[The Internet: its usefulness in dermatology].
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Biomedical subjects
Publications and source records attributed to D Lipsker.
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A 76-year-old patient developed cutaneous vasculitis on the lower legs on the 8th day of treatment with the selective cox-2-inhibitor celecoxib (Celebrex((R))) and the proton-pump inhibitor omeprazole. The patient had no history of allergic reactions. The patient had already been treated previously with omeprazole without any side effects. A cutaneous biopsy confirmed the diagnosis of leucocytoclastic vasculitis. The purpuric skin lesions regressed within 3 weeks after withdrawing the two newly introduced drugs. We discuss the potential role of Celecoxib in triggering this vasculitis.
BACKGROUND: The long-term prognosis of patients treated for erythema migrans has only rarely been assessed. OBJECTIVES: To evaluate the clinical characteristics and long-term prognosis of patients treated for erythema migrans in the region of Alsace, France. METHODS: In a prospective study, 56 consecutive patients presenting with erythema migrans at the Strasbourg University Hospital between 1995 and 1999 were examined and a Borrelia burgdorferi enzyme immunoassay was performed. Patients were treated with tetracyclines or amoxycillin. Patients were re-examined 6 weeks later and a telephone interview was performed in summer 2000 to evaluate the long-term outcome. RESULTS: There were 25 women and 31 men of mean age 49 years presenting with single (n = 54) or multiple (n = 2) erythema migrans lesions. At the time of diagnosis, 30% of the patients had systemic signs, myalgias or arthralgias and only 36% of 50 patients were seroreactive against B. burgdorferi. None of the 51 patients evaluated at 6 weeks and none of the 37 patients interviewed after a median delay of 3 years had developed complications attributable to Lyme borreliosis. CONCLUSIONS: The prognosis of patients treated for Lyme borreliosis in this part of France is excellent. Therefore, a complete clinical examination is sufficient as an initial evaluation and long-term follow-up is not necessary.
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INTRODUCTION: In Europe, Borrelia burgdorferi sensu stricto, Borrelia afzelii and Borrelia garinii are known as pathogens among the Borrelia burgdorferi sensu lato group. Since it is not yet known which Borrelia are responsible for Lyme borreliosis in France, the objective of this study was to identify the species of Borrelia responsible for erythema migrans in the region of Alsace, France. PATIENTS AND METHODS: Eighteen patients with erythema migrans (EM) of more than 5 cm of diameter were included in this prospective study. All patients were investigated at the Strasbourg University Hospital. Patients were biopsied on the active border of their lesion. Cutaneous biopsies of the active border of the lesion were cultivated in BSK-H medium (Sigma) and analysed in vitro by PCR after 8 weeks of culture, using flagellin consensus sequences which are present in all species of Borrelia burgdorferi sensu lato group as primers. Species-specific oligotyping was used for species identification. RESULTS: Among the 18 patients biopsied, 7 had evidence of borrelia infection revealed by culture and/or PCR. Borrelia afzelii was detected in 4 patients and Borrelia garinii in three. CONCLUSION: These preliminary results appear to confirm that Borrelia afzelii and Borrelia garinii are the predominant borrelial species in EM lesions in our geographic area, as in other European countries.
INTRODUCTION: We report 2 patients who developed pentamidine-induced rhabdomyolysis during treatment of leishmaniasis. This potentially harmful side effect of pentamidine has only been reported exceptionally until now. CASE REPORTS: In January 2001, we treated 2 patients, aged 31 and 38 years, with 600 mg pentamidine administered intramuscularly twice in 48 hours. The two patients developed rhabdomyolysis with elevated CPK (respectively 30-70-x normal) and myoglobinemia (respectively 20-28-x normal) levels. Outcome was good under hyperhydratation and alkaline diuresis. DISCUSSION: This underestimated side effect of pentamidine treatment is not mentioned in recent articles on the topic. In case of such treatment however, these biological parameters should be monitored in order to establish the real frequency of this side-effect.
INTRODUCTION: We report a case of symmetric lipomatosis in an unusual palmary topography. CASE REPORT: A 56 year-old woman was referred for evaluation of scleroderma. The diagnosis was made 10 years earlier because of acrosclerosis of the distal phalanges of both hands. The disease began 2 months after administration of systemic steroids for severe asthma. Since then, she was followed up for her scleroderma every 2 years without any evidence of systematization of the disease. On examination, the first phalanges appeared protruding and podgy on the palms of both hands. On palpation, the consistence was suggestive of lipomas. Similar nodules were present on the back of both hands at the proximal part of the interdigital spaces. Tomodensitometry confirmed the lipomatous nature of nodules. DISCUSSION: This patient presented with a symmetric lipomatosis of a very unusual distal localization on both hands. This unusual aspect mimicked acrosclerosis. In this case report, chronology suggests that systemic steroids might have induced this lipohypertrophy.
Since very little is known about the clinical expression of Lyme borreliosis in Western Europe, a 3-year prospective study was conducted that included all patients seen for suspected Lyme borreliosis at the Strasbourg University Hospital in northeastern France. The diagnosis of Lyme borreliosis was made on the basis of the presence of erythema migrans or on the basis of another suggestive clinical manifestation and laboratory confirmation. A total of 132 patients, 70 women and 62 men, mean age 54 years, had Lyme borreliosis according to these criteria. Within this study group, 77% of the patients were regularly exposed to tick bites and 64% could remember one. Erythema migrans, the most frequent clinical manifestation, occurred in 60% of the patients and was the only sign of Lyme borreliosis in 40%. Lymphocytoma and acrodermatitis chronica atrophicans were rare (1 and 3 patients, respectively). Nervous system involvement (mainly radiculoneuropathy), the second most common clinical manifestation, was found in 40% of the patients and was the only sign of Lyme borreliosis in 22%. Musculoskeletal involvement was present in 26% of the patients and was an isolated finding in 14%. During the study period, no patient was diagnosed with Lyme carditis. There was serological evidence of Lyme borreliosis in 75% of the cases and direct evidence of borrelial infection in 10 (7.5%). The results show that the clinical expression of Lyme borreliosis in northeastern France is similar to that in other European countries but different from that in North America.
In this work, we studied the localization and traffic of CD1a molecules in human epidermal Langerhans cells and the ability of these cells to stimulate CD1a-restricted T cell clones. We found that CD1a was spontaneously internalized into freshly isolated Langerhans cells, where it was rapidly distributed to the early/sorting endosomes and then to the early/recycling endosomes. In the latter compartments, CD1a colocalized with Rab11, a small GTPase known to be involved in the recycling of transmembrane proteins from early endosomes to the cell surface. In the steady state, intracellular CD1a was mainly located in Rab11+ recycling endosomal compartments. When endocytosis was blocked, intracellular CD1a moved rapidly from the early/recycling endosomes to the cell surface where it accumulated. The resultant increase in the cell surface expression of CD1a enhanced the capacity of Langerhans cells to stimulate a CD1a-restricted T cell clone. These findings are consistent with a dynamic exchange of CD1a between recycling compartments and the plasma membrane and suggest that the antigen-presenting function of CD1a depends on its traffic through the early/recycling endosomal pathway.
The Schnitzler syndrome is characterized by a chronic urticarial eruption with a monoclonal IgM gammopathy. The other signs of the syndrome include intermittent elevated fever, joint and/or bone pain with radiologic evidence of osteosclerosis, palpable lymph nodes, enlarged liver and/or spleen, elevated erythrocyte sedimentation rate, and leukocytosis. The mean delay to diagnosis is more than 5 years, and this syndrome is of concern to internists and many medical specialists. Patients with this syndrome are often initially considered to have lymphoma or adult-onset Still disease, which are the main differential diagnoses. However, hypocomplementic urticarial vasculitis, systemic lupus erythematosus, cryoglobulinemia, acquired C1 inhibitor deficiency, hyper IgD syndrome, chronic infantile neurologic cutaneous and articular (CINCA) syndrome, and Muckle-Wells syndrome should also be excluded, because diagnosis relies on a combination of clinical and biologic signs and there is no specific marker of the disease. The disease pursues a chronic course, and no remissions have yet been reported. Disabling skin rash, fever, and musculoskeletal involvement are the most frequent complications. Severe anemia of chronic disease is another serious complication. The most harmful complication, however, is evolution to an authentic lymphoplasmacytic malignancy, which occurs in at least 15% of patients. This hematologic transformation can occur more than 20 years after the first signs of the disease, thus patients deserve long-term follow-up. Treatment is symptomatic and unsatisfactory. The skin rash is unresponsive to treatment, and nonsteroidal antiinflammatory drugs, antihistamines, dapsone, colchicine, and psoralens and ultraviolet A (PUVA) therapy give inconstant results. Fever, arthralgia, and bone pain often respond to nonsteroidal antiinflammatory drugs. In some patients, these symptoms and/or the presence of severe inflammatory anemia require steroids and/or immunosuppressive treatment, which ameliorate inflammatory symptoms but do not change the course of the skin rash.
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BACKGROUND: The definition of the "subcutaneous cellular tissue" is still debated. METHODS: In order to establish the localisation and composition of this tissue, or, merely its existence, we interviewed French dermatologists and conducted a bibliographic study on the historical definitions of the so-called "subcutaneous cellular tissue". A questionnaire was sent to French professors of dermatology to assess their definition of the "subcutaneous cellular tissue". They were also asked to make a simple cartoon showing the anatomy of the skin and "subcutaneous cellular tissue". RESULTS: We obtained 37 answers which could be classified in three main categories: 1) "subcutaneous cellular tissue" and hypodermis are synonymous, 2) "subcutaneous cellular tissue" is an autonomous tissue which separates the hypodermis from the tissues below and 3) "subcutaneous cellular tissue" designates all structures located below the hypodermis. In an historic perspective, the "cellular system" was a macroscopic concept described in the eighteenth century as whitish fibrils delimitating "cells". It was renamed loose connective tissue in the twentieth century and thus "cellular" became obsolete. The definition of skin, and of "subcutaneous cellular tissue" in particular, has greatly changed over time. In the eighteenth century, only epidermis and dermis were considered as belonging to the skin, although some included the tela subcutanea. In the twentieth century, the "subcutaneous cellular tissue" is considered either as a part of the hypodermis, or as the hypodermis itself or as a tissue located between the hypodermis and the fascia. DISCUSSION: The difficulty in defining "subcutaneous cellular tissue" is the result of a French semantic problem. The "cellular tissue" became loose connective tissue. For French dermatologists, the skin is composed of epidermis, dermis and hypodermis and the hypodermis can therefore not be subcutaneous. In order to check whether an autonomous tissue could be evidenced under the skin, we conducted an histologic study, which is presented in a second article.
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E. Grosshans and L. Marot first described blaschkitis in 1990 as a linear inflammatory dermatitis following lines of Blaschko in an adult patient. We report another case which occurred in a 38-year-old woman who developed an extensive, linear, erythematosquamous dermatitis involving the face, all limbs and the trunk. The patient's serum tested positive for antinuclear antibodies at a dilution of 1:640. The lesions regressed spontaneously within 4 weeks. Blaschkitis is a distinct entity which corresponds neither to a known inflammatory dermatitis in the lines of Blaschko nor to an hamartoma nor to an X-linked disease. Cutaneous antigenic mosaicism, the expression of which might be induced by a viral infection, could trigger this localized inflammatory T-cell response. This hypothesis relates blaschkitis to other cutaneous autoimmune diseases, as does the presence of antinuclear antibodies. We therefore suggest renaming this type of inflammatory dermatitis Grosshans-Marot disease in honour to the dermatologists who first described the entity.
The Schnitzler syndrome is the association of chronic urticaria, intermittent fever, osteosclerotic bone lesions and a monoclonal IgM gammopathy. It is not yet firmly established whether the monoclonal immunoglobulin component plays a part in the pathophysiology of the urticarial lesions. Immunoblotting on epidermal and dermal human skin extracts as well as immunoelectron microscopic (IEM) studies on Lowicryl K4M-embedded skin sections were performed in three patients with the Schnitzler syndrome. Western blotting on epidermal extracts showed the presence of IgM-kappa antiskin autoantibodies in two patients. These antibodies displayed the same isotype as the monoclonal components and recognized a 280-290-kDa antigen in one patient and a 200-kDa antigen in the other patient. IEM studies showed sparse IgM deposits in the epidermis, around the keratinocytes, near the desmosomes in one patient and dense deposits below the lamina densa, in the region of the anchoring fibrils, in another patient. Antiskin IgM autoantibodies of the same isotype as their monoclonal gammopathies can be present in the serum of some patients with the Schnitzler syndrome. These IgM antibodies seem to deposit in vivo in the epidermis and at the dermal-epidermal junction, in the region of the anchoring fibrils. These findings suggest that the monoclonal gammopathy plays a part in the pathophysiology of the skin rash. They also suggest patient heterogeneity both in the skin antigens that are recognized as well as in their localization.