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PubMed2001

Autoimmune keratolysis in a patient with leukocytoclastic vasculitis: unusual erythema elevatum diutinum with granulomatous pattern.

PURPOSE: Leukocytoclastic vasculitis (LCCV) is an immune complex-mediated, small vessel disease that is clinically characterized by the presence of palpable purpuric lesions, most often in association with rheumatic diseases. Ocular manifestations of LCCV are rare. METHODS: We describe a patient with an unusual granulomatous pattern of erythema elevatum diutinum (EED) associated with autoimmune keratolysis. RESULTS: We studied a 64-year-old man with decreased visual acuity and nodular lesions in both hands. Ocular examination revealed bilateral superior corneal melting with perforation in the left eye and conjunctival thickening in both eyes, in association with a severe inflammatory reaction. Histopathologic examination of the conjunctiva revealed granulomatous vasculitis with neutrophilic infiltrate, giant cells, and fibroblastic proliferation. A punch biopsy taken from his skin showed similar characteristics that suggested EED; however, there were no giant cells. CONCLUSION: To our knowledge, autoimmune keratolysis secondary to cutaneous LCCV (EED) has not been described previously, and there has been no description of granulomatous reaction (in the conjunctiva) in EED.

Autoimmune Diseases↗
PubMed1989

Recurrent erythema multiforme.

In a prospective clinical study of erythema multiforme (EM), we identified 22 subjects who experienced more than 1 episode. These subjects were young, with an average age of 29 years. They had an average number of 12 previous episodes, with each episode lasting 3 weeks. The average interval between episodes was 4.9 months. We counted the number and location of each skin lesion and found that patients had an average of 188 EM skin lesions at the time of their evaluation. We found the isomorphic phenomenon, that is, lesions appearing at sites of skin trauma, in 19 of the 22 study subjects; photodistribution of skin lesions in 15 of the 22, grouping of the lesions over the elbow and knees in 7 of the 22, and nailfold involvement in 7 of the 22. In this study there was compelling evidence for herpes simplex virus association with recurrent EM. All 22 patients had histories of herpes simplex virus infections preceding at least 1 of their previous episodes of EM. Sera from all study subjects had antibodies to HSV detectable by enzyme immunoassay. None, however, had HSV isolated from the throat at the time of the EM or from an EM skin lesion. All 11 patients who were subsequently tested had positive viral cultures for HSV taken from the suspected recurrent herpes lesion. When 8 EM skin biopsies were examined by indirect immunofluorescence with a monoclonal antibody to the type common HSV glycoprotein gB, all had positive staining of keratinocytes. Only one-third of patients with a single episode of EM had a history of possible herpes lesions preceding EM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Isolation of Borrelia burgdorferi sensu lato from blood of children with solitary erythema migrans.

OBJECTIVES: To establish the frequency of isolation of Borrelia burgdorferi sensu lato from blood of children with solitary erythema migrans (EM) in Europe, to determine the strains of the isolated borreliae and to compare the clinical course and the outcome of the disease according to positive and negative blood culture result. METHODS: In the prospective study we included 134 consecutive patients younger than 15 years with solitary EM, referred to our institution in 1996 and 1997. One milliliter of blood was withdrawn before treatment and cultured in modified Kelly-Pettenkofer medium. Isolated borreliae were typed according to LRFP analysis. Patients were treated with either penicillin V or cefuroxime axetil for 14 days. The posttreatment course was surveyed by follow-up visits during 1 year. RESULTS: B. burgdorferi sensu lato was isolated in 12 of 134 (9%) patients. Eleven blood isolates were typed: 10 were found to be B. afzelii and 1 was Borrelia garinii. Comparison of blood culture-positive and -negative patients revealed no differences in pretreatment characteristics or in posttreatment clinical course. However, worsening of local and/or systemic signs and symptoms at the beginning of antibiotic therapy (Jarish-Herxheimer's reaction) was identified more often in the blood culture-positive than in the blood culture-negative group (5 of 12 vs. 17 of 122, respectively; P = 0.0274). CONCLUSIONS: The isolation rate of B. burgdorferi sensu lato from the blood of children with solitary EM was 9%. The majority of the isolates were B. afzelii. Blood culture-positive patients treated with oral antibiotics were not at greater risk for unfavorable course of the disease than patients with negative blood culture result.

Bacteremia↗
PubMed2001

Erythema migrans after ceftriaxone treatment of aseptic meningitis caused by Borrelia burgdorferi.

Erythema migrans is the characteristic exanthem of Lyme disease. The rash initially occurs at the site of inoculation; subsequently satellite lesions can occur. We describe an adolescent girl in whom the rash appeared after the initiation of ceftriaxone therapy for aseptic meningitis. We suggest that the occurrence of rash in this patient was a result of liberated toxin from local bacterial lysis.

Adolescent↗
PubMed1986

Somatostatin analog-induced remission of necrolytic migratory erythema without changes in plasma glucagon concentration.

A 41-year-old woman with metastatic glucagonoma and the characteristic disabling rash, necrolytic migratory erythema, was treated with a synthetic somatostatin analog while waiting to undergo curative surgical resection. Plasma glucagon concentration (1,500-3,300 pg/ml, normal less than 200) remained elevated during analog therapy as the rash cleared. Only with surgical resection (partial pancreatectomy and partial hepatectomy) did glucagon levels return to normal. The therapeutic benefit caused by the analog in this syndrome differs from that in other endocrine tumor syndromes such as pancreatic cholera, carcinoid, or gastrinoma where circulating levels of tumor-produced agents are suppressed in conjunction with control of symptoms.

Adult↗
PubMedDate not supplied

Recurrent herpes simplex virus infections and erythema multiforme: a report of three patients.

The widespread preoccupation of the media and patients with herpes prompts this report of two patients who developed erythema multiforme, an allergic response to the herpes simplex virus. While this complication is not new, physicians and nurses working in clinics for sexually transmitted diseases should be aware of this allergic response to infection with herpes simplex virus.

Adult↗
PubMed1978

Erythema multiforme and the Stevens-Johnson syndrome.

Erythema multiforme (EM) is clinically characterized by a "minor" form and a "major" form. The latter is known as the Stevens-Johnson syndrome. Infections (particularly herpes simplex and Mycoplasma pneumoniae) and drugs seem to predispose toward the development of EM. The pathogenesis is poorly understood. The treatment is supportive. Prognosis varies with the severity of the eruption. Recurrences are commonly seen.

Diagnosis, Differential↗
PubMed1986

Erythema multiforme due to herpes simplex: treatment with oral acyclovir.

We have reported a case of severe erythema multiforme caused by outbreaks of recurrent HSV-2 infection. The EM was debilitating and responded to the treatment of HSV with oral acyclovir. On stopping the oral acyclovir, the HSV and the EM both recurred. We recommend a trial of oral acyclovir in cases of severe EM caused by recurrent HSV.

Acyclovir↗
PubMed2005

Erythema elevatum diutinum in the setting of connective tissue disease and chronic bacterial infection.

Erythema elevatum diutinum (EED) is a rare and chronic cutaneous leukocytoclastic vasculitis. It is predominantly seen on the extensor surfaces of the extremities. Although a specific cause is largely unknown, EED has been noted to occur in association with a wide variety of diseases. A 28-year-old man with systemic lupus erythematosus (SLE) and a 53-year-old woman with an overlap syndrome of rheumatoid arthritis and polymyositis are presented. Both patients developed EED in the setting of chronic recurrent bacterial infections. Patients with a connective tissue disease are at increased risk for such infections secondary to immunosuppression, either from the disease itself or secondary to immunosuppressive therapy. EED has been independently reported to occur in the setting of connective tissue disease as well as in the setting of chronic infection. Our patients had both of these underlying conditions, which are known to predispose patients to immune complex-mediated vasculitides, in this case EED. One patient's EED responded to treatment of the SLE and the other improved, as has been previously reported with dapsone.

Adult↗
PubMed2003

Improved serodiagnosis of erythema migrans using novel recombinant borrelial BBK32 antigens.

The performances of recombinant borrelial BBK32 proteins as antigens in the serology of erythema migrans (EM) were evaluated in an ELISA. Serum samples were obtained from 75 patients from different geographic areas where three borrelial species, Borrelia burgdorferi sensu stricto, Borrelia afzelii or Borrelia garinii, cause Lyme borreliosis. Antibodies to variant BBK32 proteins were compared with anti-flagella or with anti-IR(6) peptide antibodies. In IgG ELISA at presentation of EM, 65/75 (87 %) patients had antibodies to one or more variants of BBK32, 29/75 (39 %) had antibodies to flagella and 29/75 (39 %) had antibodies to the VlsE IR(6) peptide antigen. The immunoreactivity against variant BBK32 proteins differed in patients from different geographic regions. The present results suggest that the BBK32 proteins used in combination or in parallel may improve the laboratory diagnosis of EM.

Adult↗
PubMed1985

The relationship of skin color, UVB-induced erythema, and melanogenesis.

The relationship between skin color, delayed erythema, and delayed tanning (DT) elicited by a single exposure of UVB was investigated. Both constitutive and facultative pigmentation were determined by skin reflectance using a melanometer. Skin reflectance using visible light was well correlated to the minimal immediate pigment darkening dose elicited by UVA irradiation, which may relate to epidermal melanin content, a determinant of skin color. Minimal erythemal dose (MED) was well correlated to skin color, but there was less correlation between minimal melanogenic dose and skin color or the MED, since melanogenesis is controlled by genetic factors. DT also correlated to the dose of UVB in terms of MED. A coefficient of the regression line of DT may suggest the tanning capacity of skin. The possibility of detecting mild photosensitivity in individuals from a regression line of the MED on skin color is suggested.

Erythema↗
PubMed1989

Detection of herpes simplex virus DNA in cutaneous lesions of erythema multiforme.

The association between erythema multiforme (EM) and herpes simplex virus (HSV) infection has long been appreciated, although the exact role which HSV may play in the pathogenesis of this herpes-associated EM (HAEM), is unknown. Previous studies have suggested, but not definitively demonstrated, the presence of HSV in lesions of HAEM. The presence of HSV would support the hypothesis that an immune-mediated response directed against HSV-specific antigens in the skin is central to lesion development in HAEM. The purpose of this study was to examine lesions of EM for the presence of HSV DNA by using the polymerase chain reaction (PCR). In addition, in situ hybridization using an HSV-specific RNA probe was performed to further localize the HSV nucleic acids within the skin. DNA was extracted from formalin-fixed, paraffin-embedded specimens of cutaneous lesions of HAEM and also from EM for which no precipitating factor could be documented, otherwise known as idiopathic EM (IPEM). DNA from lesions of bullous pemphigoid served as a negative control. Using PCR to specifically amplify HSV sequences which might be present, and then performing Southern analysis, we demonstrated HSV DNA in 9/13 HAEM and 6/9 IPEM biopsies. No HSV was detected in six lesions of bullous pemphigoid. In situ hybridization of three cutaneous HAEM lesions using an 35S-labeled HSV-specific RNA probe localized the HSV nucleic acids predominantly to the epidermis. Three biopsies of chronic dermatitis, used as negative controls, did not demonstrate this specific hybridization. These findings confirm the presence of HSV in lesions of HAEM and are consistent with the concept of an HSV-specific immune-mediated pathogenesis for this disease. In addition, most cases of IPEM appear to be herpes associated despite the absence of clinically apparent HSV infection.

DNA, Viral↗
PubMed1997

Expression of herpes simplex virus DNA fragments located in epidermal keratinocytes and germinative cells is associated with the development of erythema multiforme lesions.

Skin from acute and healed herpes simplex virus or herpes simplex virus-associated erythema multiforme (HAEM) lesions was examined by polymerase chain reaction with primers for DNA polymerase, ICP8, thymidine kinase (5' end of herpes simplex virus genome), and ICP27 (3' end of herpes simplex virus genome). The primers were herpes simplex virus specific and equally sensitive. The four herpes simplex virus genes were seen in acute herpes simplex virus lesions, but except for one patient, only polymerase (or polymerase and ICP8) were seen in 7-d healed lesional skin. Herpes simplex virus DNA was not seen 1-1.5 mo after healing. HAEM skins from 18 of 24 patients (75%) were positive for polymerase DNA and four of 24 (17%) were also positive for ICP8 or thymidine kinase DNA. Only one tissue (4%) was positive for polymerase, ICP8, and ICP27 DNA. Skin from healed HAEM lesions was still polymerase DNA positive 1-3 mo after lesion resolution. The polymerase DNA signal was in the basal and spinous cell layers of the epidermis and in the outer root sheath of the hair follicle. Polymerase RNA was identified by reverse transcriptase polymerase chain reaction in skin from acute, but not healed polymerase DNA positive HAEM lesions, suggesting that polymerase expression is associated with HAEM lesion development.

DNA Fragmentation↗
PubMed1996

Autoantibodies against desmoplakin I and II define a subset of patients with erythema multiforme major.

In a previous report, we described autoantibodies against the desmosomal plaque proteins desmoplakin I and II (dp I and II) in patients with erythema multiforme (EM) major. In the present study we investigated ten EM major and eight EM minor patients for circulating autoantibodies and performed clinical and immunomorphological evaluations. Seven out of ten EM major patients revealed anti-dp I and II autoantibodies. Antigens were biochemically characterized by Western blotting and immunoprecipitation of epithelial-cell-derived protein extracts. These autoantibodies bind in vivo to lesional skin/mucosa in a pemphigus-type dotted pattern along the cytoplasmic membranes of keratinocytes. Ultrastructural immunolocalization studies confine in vivo bound autoantibodies to the cytoplasmic desmosomal plaque. Autoantibody binding studies with the sera of such patients demonstrate that the target antigens are not restricted to squamous epithelia but are also expressed in simple and transitional epithelia, on hepatocytes, and on cells of mesenchymal origin, e.g., myocardial cells. Comparing the clinicopathological features of ten patients with EM major, we could not define any discriminating clinical symptoms among patients with or without autoantibodies. Histopathological examination, however, revealed that only patients with EM major and autoantibodies against dp I and II show suprabasal acantholysis in lesional skin and mucous membranes, suggesting a potential role of the humoral immune response in the pathogenesis of this disease. These findings suggest that these autoantibodies define a subset of patients within the clinical spectrum of EM.

Adult↗
PubMed1986

IgM and IgG antibodies to phenolic glycolipid I from Mycobacterium leprae in leprosy: insight into patient monitoring, erythema nodosum leprosum, and bacillary persistence.

Serum IgM and IgG antibodies against Mycobacterium leprae-derived phenolic glycolipid I (PG) were determined in leprosy patients, contacts, and controls by enzyme-linked immunosorbent assay (ELISA). Anti-PG IgM levels increased from the tuberculoid (TT) to the lepromatous (LL) pole of the disease spectrum. There was a positive linear correlation between anti-PG IgM and bacillary index (BI). Patients with erythema nodosum leprosum (ENL) had lower levels of serum anti-PG IgM than non-ENL patients of comparable BI, suggesting that anti-PG IgM is involved in the pathogenesis of ENL. Initial observations indicate that high anti-PG IgM levels in bacillary-negative patients might reflect bacillary persistence. A study of 2 different substrate reagents in the ELISA [2,2'-azino-di(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), 0.1 mM H2O2, serum diluted 1:20, and o-phenylenediamine (OPD), 5 mM H2O2, serum diluted 1:300] showed generally good correlation in detection of anti-PG IgM. However the OPD system detected more paucibacillary disease (BT), while the ABTS system detected the significant effect of ENL on the relationship between BI and anti-PG IgM. Anti-PG IgM was clearly dominant over anti-PG IgG. However, certain patients, including several patients who had upgraded from LL and borderline lepromatous leprosy (BL), showed high levels of anti-PG IgG. Since studies have shown that LL patients are selectively deficient in cell-mediated immunity, T-cell products may be required for the IgM to IgG isotype switch. We conclude that anti-PG IgM is useful for monitoring the bacillary load in individual patients and should prove useful for leprosy control strategies.

Antibodies, Bacterial↗
PubMed1991

The expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in experimental cutaneous inflammation: a comparison of ultraviolet B erythema and delayed hypersensitivity.

Endothelial cell adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-regulated cell surface molecules involved in leukocyte adhesion. We have studied two forms of cutaneous inflammation to investigate in vivo the kinetics of adhesion molecule expression in relation to tissue accumulation of leukocytes. Immunohistology was performed on skin biopsies taken from human volunteers at 1, 6, 24, 72 h, and 1 week after two minimal erythema doses (MED) of ultraviolet B (UV-B) or intra-cutaneous tuberculin-purified protein derivative (PPD) (10-100 U). ELAM-1 expression on vascular endothelium and polymorphonuclear leukocyte infiltration were first observed at 6 h and maximal at 24 h after both UV-B and PPD. At 72 h and 1 week, however, endothelial ELAM-1 was more strongly expressed in PPD biopsies. VCAM-1 was minimally expressed in control skin, and was induced above background levels on endothelium, on some perivascular cells, and on stellate-shaped cells in the upper dermis at 24 h after injection of PPD; it was maintained up to 1 week. In contrast, no induction of VCAM-1 was seen following challenge with either 2 or 8 MED UV-B. Following PPD, but not UV-B, there was marked induction of ICAM-1 expression on basal keratinocytes. In these biopsies, the inflammation induced in response to PPD therefore differed from UV-B-induced inflammation in showing prolonged expression of endothelial ELAM-1, induction of VCAM-1 on endothelium and other cells, and induction of keratinocyte ICAM-1. These differences may result from differences in the cytokines released and may in turn be responsible for the differences in the nature of the leukocytic infiltration during the two types of inflammatory response.

Cell Adhesion↗
PubMed1988

Urinary excretion of 5-S-cysteinyldopa in relation to skin type, UVB-induced erythema, and melanocyte proliferation in human skin.

5-S-Cysteinyldopa (5-S-CD) is found in all pigment-producing cells and is the major precursor of phaeomelanin. However, the melanocyte specificity of the compound has been questioned. In order to elucidate the origin of 5-S-CD, we have now systematically studied the relationship between the 5-S-CD excretion in urine and the size of the melanocyte organ, UV-induced melanocyte proliferation, skin type, and the erythemal reaction. The skin type had no influence on the basal excretion of 5-S-CD. There was no significant correlation between the basal 5-S-CD excretion and the size of the melanocyte organ; that is, the number of skin melanocytes and nevi. During the irradiation, subjects with skin type II developed a more pronounced erythema (p less than 0.01) and had a significantly higher 5-S-CD excretion than those with skin type III-IV (p less than 0.01). No correlation was found between 5-S-CD excretion and UV-induced melanocyte proliferation. The lack of correlation between the basal 5-S-CD excretion and skin type or number of melanocytes suggests that the basal 5-S-CD in urine is mainly of extra-melanocytic origin. Our findings favor the view that the increase in 5-S-CD excretion during UV irradiation is due to UV damage.

Adult↗