Erythema Migrans Borreliosis: An HLA‐associated Disease?

Pflüger, K. H.; Reimers, Carl D.; Neubert, U.; Meisel, Christian; Trapp, Bruce D.; Leititis, J. U.; Völker, B.; Münchhoff, Peter; Litzenberger, J.; Holthausen, Hans; Pongratz, E.

doi:10.1111/j.1749-6632.1988.tb31889.x

Cited by 10 publications

(1 citation statement)

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“…Steere 23 reported that patients with neuroborreliosis or Lyme arthritis had a significantly increased frequency of HLA-DR4 or DR2, although this was not confirmed by others. 24 Pfluger et al 25 reported that the haplotype combination HLA-A2 and HLA-Cw3 is more frequent in patients with EM. The present patient with facial nerve palsy presented with HLA-DR4, but not HLA-A2 or Cw3.…”

Section: Discussionmentioning

confidence: 99%

Lyme disease with facial nerve palsy: rapid diagnosis using a nested polymerase chain reaction–restriction fragment length polymorphism analysis

Hashimoto

Takahashi

Kishiyama

et al. 1998

British Journal of Dermatology

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A 64-year-old woman with Lyme disease and manifesting facial nerve palsy had been bitten by a tick on the left frontal scalp 4 weeks previously. Erythema migrans appeared on the left forehead, accompanied by left facial paralysis. Nested polymerase chain reaction-restriction fragment length polymorphism analysis (nested PCR-RFLP) was performed on DNA extracted from a skin biopsy of the erythema on the left forehead. Borrelia flagellin gene DNA was detected and its RFLP pattern indicated that the organism was B. garinii, Five weeks later, B. garinii was isolated by conventional culture from the erythematous skin lesion, but not from the cerebrospinal fluid. After treatment with ceftriaxone intravenously for 10 days and oral administration of minocycline for 7 days, both the erythema and facial nerve palsy improved significantly. Nested PCR and culture taken after the lesion subsided, using skin samples obtained from a site adjacent to the original biopsy, were both negative. We suggest that nested PCR-RFLP analysis might be useful for the rapid diagnosis of Lyme disease and for evaluating therapy.

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Section: Discussionmentioning

confidence: 99%

Lyme disease with facial nerve palsy: rapid diagnosis using a nested polymerase chain reaction–restriction fragment length polymorphism analysis

Hashimoto

Takahashi

Kishiyama

et al. 1998

British Journal of Dermatology

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Lyme disease in a 74‐year‐old forest owner with symptoms of dermatomyositis

Hoffmann

Stichtenoth²,

Zeidler³

et al. 1995

Arthritis & Rheumatism

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We describe a 73-year-old forest owner with widespread erythema, myalgia, and proximal muscle weakness. The clinical signs and the results of electromyography, magnetic resonance imaging, and a muscle biopsy were consistent with dermatomyositis. However, serology was positive for Borreliu burgdorferi. More importantly, B burgdorferi DNA was detected in skin by polymerase chain reaction techniques, and spirochetelike organisms were detected in the muscle by silver staining. Lyme disease with muscle involvement can mimic or trigger dermatomyositis and should be considered in the differential diagnosis of dermatomyositis.Lyme disease is a multisystem organ disease caused by Borreliu burgdorferi. It primarily affects the skin, joints, nervous system, and heart (I). Although this is uncommon, B burgdorferi has been shown to infiltrate into the muscles, causing a special form of myositis, which is usually localized and is often associated with neurologic symptoms (2-1 1).We report the case of a patient with typical features of dermatomyositis, including recurrent rashes and proximal muscle weakness. Examination of skin and muscle biopsy samples, however, showed invasion by B burgdorferi, spirochete-like organisms, and mononuclear cell infiltrates. To our knowledge, this is the first report of a patient with definite Lyme disease that is clinically almost indistinguishable from dermatomyositis. CASE REPORTThe patient, a 73-year-old white man, was admitted to the Hannover Medical School Hospital because of muscle pain and weakness in his shoulders and thighs, as well as erythematous lesions on his face, hands, and forearms. His symptoms had begun 3 months prior to admission, when he consulted a local dermatologist. He was started on methylprednisolone, 16 mg daily. There had been no improvement in his condition, and he was therefore referred to our institution.On admission, the patient was found to have diffuse pruritic erythema with edema of his hands, induration and partial epidermal atrophy of his forearms, and a pale violaceous heliotrope erythema of his face. In addition, there was marked proximal muscle weakness and atrophy in his shoulders and thighs in a symmetric distribution. On direct questioning, he mentioned several tick bites that had occurred over recent years as he was working in his forest. However, he denied having any symptoms of erythema migrans.The patient's creatine kinase (CK) level was 195 unitsfliter (normal <70) with an MB isoenzyme level of 5.6 unitsfliter, aldolase was 4.6 unitdliter (normal <3), serum glutamic oxaloacetic transaminase (SGOT) was 25 unitdliter, lactic dehydrogenase (LDH) was 416 unitsfliter, IgG was 21.4 gmiliter, IgM was 3.9 g d i t e r , and serum electrophoresis showed 26% gamma globulins and 50% albumin. Antinuclear antibodies were positive at a titer of 1:160. Rheumatoid factor, anti-extractable nuclear antigen, anti-DNA, anti-Scl-70, anti-Jo-l , anti-PL7, anti-PL12, anti-Ku-l , anti-Mi-2, and anti-PM1 were negative.Serum antibodies to B burgdorferi, as determined by in...

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