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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↗

PubMed1988

Borrelia burgdorferi in the nervous system: the new "great imitator".

There are many obvious similarities between Lyme disease and syphilis. The major ones are their spirochetal etiology, the ability of the spirochetes to stay alive in human tissue for years, occurrence of clinical manifestations in stages, early disease in the skin and later disease in the brain, and susceptibility to antibiotic treatment. Thus, one can assume that many of the same lessons learned from the centuries of experience with syphilis will apply to Lyme disease. One of these lessons that should be constantly borne in mind is that spirochetal disease of the brain can mimic many other neurological diseases. Thus, the "effective clinician" must take special care to consider Lyme disease primarily because of the excellent response to antibiotics early in its course in relationship to some of the diseases it mimics. Lyme meningitis, occurring in the "second stage" of the disease, usually is fairly easily recognized because it occurs in the summer or early fall, often is associated with ECM or a recent history of it, and has a characteristic clinical picture of lymphocytic meningoradiculoneuritis. Many patients with Lyme meningitis or ECM have very mild symptoms, and it is likely that a large percentage of patients go undiagnosed and untreated. The frequency of progression of these patients to third-stage disease is unknown but may be quite high. This can be inferred from a similar situation in the other major late manifestation of Lyme disease: Lyme arthritis. A large number of patients present with joint involvement as their only manifestation of Lyme disease. Similarly, patients may present with symptoms of third-stage Lyme disease affecting the CNS, but they may not be recognized because of the lack of earlier stages usually associated with the disease. Thus, serology has become a very important tool for identifying patients exposed to B. burgdorferi. At the present time, serologic tests are the key to diagnosis of Lyme disease in its later stages, since, as in neurosyphilis, cultures and tests for antigen have not proven useful. Lyme arthritis and acrodermatitis atrophicans (ACA) both are associated with quite high antibody titers to the organism, while the test is understandably unreliable for identification of patients with ECM. Antibody titers in Lyme meningoradiculoneuritis are generally positive but often are not as high as those in ACA or arthritis. The antibody response in serum in CNS Lyme disease seems to be related to the presence of other manifestations; patients who have had both arthritis and CNS disease have quite high titers, while those with only CNS disease sometimes do not.(ABSTRACT TRUNCATED AT 400 WORDS)

Borrelia Infections↗

PubMed1989

[Articular involvement in Swiss patients with a Borrelia burgdorferi infection--report of 8 cases].

Eight cases of Lyme's arthritis are reported. In four of them, they are related to an erythema chronicum migrans, in two to an acrodermatitis atrophicans. In two cases, there was no cutaneous manifestation, but the serology was strongly positive for Borrelia burgdorferi, and there was rapid relief of the pain with antibiotic therapy. It is suggested that Lyme's arthritis is not rare in Switzerland and that it must be searched for in every case of arthritis of unknown etiology, especially when there is a history of cutaneous involvement. The arthritis is cured by antibiotics.

Adolescent↗

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↗

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↗

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↗

PubMed1997

A two year prospective study to compare culture and polymerase chain reaction amplification for the detection and diagnosis of Lyme borreliosis.

AIM: To compare polymerase chain reaction (PCR) amplification of borrelial DNA and culture isolation of spirochaetes for the diagnosis of Lyme borreliosis by direct detection of Borrelia burgdorferi sensu lato in patients with erythema migrans and acrodermatitis chronica atrophicans lesions. METHODS: Skin biopsy specimens from erythema migrans and acrodermatitis chronica atrophicans lesions were subdivided and tested by PCR amplification assay and culture using two artificial growth media, Barbour-Stoenner-Kelly II (BSK II) and modified Kelly-Pettenkofer (MKP). Five classes of lesions were studied: typical erythema migrans, spontaneously resolved erythema migrans, atypical/partially treated erythema migrans, typical acrodermatitis chronica atrophicans, and atypical/partially treated acrodermatitis chronica atrophicans. RESULTS: For both erythema migrans and acrodermatitis chronica atrophicans lesions, the most sensitive detection method was MKP culture. PCR was less sensitive than MKP culture, but more sensitive than BSK II culture. Results for 758 typical erythema migrans specimens showed positivity rates of 36% for MKP, 25% for PCR, and 24% for BSK II. Differences were statistically significant. The overall positivity rate for all three methods combined was 54%, but few specimens (6%) were positive by all three methods. Examination of multiple erythema migrans lesions from the same patient increased the diagnostic yield. These findings, and similar results for acrodermatitis chronica atrophicans lesions, suggest that the distribution of spirochaetes in skin biopsies is not homogeneous. CONCLUSIONS: Although possessing the potential to provide a rapid diagnosis, PCR is not more sensitive than culture for the direct detection of borrelia. Spirochaetes appear to be unevenly distributed throughout biopsy specimens, suggesting that diagnosis of Lyme borreliosis by direct detection of the causative agent in skin lesions in vulnerable to sample bias.

Acrodermatitis↗

PubMed1991

Borrelia burgdorferi-associated cutaneous B cell lymphoma: clinical and immunohistologic characterization of four cases.

Four patients with low-grade malignant B cell lymphoma of the skin in association with chronic Borrelia burgdorferi infection are presented. Plaque-shaped or nodular erythematous lesions with ill-defined borders were seen. Clinical progression was slow; the skin tumors occurred for up to 7 to 15 years. Extracutaneous involvement was found in only one case. Immunohistologic investigations showed an expression of B cell markers with restriction to only one light chain type and absence of T cell antigens. The growth fraction was 5% to 30%, as shown with the monoclonal antibody Ki-67. The immunoarchitecture of the tumors in three patients was unusual compared with established criteria for cutaneous B cell lymphoma and revealed similarities to mucosa-associated B cell lymphoma. Some immunohistologic heterogeneity may indicate the development of monoclonal proliferation that originated from different phases of B lymphocytic differentiation. In three cases no clinical signs of B. burgdorferi infection were found; in one patient acrodermatitis chronica atrophicans was present. The occurrence of acrodermatitis chronica atrophicans and malignant lymphomas was frequently reported in the European literature before B. burgdorferi was recognized. These findings suggest a relation between B. burgdorferi infection and cutaneous B cell lymphoma. In geographic regions where infected ticks are present, borreliosis should be considered in patients with cutaneous B cell lymphoma.

Aged↗

PubMed1988

[Thrombocytopenic purpura caused by Borrelia burgdorferi?].

In November 1983 a woman born in 1902 was found to have thrombocytopenic purpura with a platelet count of 14,000/microliter. Examination of the sternal marrow resulted in a suspected diagnosis of Werlhof's disease. Platelet counts dropped at times to below 7,000/microliter during immunosuppressive treatment with corticosteroids and azathioprine of three months' duration. When this treatment was discontinued spontaneous remission occurred until July 1984. Acrodermatitis chronica atrophicans was diagnosed in August 1987. The IgG antibody titre against Borrelia burgdorferi of 1:2,000 in whole blood and the late manifestation of Lyme disease (chronic acrodermatitis atrophicans) suggest a causal relationship with the previous thrombocytopenic purpura.

Administration, Oral↗

PubMedDate not supplied

Polymerase chain reaction control of antibiotic treatment in dermatoborreliosis.

Assessment of the efficacy of an antibiotic drug used in patients with various manifestations of dermatoborreliosis is crucial. Clinical judgement alone (resolution of the present dermatologic lesion, prevention of later major or minor sequelae) is not sufficient in erythema migrans and acrodermatitis chronica atrophicans. Thus, laboratory tests are desirable to prove the benefit of an antimicrobial agent. It was intended to establish a constant parameter--besides the clinical picture--for assessing the efficacy of antibiotic treatment in patients with dermatoborreliosis in terms of eradication of Borrelia burgdorferi from the site of infection. Polymerase chain reaction (PCR) was therefore performed from pretreatment biopsy specimens from lesional skin of 36 erythema migrans patients (m:f = 15:21, mean age 49 years) and seven acrodermatitis chronica atrophicans patients (m:f = 0:7, mean age 59 years), respectively. After antibiotic therapy with minocycline (100 mg, orally twice daily, 14 days) for erythema migrans, and ceftriaxone (2 g, intravenously once daily, 14 days) for acrodermatitis chronica atrophicans another punch biopsy was obtained and analysed by PCR. In pretreatment specimens, B. burgdorferi-specific DNA was amplified by PCR in 23/36 erythema migrans patients (69%), and in 5/7 acrodermatitis chronica atrophicans patients (71%). After antibiotic therapy, PCR yielded negative results in all of these cases. Clinically, all patients showed complete recovery or at least marked improvement of lesions at this time. PCR appears to be a reliable parameter for the assessment of the efficacy of antibiotic treatment in dermatoborreliosis.

Acrodermatitis↗

PubMedDate not supplied

Cutaneous manifestations of Lyme borreliosis.

The dermatological symptoms of Lyme borreliosis present with a typical clinical pattern and characteristic time of appearance. In contrast to other manifestations of Lyme borreliosis they are easily recognizable in most of the cases. In the first stage, erythema migrans arises at the tick bite site. With this symptom the diagnosis of Lyme borreliosis can be established. During all manifestations of Lyme borreliosis the history of erythema migrans is an important parameter to verify the diagnosis. In the early stage of disease a lymphocytic proliferation can appear at the tick bite site, at the ear lobe, or at the mamilla. Borrelia lymphocytoma can be diagnosed when antibodies against Borrelia burgdorferi are positive. Years after infection, acrodermatitis chronica atrophicans arises at distal body sites causing livid swelling and gradually skin atrophy. Skin lesions can be accompanied by neuropathies, mostly of the lower legs, which in contrast to the skin lesions, do not respond well to antibiotic therapy. There is evidence that some cases of Shulman syndrome, morphea and lichen sclerosus et atrophicus might be related to a borrelia infection as indicated by cultivation of B. burgdorferi from skin biopsies of morphea and response to antibiotic treatment in some cases. The classical dermatological symptoms of Lyme borreliosis, erythema migrans, borrelia lymphocytoma and acrodermatitis chronica atrophicans respond to oral antibiotic treatment. In acrodermatitis chronica atrophicans parenteral antibiotic therapy is sometimes necessary.

Acrodermatitis↗

PubMed1994

No association with HLA class II alleles in Swedish patients with cutaneous manifestations of Lyme borreliosis.

The possibility of an association between manifestations of Lyme borreliosis and HLA class II alleles has been investigated with varying results. In the present study, we used genomic typing techniques to determine the DR, DQ and DP allele frequencies in 29 patients with erythema migrans and 36 patients with acrodermatitis chronica atrophicans. We did not find a significant deviation from controls in the distribution of the HLA class II alleles in any of these disease manifestations, nor in the subgroup of 8 patients with acrodermatitis chronica atrophicans and long-standing arthritis. With the additional information obtained by the typing techniques used, our results are thus in accord with those studies where no association between the development of the late disease manifestation acrodermatitis chronica atrophicans and HLA class II alleles has been found.

Acrodermatitis↗

PubMed1995

Polymerase chain reaction for detection of Borrelia burgdorferi DNA in skin lesions of early and late Lyme borreliosis.

The aim of this study was to evaluate the polymerase chain reaction (PCR) as a diagnostic tool for Lyme borreliosis on large numbers of samples from clinically well-defined cases of early and late cutaneous borreliosis. Skin biopsy specimens from patients with erythema migrans and acrodermatitis chronica atrophicans were analysed blindly together with an equal number of control biopsies. Using two different dilutions of each DNA specimen increased the number of total positives detected. All of the 76 control biopsies were PCR negative. Biopsy specimens from 18 of 26 (69%) erythema migrans lesions and from 22 of 36 (61%) acrodermatitis chronica atrophicans lesions were PCR positive. Fourteen post-therapy biopsies from patients with acrodermatitis chronica atrophicans were all negative, supporting the opinion that antibiotic therapy is successful in this chronic manifestation of Lyme borreliosis.

Acrodermatitis↗

PubMed2007

Course of Borrelia burgdorferi DNA shedding in urine after treatment.

Diagnosis of Lyme borreliosis by urine polymerase chain reaction (PCR) has been recognized as having better diagnostic sensitivity in patients with erythema migrans than serological methods. We made serial tests with 192 urine specimens from 70 patients with erythema migrans and 60 urine specimens from 21 patients with acrodermatitis chronica atrophicans to evaluate the course of positive urine PCR after antibiotic treatment. Before treatment, urine samples from patients with erythema migrans showed a positive PCR in 27/34 samples (79%), and those from patients with acrodermatitis chronica atrophicans in 7/11 (63%). The specificity of bands was proven by hybridization with GEN-ETI-KTM-DEIA kit in 40/41 samples. Borrelia DNA in urine decreased gradually within the observation period of one year in both patients with erythema migrans and acrodermatitis chronica atrophicans, and persisted without clinical symptoms in 4/45 patients with erythema migrans (8%) after 12 months. Urine PCR can serve as a diagnostic method in early Lyme borreliosis and also in seropositive patients with unclear clinical symptoms.

Adolescent↗

PubMed1995

No evidence for Borrelia burgdorferi-specific DNA in lesions of localized scleroderma.

A possible association of Borrelia burgdorferi with localized scleroderma is currently the focus of intense research and discussion. Skin biopsies from 30 patients with localized scleroderma (28 of the plaque type/morphea; two linear scleroderma) were analyzed for the presence of Borrelia burgdorferi using three different polymerase chain reaction systems for amplification of segments of borrelial genes. Formalin-fixed, paraffin-embedded biopsies of 14 patients and fresh-frozen, cryo-conserved biopsies of 16 patients with localized scleroderma were obtained. Lesions of all patients showed clear signs of scleroderma and disease progression at the time of biopsy. Fresh-frozen as well as formalin-fixed biopsies from patients with erythema migrans or acrodermatitis chronica atrophicans were used as positive controls. With all three polymerase chain reaction systems, borrelial DNA was detected in none of the 30 specimens of localized scleroderma. In contrast, with one polymerase chain reaction system, Borrelia burgdorferi-specific DNA was found in 24 of 27 frozen biopsies from patients with erythema migrans and in all 5 analyzed frozen biopsies of patients with acrodermatitis chronica atrophicans. In approximately half of the paraffin-embedded biopsies from patients with erythema migrans (nine of 23) and acrodermatitis chronica atrophicans (13 of 27), Borrelia burgdorferi-specific DNA was identified. These results question the association of localized scleroderma with known subtypes of Borrelia burgdorferi.

Acrodermatitis↗

PubMedDate not supplied

Dermatological manifestations of Lyme borreliosis.

Lyme borreliosis is a multisystem infectious disease caused by the tick-transmitted spirochete Borrelia burgdorferi sensu lato. About 80% of all Lyme borreliosis cases represent skin manifestations (dermatoborrelioses). The three characteristic dermatoborrelioses are erythema migrans, borrelial lymphocytoma, and acrodermatitis chronica atrophicans, which occur in different stages of the disease. Erythema migrans is the hallmark of early Lyme borreliosis, whereas acrodermatitis chronica atrophicans is the characteristic manifestation of late Lyme borreliosis. Several spirochetal factors (e.g. infection with different genospecies, co-infection with other tick-transmitted pathogens) as well as host factors (e.g. cytokine patterns at the site of infection) influence the course of the disease. Diagnosis in the early stage of Lyme borreliosis relies on the clinical picture, whereas serological, molecular, microbiological, and histopathological findings are important adjuncts in the diagnosis of later stages of the infection. Antibiotic treatment is necessary for all stages and manifestations of Lyme borreliosis. Doxycycline is the antibiotic of choice for most patients with dermatoborrelioses.

Animals↗

PubMed1991

Diagnosis of Lyme disease based on dermatologic manifestations.

Lyme disease, or Lyme borreliosis, is an infection caused by the spirochete Borrelia burgdorferi, which is most commonly transmitted to humans by a tick bite. Characterized by early and late phases, Lyme disease is a multisystem illness involving the skin, heart, joints, and nervous system. Diagnosis is based predominantly on clinical manifestations, the most specific being dermatologic. Thus, recognizing the dermatologic manifestations of Lyme disease is important for diagnosis and institution of appropriate, effective therapy. Approximately 75% of patients with Lyme disease present with the pathognomonic skin lesion erythema migrans, an expanding erythematous lesion. During early infection, secondary erythema migrans lesions or Borrelia lymphocytoma may occur. Borrelia lymphocytoma commonly presents as an erythematous nodule on the ear lobe or nipple. During late infection, acrodermatitis chronica atrophicans, an erythematous, atrophic plaque unique to Lyme disease may appear; it has been described in about 10% of patients with Lyme disease in Europe. Fibrotic nodules associated with acrodermatitis chronica atrophicans as well as other sclerotic and atrophic lesions, such as morphea, lichen sclerosus et atrophicus, anetoderma, and atrophoderma of Pasini and Pierini, have been seen late in the course of Lyme disease. In a few cases, other sclerodermatous lesions, such as eosinophilic fasciitis and progressive facial hemiatrophy, have been linked to B. burgdorferi infection. We review the cutaneous lesions associated with Lyme disease.

Acrodermatitis↗

PubMed1998

Analysis of antibody response to the outer surface protein family in lyme borreliosis patients.

Studies on frequencies of serum antibodies to outer surface proteins (Osps) in Lyme disease have produced conflicting results. Osp antigens (A, B, and C) enriched by butanol extraction, which aids band identification in immunoblotting, were used to test sera for IgG antibody to Osp antigens from Borrelia burgdorferi isolates from each subspecies (sensu stricto, afzelii, and garinii). Individual isolates were selected to include all five known European OspA genotypes. Of arthritis sera, 83% (n=29), and of acrodermatitis chronica atrophicans sera, 81% (n=26), recognized OspA, B, and/or C. Of erythema migrans sera, 23% recognized OspA and/or B and a further 15% OspC alone. Only 5 (6%) of 86 sera (4 arthritis, 1 acrodermatitis chronica atrophicans, 0 erythema migrans) recognized all five OspA phenotypes tested. Marked differences in the reactions of individual sera to the various Osp antigens were seen, which helps reveal the causes of discrepancies between previous reports.

Acrodermatitis↗