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[Lyme borreliosis: review of present knowledge].

The author reviews hitherto assembled knowledge on a bacterial disease, Lyme borreliosis transmitted by ticks. Initial information on Lyme borreliosis appeared at the beginning of the 20th century. In Czechoslovakia attention to the disease was paid since cca 1960. The infection occurs as a rule in the summer months during the period when ticks are parasitic and at that time the causal agent of the disease is transmitted to hosts. Information on the prevalence and incidence of Lyme borreliosis in Europe is not complete and so far we do not possess a standardized diagnostic method for assessment of circulating antibodies in the patients' serum and cerebrospinal fluid. The infectious disease is caused by the gram-negative spirochete Borrelia burgdorferi. The Borrelia cell has a similar morphological structure as cells of other gram-negative bacteria. Chemical analysis of the external membrane of B. burgdorferi revealed the presence of 46% proteins, 51% lipids and 3% carbohydrates. The typical shape of borrelias indicates marked ondulation of 8-14 periplasmatic flagellae along the cell body. Borrelias can be cultivated in vitro in modified Barbour-Stoenner-Kelly medium at an optimal temperature of 30-37 degrees C. The change of morphology during cultivation is typical for B. burgdorferi. Clinically Lyme borreliosis is manifested in two stages. A typical manifestation of the early stage is a skin lesion--erythema migrans. The later stage is characterized above all by relapsing arthritis, CNS infection and chronic acrodermatitis chronica atrophicans. The disease is treated by administration of a number of antibiotics either by the oral route or by injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

[Diagnosis and therapy of Lyme arthritis].

Several distinct patterns of rheumatic manifestations can be seen throughout the course of Lyme borreliosis: intermittent and migratory musculoskeletal pain without objective findings, intermittent arthritis, chronic erosive arthritis, and joint deformities under affected skin in acrodermatitis chronica atrophicans. Commonly, Lyme arthritis is a late disease manifestation. A clinical history of extra-articular disease manifestations is the most reliable key to Lyme arthritis. However, arthritis often occurs without antecedent early-disease manifestations. The diagnostic significance of serological findings suggesting Lyme arthritis must be considered carefully with regard to the typical clinical features of Lyme arthritis and its potential differential diagnoses. Otherwise, Lyme arthritis will be frequently over-diagnosed. Lyme arthritis can be cured with antibiotics. However, treatment failures occur with any of the hitherto recommended regimens.

Anti-Bacterial Agents↗

[The clinical and serological manifestations of Lyme disease in Russia].

Out of 86 Lyme's disease patients with a history of migrating erythema nervous system, cardiovascular and articular involvement was observed in 27, 6 and 43% of cases. Acrodermatitis was diagnosed in 2% of patients. Affection of locomotor system manifested with acute arthritis episodes or pains in major joints. 11 patients of 12 examined at arthritis onset showed elevated titer of anti-Borrelia IgG antibodies. Serologically, of 80 patients with arthritis or arthralgia without prior migrating erythema 6 demonstrated antibodies to 5 and more Borrelia polypeptides.

Adolescent↗

[Essential trace element and skin diseases].

We have described herein various skin diseases which are caused by essential trace element deposition, deficiency, allergy, etc. Pigmentation of hemochromatosis and hemosiderosis are recognized by hemosiderin deposition in the dermis. Acrodermatitis enteropathica is caused by a deficiency of Zn and is classified as either a hereditary type or as an acquired type. The former is autosomal recessive and the latter is caused by a low intake of Zn. Wilson's disease and Menkes' kinky hair syndrome, which are caused by abnormal Cu metabolism, elicit hyperpigmentation and morphological changes of the hair, respectively. It appears that kinky hair formation results from low activity of sulfhydryl oxidase which is a Cu enzyme. Bowen disease, which is carcinoma in situ, is caused by As toxicosis. Some cases, such as palmo-plantar-pustulosis, lichen planus and oral lichen planus are caused by allergies to metals used in dental surgery, especially Ni, Co, Cr and Sn.

Bowen's Disease↗

[Frequency of the clinical manifestations of Lyme borreliosis in Spain].

INTRODUCTION: There are differences in the clinical manifestations of Lyme borreliosis (LB) in different parts of the world. The aim of this work was to analyze its clinical manifestations in Spain. METHODS: We evaluated by ELISA and IFI the sera of 1,500 patients with clinical suspicion of LB between January 1987 to February 1993. Spanish criteria of LB (amplified CDC criteria of LB for epidemiological purpuse) were used. Clinical and serological data were evaluated with the patients' physicians and other etiologies were reasonably excluded in accepted cases of LB. RESULTS: Sixty-four patients of 138 with a positive serology (46%) met the LB criteria. Neurological manifestations were presented by 40 patients (62.5%) (in control group 23%, p < 0.05) cutaneous lesions by 20 patients (31%), articular manifestations by 18 patients (28%) (in control groups 56%; p < 0.05) and cardiac manifestations in two. Cutaneous manifestations included 17 erythema migrans, 2 acrodermatitis chronica atrophicans and 1 lymphocytoma). Artritis was present in 18 cases. Neurological manifestations included 16 cases of meningitis (2 with encephalitis), 11 of craneal neuropathy and 25 of peripheral neuropathy (13 of polyneuropathy). Cardiac manifestations acepted was 2 atrioventricular blockade. We detected 21% of false positive serology and in 33% of the positive cases, the LB criteria was not met. CONCLUSIONS: The low percentage of cutaneous manifestations is probably due to the fact that this series consist predominantly of hospital patients. In Spain, as in the rest Europe the predominant manifestations are neurological, however artritis are not infrequent manifestations.

Adolescent↗

[Post-traumatic psoriatic arthritis. 2 cases].

Physical trauma is generally accepted as a possible factor in the pathogenesis of rheumatoid arthritis. In the last ten years, there have been a few rare case reports of physical trauma precipitating psoriasic arthritis. We observed two such cases following an occupational accident discovered one and a half year and two and a half year after onset of the first clinical manifestations. In the first case, a 43-year-old man had a fracture of the right calcaneus in March 1991. He was treated with nailing and also required emergency surgery of the posterior tibial artery. The tibiotarsal joint was normal radiologically. Pain persisted after treatment and in 1993 he presented with psoriasis of the scalp and several other localizations together with Hallopeau's acrodermatitis continua of the ankle, pathognomonic for psoriasic arthritis. Salazosufapyridin was given. The second case was a 50-year-old man who had major pain in both wrists immediately after falling on the palm of his hands in 1992. Bilateral carpal tunnel syndrome developed which did not respond well to surgery. In 1993, he developed inflammatory synovitis and also had psoriasis mainly located at the elbows. Immunological tests were negative. Cortisone and salazosulfapyridin were not particularly effective and the patient later developed arthritis of the hip and ankle joints. Physicians should be aware of physical trauma as a causative factor in psoriasic arthritis due to the potential legal implications. Criteria for imputability are: single major physical trauma, absence of clinical signs prior to the trauma, continuous clinical course, first signs occurring then predominating at the joint exposed to trauma. The pathophysiology of this type of arthritis is not well understood. Deep Koebner's phenomena could be involved. Activation of substance P has also been hypothesized.

Adult↗

[Necrolytic migrating erythema without glucagonoma].

INTRODUCTION: The glucagonoma syndrome is an uncommon but well-known entity associating erythema necroticans migrans (ENM) with glucagonoma. CASE REPORT: A 43-year-old man with a past history of alcoholic cirrhosis and ascitis was hospitalized for skin disorders which had developed over the past 4 months. Centrifugal erythematous skin lesions were observed, some with non-turgid bullae and marginal desquamation, others with an erosive center. Lesions first appeared on the hands then diffused widely without involving the periorifical areas, folds and lower limbs. Laboratory results revealed an anemia, hypovitaminosis K, cholestatic liver failure, a beta-gamma block and low zinc levels. Histology study of the skin biopsy demonstrated a << Neapolitan trench >> image suggestive of ENM. A paraneoplasic syndrome and pancreas tumor were not found. Despite supplementation with zinc, amino acids and vitamins, the patient died from his liver disease. DISCUSSION: There have been 4 cases of ENM reported in the literature, all in cirrhosis patients, two of which had low zinc levels. Our case is thus the third with cirrhosis and low zinc. Bazex's syndrome, acrodermatitis enteropathica, annular chronic lupus erythematosis and annular superficial pemphigus were eliminated as possible diagnoses. The failure of zinc and amino acid supplementation would favor the secondary nature of the zinc deficiency and the predominant role of cirrhosis in this skin disease. The possible role of essential fatty acids in ENM is raised.

Adult↗

[Musculoskeletal symptoms often incorrectly attributed to Lyme disease].

OBJECTIVE: To establish, in patients referred with persisting noninflammatory musculoskeletal complaints. diagnosed elsewhere with Lyme disease, whether Lyme disease was present. SETTING: Outpatient Clinic for Rheumatology. Eemland Hospital Amersfoort and University Hospital Utrecht, the Netherlands. DESIGN: Descriptive, prospective. METHOD: Patients were classified as having had Lyme disease in the past, having ongoing Lyme disease of no Lyme disease at all, on the basis of clinical history, physical examination, and classification criteria for Lyme disease. RESULTS: In a two-year period 37 consecutive patients (mean age 50 years) were examined, 20 (54%) of whom had (a history of) Lyme disease. Of these 20, two suffered from erythema migrans, one of synovitis of the knee, and one of acrodermatitis chronica atrophicans (these four had not been treated). while one had persistent chronic oligoarthritis. Seventeen patients did not have Lyme disease, but were suffering from aspecific, noninflammatory musculoskeletal problems. CONCLUSION: In this patient group with persisting musculo-skeletal complaints, 'Lyme disease' had been diagnosed correctly as often as incorrectly.

Adolescent↗

Kwashiorkor-like zinc deficiency syndrome in anorexia nervosa.

This report deals with a 26-year-old white woman exhibiting signs of both Kwashiorkor (marasmus, pallor, hypopigmentation of hair and hepatomegaly) and acrodermatitis enteropathica (eczematous dermatitis predominantly on acral areas). Clinical and laboratory examinations excluded malabsorption syndrome and glucagonoma syndrome and revealed hypoproteinemia and marked zinc deficiency. Psychiatric examination disclosed anorexia nervosa. Substitution therapy led to rapid clearing of the skin lesions.

Adult↗

Clioquinol-zinc chelate: a candidate causative agent of subacute myelo-optic neuropathy.

BACKGROUND: 5-chloro-7-iodo-8-hydroxyquinoline (clioquinol) was used clinically three decades ago as an oral antiparasitic agent and to increase intestinal absorption of zinc in patients with acrodermatitis enteropathica, a genetic disorder of zinc absorption. Use of clioquinol was epidemiologically linked to subacute myelo-optic neuropathy (SMON), characterized by peripheral neuropathy and blindness, which affected 10,000 patients in Japan. Discontinuation of oral clioquinol use led to elimination of SMON, however, the mechanism of how clioquinol induces neurotoxicity is unclear. MATERIALS AND METHODS: We tested the effect of clioquinol-metal chelates on neural crest-derived melanoma cells. The effect of clioquinol chelates on cells was further studied by electron microscopy and by a mitochondrial potential-sensitive fluorescent dye. RESULTS: Of the ions tested, only clioquinol-zinc chelate demonstrated cytotoxicity. The cytotoxicity of clioquinol-zinc chelate was extremely rapid, suggesting that its primary effect was on the mitochondria. Electron microscopic analysis demonstrated that clioquinol-zinc chelate caused mitochondrial damage. This finding was further confirmed by the observation that clioquinol-zinc chelate caused a decrease in mitochondrial membrane potential. CONCLUSIONS: We demonstrate that clioquinol, in the presence of zinc, is converted to a potent mitochondrial toxin. The phenomenon of clioquinol mediated toxicity appears to be specific to zinc and is not seen with other metals tested. Since clioquinol has been shown to cause increased systemic absorption of zinc in humans, it is likely that clioquinol-zinc chelate was present in appreciable levels in patients with SMON and may be the ultimate causative toxin of SMON.

Chelating Agents↗

[Lyme borreliosis: therapeutic aspects].

CAUSAL AGENTS: Several Borrelia burgdorferi sensu lato species have been recently described which cause different clinical forms of Lyme disease. B. garinii is implicated in neurological forms, B. burgdorferi sensu stricto in articular forms and B. afzelii in late cutaneous forms. As such disease diversity is seen only in Europe and Asia, clinical management in Europe is somewhat different than in North America. NUMEROUS CLINICAL TRIALS: A recently proposed classification of the European forms of Lyme disease is based on clinical presentation: contagious conditions or erythema migrans, early neurologic or cardiologic complications, late articular, neurologic or cutaneous complications. Therapeutic proposals should be guided by the results of European trials, taking into account this classification. ADAPTED MANAGEMENT: For contagious conditions or erythema migrans, amoxicillin and doxycycline are the first intention antibiotics and should be given for 14 to 21 days. Other antibiotic classes (macrolides, oral cephalosporins) have not been found be more effective and should be reserved for second line treatment. Early neurological involvement requires penicillin, a third generation cephalosporin or doxycycline for one month. Oral antibiotics are preferred in case of joint involvement using amoxicillin or doxycycline as first line therapy. A second regimen could be proposed in case of failure. Parenteral administration should be reserved for second line treatment. There is little data available on chronic atrophic acrodermatitis and protocols are based on ceftriaxone, doxycycline or penicillin.

Amoxicillin↗