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At least 1,063 records · Page 59Linked to original sources
PubMed1993

Monoclonal antibodies for identification of Borrelia afzelii sp. nov. associated with late cutaneous manifestations of Lyme borreliosis.

Borrelia isolates associated with Lyme borreliosis were previously divided into 3 genospecies, B. burgdorferi sensu stricto, B. garinii and group VS461, on the basis of DNA homology. B. burgdorferi sensu stricto and B. garinii were identified by monoclonal antibodies (MAbs), H3TS and D6 respectively, but no MAbs were available to identify group VS461. Two MAbs were produced, I 17.3 and J 8.3 which reacted with OspB and OspA proteins, respectively, of strains belonging to group VS461, which should be named B. afzelii sp. nov. 24 strains were assigned to B. afzelii sp. nov., 11 of them being isolated from skin lesions, 6 from acrodermatitis chronica atrophicans (ACA) and 5 from erythema chronicum migrans (ECM). Although quite unknown in the USA, ACA has frequently been reported in northern Europe where B. afzelii sp. nov. is commonly isolated. This study documents the involvement of B. afzelii sp. nov. as a specific aetiological agent of ACA.

Acrodermatitis↗
PubMed1981

Severe zinc deficiency in humans: association with a reversible T-lymphocyte dysfunction.

Two patients developed severe zinc deficiency with acrodermatitis during parenteral hyperalimentation. The response of circulating T-lymphocytes to phytohemagglutinin was assessed both during the episode of clinical zinc deficiency and after intravenous zinc supplementation as the sole means of nutritional intervention. Maximum T-cell response to phytohemagglutinin, expressed as percent of simultaneous normal control response, was 2.1% and 27.9% in Patients 1 and 2 respectively. After 20 days of intravenous zinc supplementation (12 mg/d), repeat studies showed the T-cell response of Patient 1 to be 221% of the control, and that of Patient 2 to be 139% of control. In addition, Patient 1 was anergic during the period of zinc deficiency and normally reactive after zinc supplementation. These findings agree with extensive animal studies showing the detrimental effect of zinc deficiency on cellular immunity.

Acrodermatitis↗
PubMed1978

[Zinc in digestive diseases (author's transl)].

The present review is concerned by the main features of zinc metabolism (requirements, intestinal absorption, tissue distribution, excretion). The relationships between zinc variations and gut pathology are discussed with respect to the following points: criteria for the diagnostic of zinc deficiency, pathophysiological mechanisms, clinical consequences, therapeutic implications. Evidence for zinc malabsorption is present in Acrodermatitis enteropathica and in chronic zinc deficiency observed in Middle-East. During last decade zinc deficiency has been frequently reported in total parenteral feeding. Alterations in plasma zinc concentrations have been described in coeliac disease and inflammatory bowel disease but a true deficiency remains to be established in this pathological states.

Acrodermatitis↗
PubMedDate not supplied

Current status of zinc deficiency in the pathogenesis of neurological, dermatological and musculoskeletal disorders.

Recent clinical and experimental studies suggest that zinc deficiency may play an important role in the pathogenesis of (1) acrodermatitis enteropathica, and in certain cases of (2) hypogonadal dwarfism, (3) congenital malformations, (4) hypogeusia and hyposmia, (5) nyctalopia and (6) impaired wound healing. Distrubances of zinc metabolism also occur in a broad spectrum of other clinical disorders. The pathophysiological factors which are responsible for hypozincemia include: (1) nutritional deficiency and/or intestinal malabsorption of zinc; (2) hyperzincuria secondary to aminoaciduria; (3) hormonal effects (cortisol, growth hormone, estrogens); (4) hypoalbuminemia; and (5) effects of leukocytic endogenous mediator. The clinical diagnosis of zinc deficiency in patients with specific neurological, dermatological and musculoskeletal disorders is complicated by the complex interactions of these pathophysiological factors and by the need for more dependable laboratory indices of zinc deprivation.

Acrodermatitis↗
PubMed1992

Neurological complications of Lyme borreliosis.

Lyme disease, like syphilis, a spirochetal infection, can appear with exacerbations and remissions in different stages. The clinical picture is marked by dermatological, neurological, rheumatic and cardiological complications. PNS complications appear in the second and third stage. Tick bite meningoradiculoneuritis neuritis (Garin-Bujadoux-Bannwarth-Syndrome), characterized by painful asymmetrical sensory and motor dysfunctions and inflamed CSF, is a typical manifestation of the second stage. Mononeuritis multiplex appearing in conjunction with acrodermatitis chronica atrophicans is a typical PNS manifestation of the third stage. CNS involvement may also occur in early and late stages of Lyme-Borreliosis, presenting as myelitis or progressive encephalomyelitis. Lyme-Borreliosis is a treatable condition, which should not be missed in the differential diagnosis of PNS and CNS disorders.

Acrodermatitis↗
PubMedDate not supplied

Unusual musculoskeletal manifestations of Lyme disease.

We report on the imaging features of musculoskeletal abnormalities in a 52-year-old woman suffering from Lyme disease presenting with acrodermatitis chronica atrophicans (ACA). The patient developed recurrent attacks of migratory asymmetrical oligoarthritis, involving articular and peri-articular structures, including the metatarsophalageal (MTP) joints, scapular bone, thoracic spine, elbow, gluteal area, knee, ankle and metacarpophalangeal (MCP) joints. Six months after the first symptoms, Magnetic Resonance Imaging (MRI) showed bone marrow oedema within the proximal phalanx of the right fifth toe, adjacent to an ACA rash. A year after the onset of the disease, swelling at the right scapular region occurred, and MRI showed osseous, periosteal and soft tissue involvement of the superior margin of the right scapula and adjacent rib. On MRI of the spine, there was bone marrow infiltration with irregular delineation of the anterior corner of the thoracic vertebrae 4 to 6, corresponding to an osteoblastic bony lesion on radiographic examination. This case report is unique, because MRI documentation of bony abnormalities and periarticular soft tissue swelling, accompanying an attack of ACA has never been reported previously. Moreover, involvement of the osseous spine and the scapular bone have never been described in the radiological literature.

Acrodermatitis↗
PubMed2004

Gianotti-Crosti syndrome following milkers' nodules.

Gianotti-Crosti syndrome (GCS), or papular acrodermatitis of childhood, is a distinctive self-limiting rash with symmetrically distributed papules on the face, buttocks, and extremities that has been related to several underlying viral diseases. We report a case of a boy exhibiting involutive lesions of milkers' nodules who subsequently developed a rash with the clinical features of GCS. The temporal relationship suggested the possibility of a causal association.

Acrodermatitis↗
PubMed1992

Contributions to the treatment of dermatologic manifestations of Lyme borreliosis.

Lyme borreliosis was identified in Czechoslovakia for the first time in 1985. Since then, more cases have gradually been identified. Since 1989, about 1,500 patients per ten million inhabitants have been reported every year. Having summarized the results of the therapy of 371 patients with dermatologic manifestations of lyme borreliosis (erythema migrans in 315, borrelial lymphocytoma in fifteen, and acrodermatitis chronica atrophicans in forty-one) we present the antibiotic regimens used by Czechoslovak dermatologists in clinical practice.

Acrodermatitis↗
PubMed2006

[Stage-oriented treatment of Lyme borreliosis].

Every manifestation of Lyme borreliosis needs to be treated with antibiotics. The type of antibiotic applied and duration of treatment will depend on the stage and severity of the disease. Erythema migrans, Borrelia lymphocytoma, Lyme arthritis and acrodermatitis chronica atrophicans are primarily treated orally. If neurological symptoms, severe Lyme carditis or eye manifestations are present, intravenous treatment is initially recommended. For oral therapy, doxycycline, amoxicillin, cefuroxime and, if intolerance is shown, azithromycin, are available. For intravenous treatment ceftriaxone, cefotaxime or penicillin G is employed. The overall prognosis for treated Lyme borreliosis is good. However, in particular when manifestations with substantial organic injury have persisted, incomplete healing must be expected. With the exception of erythema migrans, every manifestation should be subjected to a careful diagnostic work-up prior to the start of treatment, because premature antibiotic administration is not only associated with an elevated risk for the patient, but can also mask important diagnostic signs.

Acrodermatitis↗
PubMed1999

[Clinical picture of Lyme boreliosis].

Prevalence of Lyme borreliosis in Europe has been well esablished during the last decade. The highest morbidity in Poland, exceeding 100 cases (100.000) year, was demonstrated in north-estern part of the country. Additional small endemic areas were also described in south-western and central part of the country. Clinical picture of the disease do not differ significantly from observed in other parts of Europe. Lyme borreliosis is characterized with a wide variety of manifestations recognized as typical: erythema migrans, borrelial lymphocytoma, acrodermatitis chronica atrophicans, arthritis, facial palsy, lymphocytic meningitis and cardiac transduction disturbances. However there are also controversial syndroms, that have confirmed etiology of Borrelia burgdorferi but only in some cases, such as: morphea sclerodermatous lesions, cardiomyopathy and some neurologic disorders. Diagnosis of Lyme borreliosis is still based on typical signs of the disease and laboratory techniques can not solve clinical doubts.

Acrodermatitis↗
PubMed2006

[Skin manifestations of Lyme borreliosis].

Lyme borreliosis is the most common tick-borne disease which is caused by Borrelia burgdorferi and transmitted in the Poland, as well as Europe, primarily by Ixodes ticks. After inoculation spirochetes spreads in the skin, activate locally immune response mechanisms and cause characteristic skin lesions like erythema migrans, lymphadenosis benigna cutis, erythema migrans multiplex and acrodermatitis chronica atrophicans. The correct clinical diagnosis of skin lesions and antibiotic treatment is most important for regression of symptoms and prevention of late manifestations of Lyme disease.

Acrodermatitis↗
PubMed1991

[Borrelia infections of the skin--progress of knowledge since the discovery of Lyme disease].

The description of Lyme disease in 1976 and the detection of its causative agent, the spirochete Borrelia burgdorferi (B. burgdorferi), in 1982 led to an increase in our knowledge of the course of B. burgdorferi infection and its clinical manifestations. The classic tick-borne dermatoses erythema chronicum migrans (ECM), lymphadenosis benigna cutis (LABC) and acrodermatitis chronica atrophicans (ACA) were proven by isolation of the spirochete from skin lesions to be caused by B. burgdorferi infection. In early disease (less than 1 year) ECM and LABC can develop locally at the site of infection (stage I), but both these skin manifestations can also occur together with multiple lesions after dissemination of the causative organism (stage II). ACA is typical for late infection (greater than 1 year, stage III). High titres of B. burgdorferi antibodies have been found in patients with localized sclerodermalike lesions (circumscribed scleroderma, lichen sclerosus et atrophicus, anetoderma), and frequent simultaneous occurrence of ACA suggests an association with late B. burgdorferi infection. Similarly, we found four cases of cutaneous B-cell lymphoma possibly arising from LABC in association with the same markers of late B. burgdorferi infection. Additionally, some cases of Schönlein-Henoch purpura and of Shulman syndrome may be associated with Lyme borreliosis. The disease is endemic in central Europe, and almost exclusively ticks of the Ixodes ricinus complex seem to transmit B. burgdorferi to humans, whereas the reservoir of infection seem to be rodents, especially mice. The main diagnostic tool is serological examination for B. burgdorferi antibodies, which will become detectable 3-6 weeks after infection. Enzyme-linked immunosorbent assay (ELISA) and the indirect immunofluorescence test (IFT) revealed similar sensitivity. In early disease, sensitivity for antibody detection could be improved by immunoblot technique and by flagellum-ELISA, which is specific for this early sensitizing B. burgdorferi antigen. For treatments, penicillin is no longer recommended as the drug of first choice, because low sensitivity of B. burgdorferi has been observed in vitro and in vivo. Tetracycline, doxycycline and amoxicillin p.o. are now preferred for the treatment of Lyme borreliosis, and in neurologic and cardiac abnormalities ceftriaxone i.v. is recommended. Treatment duration should be 14 days in early disease and 30 days in late disease.

Acrodermatitis↗
PubMed1991

[Borrelia infections from a dermatological viewpoint].

Erythema migrans (EM), Borrelia lymphocytoma (BL) and acrodermatitis chronica atrophicans (ACA) are the established dermatological manifestations of borrelia infection, a complex multiorganic disease. Analogous to syphilis Borrelia infection can be classified by three stages, at which stage I (localized infection) and II (disseminated infection) are manifestations of early infection and stage III (persistent infection) a symptom of late infection. At all stages skin manifestations can be present, the above mentioned as stage-marker as well as other non-specific polymorphous skin lesions which sometimes appear at stage II. Because of its frequent (60-80%) occurrence in all borrelia infections EM has a pathognomonic importance for borrelia infection. In diagnosis serology is currently the only practical laboratory aid. False negative and false positive results must be considered. Treatment of choice is ceftriaxone, penicillin G (or amoxycillin) or tetracycline. Prophylactic antibiotic therapy for tick bites is not recommended. Congenital borrelia infections seem to be unusual, but it is likely that they can occur and cause different adverse fetal outcome or abortion.

Acrodermatitis↗
PubMed1990

[Cutaneous manifestations of infection due to hepatitis B virus].

Two entities can precede the clinical and biological signs of hepatitis B virus (HBV) infection: the various lesions of the serum sickness-like prodrome (urticaria, maculopapular exanthem, purpura, etc.) induced by the deposition of intravascular circulating immune complexes and papular acrodermatitis of childhood in which the physiopathological role of HBV has not yet been established. The persistence of HBs antigen (HBs Ag) may give rise to the purpuric lesions of essential mixed cryoglobulinemia and to the livedo, the nodules and ulcerations of poly-arteritis nodosa.

Acrodermatitis↗
PubMed1990

[Hand dermatoses in children].

Dermatoses of the hand in children are part of an original entity which can be classified in two groups: a group involving exclusively the hands and another one which is predominantly involving the hands. Attention has been focussed mostly on hand dermatoses in children (acropustulosis of infancy, papular, acrodermatitis, hand foot and mouth disease, subungual, exostosis). We discuss also the diagnostic and therapeutic aspects of scabies in children.

Acrodermatitis↗
PubMed1990

[Serodiagnosis in dermatological diseases in Borrelia burgdorferi infections].

185 patients with dermatological symptoms of Borrelia burgdorferi infection (erythema migrans, lymphadenosis cutis benigna, acrodermatitis chronica atrophicans) and morphea were examined for Borrelia burgdorferi antibodies; in addition, sera from 173 patients were tested for exclusion of Borrelia infection. Commercially available immunofluorescence tests and enzyme immunoassays supplied by four different companies were evaluated. To investigate the specificity of these assays, sera of 34 patients with syphilis in different stages and sera from 98 control persons were examined. None of the assays evaluated was suitable for the diagnosis of early infection (sensitivity 4-35%). However, they are more reliable for the diagnosis of late infection (sensitivity 56-100%). The variation in specificity between the different assays was 82-100%. Crossreactions with Borrelia burgdorferi antibodies occurred frequently in patients with syphilis (3-47%). The reliability of serological assays should be improved by antigen purification and combination of screening and confirmatory assays. After treatment the decline in IgG and IgM antibodies is very slow.

Acrodermatitis↗
PubMed1989

[Lyme disease and Borrelia burgdorferi infections in Europe].

Lyme disease is endemic in Europe. The strains of the causative agent, Borrelia burgdorferi, seem to be antigenically more heterogeneous than the North American isolates. The only documented vector for this bacterium in Europe is ixodes ricinus, but other vectors might be involved as observed in the United States. The tick hosts are not yet well documented in Europe. Human infection occurs principally during summer months. The clinical aspect of the disease has particular features in Europe: at the early stage of the disease, a single and large erythema chronicum migrans is observed on the skin; complications often include meningoradiculonevritis (Bannwarth's syndrome) and later, acrodermatitis chronica atrophians; arthritis is less frequent in Europe than in the USA. The culture of B. burgdorferi from the lesions is difficult. The diagnosis of the disease is performed on the basis of serological tests: immunofluorescence assay where the important thing is to define a cutoff titer; ELISA tests using either whole cells or supernatant of sonicated cells or flagellar antigen; passive haemagglutination for IgG; IgM solid phase haemadsorption; Western blot (immunoblot) seems interesting to perform on a research basis to determine to which protein antigens patients are responding with antibody. Once antibody production begins, it is usually in the form of IgM antibody to flagellin protein (41 kD), with time, both IgM and IgG antibodies to a variety of other antigens appear. Prophylaxis is based on health services and public education because a prompt removal of the tick diminishes risk of infection with B. burgdorferi (4 p. cent of cases after tick bite). The treatment includes aminopenicillins or tetracyclines at the early stage. The second and third stages of borreliosis are treated by high doses aminopenicillins or cetriaxone.

Acrodermatitis↗
PubMed1989

[Serodiagnosis of Lyme borreliosis: antibody titer and specificity in the IFT and western blot].

Out of 334 sera from healthy persons from northern Bavaria 6% reacted positive in the indirect immunofluorescence test (IFT, titre greater than or equal to 1:64). The percentage of positive cases in patients with erythema chronicum migrans (ECM), meningoradiculitis (M. Bannwarth), or acrodermatitis chronica atrophicans (ACA) was 43, 83 and 78%, respectively. In other patients with less characteristic symptoms in which an infection with B. burgdorferi was suspected the number of positive cases was only about 20%. A positive IgM-IFT was most often associated with ECM and M. Bannwarth; however, even in these cases IgM was only found in 30%. The serodiagnosis of Lyme disease required simultaneous serum testing of T. pallidum antibodies (TPHA) to exclude a syphilis with cross-reacting antibodies. In cases with a positive B. burgdorferi-IFT and TPHA the final diagnosis of Lyme disease was possible on the basis of Western blot analysis. The prominent antigens detected by sera from patients with Lyme disease--but not with syphilis--had molecular weights of 18, 22, 41 and 60 K; IgM antibodies were mainly directed against the 22 K and 41 K antigens. The antigen pattern was not characteristic for different disease stages.

Acrodermatitis↗