucleotide primers used in the reaction flank a 244-base-pair representing part of the variable region V4 of the B. burgdorferi 16S rRNA from biopsies of patients with acrodermatitis, and in synovial fluid from a dog with arthritis. These data suggest the presence of the disease in our state.

Animals↗
PubMed1995

Clinical and serologic features of Lyme borreliosis in Russia.

OBJECTIVE: To describe clinical and serologic features of Lyme borreliosis, particularly the joint abnormalities, in Russian patients. METHODS: Physicians were invited to refer patients with past or present erythema migrans to the Rheumatology Institute in Moscow; field studies were done of residents in an area endemic for Lyme borreliosis, and a serosurvey was conducted of patients with nonspecific neurologic, cardiac, or joint symptoms. Serologic testing was done by ELISA and Western blotting using a strain of Borrelia afzelii, a member of the B. burgdorferi sensu lato complex, recovered from ticks from the field study site. RESULTS: Of 86 patients with erythema migrans, neurologic abnormalities developed in 26 (30%), cardiac involvement in 5 (6%), arthritis or arthralgia in 35 (41%), and acrodermatitis in 2 (2%). Joint involvement was usually characterized by one or a few brief episodes of joint swelling or pain in one large joint at a time. However, 69 of the 86 patients (80%) received antibiotic therapy early in the infection. The majority of patients with active infection had elevated levels of IgM or IgG antibody to B. afzelii by ELISA, and those with late infection often had IgG reactivity with > or = 5 spirochetal proteins, particularly the 37, 39, 41, 60, and 93 kDa antigens. In a serosurvey of 75 patients with facial palsy, atrioventricular block, or arthritis or arthralgia of uncertain cause, 6 had IgG reactivity with > or = 5 spirochetal proteins. CONCLUSION: Lyme borreliosis in Russia is similar to that in other parts of Europe. Brief episodes of arthritis or arthralgia were a common feature of the illness.

Adolescent↗
PubMed1995

[Lyme disease].

The history of Lyme disease, a contagious condition caused by Borrelia burgdorferi transmitted to man by ticks offers infectiologists a formidable lesson on how medicine progresses. Clinical description started in Europe at the turn of the century with Pick's description of what was then labelled chronic atrophic acrodermatitis. Fifty years later Hauser noted the affection was transmitted by ticks. Independently, Afzelius, then Lipschutz, described erythema chronicum migrans and its relationship with tick bites. Neurological involvement was also described with the skin signs. These early dermatological descriptions suddenly came into the limelight in 1975 when an epidemia of arthritis occurred in children in Lyme, Connecticut, USA. Many of the affected children had erythema chronicum migrans. Based on these observations and an epidemiological analysis of the epidemia, Steele and co-workers defined "Lyme disease" as a rheumatological disorder commonly associated with erythema chronicum migrans and sometimes with multiple organ involvement. In 1982 Borgdorfer suggested that tick bites transmitted a Spirochaeta which was later authentified as the causal agent: Borrelia burgdorferi. Immunofluorescence and ELISA tests were rapidly developed for the diagnosis of infection by this germ which is very difficult to culture. Antibiotic curative treatment was immediately available and in 1991 a consensus conference established recommendations for treatment of isolated and disseminated forms. Antibiotic prophylaxis is not necessary but rapid extraction of the tick after the bite can prevent the disease as transmission from tick to man takes several hours. And medical progress continues. Work is now being conducted on evaluating the extent of late neurological manifestations, on developing polymerase chain reaction methods to identify B. burgdorferi infection in specific organs and on developing a vaccine.

Humans↗
PubMed1994

[Lyme disease].

Lyme disease is an infectious disease due to Borrelia burgdorferi, which is transmitted by a tick bite. Bearing ticks belong to the "Ixodes" type. Germ reservoirs include rodents, birds, deers... The disease onset usually takes place in summer or in autumn. Its early stage is characterized by erythema chronicum migrans. The secondary stage, initiated by a virus-like syndrome indicating the hematogenous and lymphatic dissemination may include neurologic symptoms and signs--the most frequent ones in France and Europe (meningoradiculitis, meningitis, palsy of one or several cranial nerves), cardiac symptoms (conduction dysfunction), a relapsing oligoarthritis, and sometimes ocular signs. In some cases, joint and/or nervous system symptoms may become chronic: it's the tertiary (late) stage, which may include, too, acrodermatitis chronica atrophicans. Any of these symptoms may initiate the disease or be its only manifestation. When erythema chronicum migrans is missing, diagnosis lays upon serology which may turn positive only lately, or remain negative; the possibility of false positivity must also be noticed. Antibiotherapy must be initiated as soon as possible; even when started lately, it may prove beneficial. It consists essentially of beta lactamins or doxycyclin. Studies are progressing in view of the elaboration of a vaccine.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Neuroborreliosis: diagnostic difficulties].

Borreliosis is a condition caused by spirochaete-Borrelia burgdorferi, characterised by multiorgan changes and prolonged course with three consecutive stages. The number of diagnosed cases in Poland tends to increase. This is due to the availability of diagnosis tests. Owing to the analysis of blood and CSF by the fluorimetric method 3M IgG/IgM Fastlyme, neuroborreliosis was confirmed in 5 patients (hospitalised in Neurological Clinic of Medical Academy in Białystok). Three of the cases were characterised by a bilateral palsy of facial nerve and abnormal CSF, as evidenced by pleocytosis (100% lymphocytes) and elevated protein. Patient 4 diagnosed by dermatologists as having Acrodermatitis atrophicans, should be classified, however, as the third stage of the disease, while according to neurological changes--namely a lesion of shoulder plexus--as the second stage. Evaluation of patient 5 presented most difficulties. Considering long-term disease and the time from the onset to the admission to the neurological clinic, she was likely to develop the third stage of the disease, and therefore, our treatment failed to be so effective as in aforementioned cases.

Adult↗
PubMed1976

Skin lesions during intravenous hyperalimentation: zinc deficiency.

Of 54 patients who received prolonged intravenous hyperalimentation during the past 4 years, six developed progressive, characteristic skin lesions. These cutaneous manifestations frequently were accompained by abdominal symptoms resembling those of acrodermatitis enteropathica in many respects. In the first four of these six patients, skin eruptions disappeared promptly after the initiation of oral feeding, which led us to assume that these skin manifestations are due to some unknown nutrient deficiency. Our experience in the remaining two patients enabled us to presume the underlying pathology to be zinc deficiency.

Adult↗