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Skin ulcers are commonly described in the juvenile form of dermatomyositis; however, in the adult form they are rarely described. We report on a patient with adult dermatomyositis, deep cutaneous ulcers in the skin folds and livedo reticularis eruption.
Skin and serum zinc measurements have been made in patients with leprosy with and without trophic skin ulceration and in several other groups. Serum zinc concentrations were decreased in leprosy irrespective of the presence or absence of skin ulceration. Serum zinc concentrations in leprosy were also unrelated to smears positive for Mycobacterium leprae and to the clinical type of leprosy. Since a decrease of the serum zinc was also found in patients with dermatitis herpetiformis and pulmonary tuberculosis it seems likely that the decreased serum zinc in leprosy is a nonspecific metabolic consequence of chronic skin and internal disease. The mean skin zinc concentration in leprosy did not differ significantly from the corresponding value in control subjects, the lack of agreement between serum and skin concentrations being possibly related to the presence of nonexchangeable keratin-bound zinc in skin. Though the clinical significance of lowered serum zinc concentrations in leprosy is uncertain therapeutic trials of zinc treatment in leprosy with trophic skin ulceration seem justifiable.
Chronic skin ulceration is a common complication of diabetes, peripheral vascular disease, and disorders that decrease mobility. Local ulcer care will be successful only if the underlying cause is correctly identified and steps are taken to reverse it. This article reviews the emergency department assessment and management of the patient with chronic skin ulceration.
Mycobacterium haemophilum has recently been recognized as a newly emerging cause of osteomyelitis in immunocompromised patients. While still uncommon, its incidence has increased significantly with the growing AIDS epidemic. Like its relative M. tuberculosis and M. intracellulare, this organism is acid-fast positive; yet unlike its more well-known counterparts, M. haemophilum requires iron-supplemented culture media and low incubation temperatures (30-32 degrees C) for growth. We describe a case of M. haemophilum osteomyelities in the distal femur of a 36-year-old HIV-positive male, who also presented with multiple skin ulcerations. In an AIDS patient with a lytic bone lesion and concomitant skin eruptions, the diagnosis of M. haemophilum should be entertained so that special culture media can be used and appropriate treatment administered.
This is the case report of a seventy-seven-year-old woman with ulcerated skin vasculitis of the lower extremities that preceded the appearance of myelofibrosis. No previous report of this association has been found in a survey of the literature.
Skin ulceration produced by inadvertently extravasated doxorubicin is characterized by a prolonged course accompanied by severe morbidity, and it has proven to be notoriously difficult to treat. In attempts to identify possible antidotes, 11 different pharmacologic agents were tested using piglets, because their skin is anatomically similar to that of man. Among the agents studied, topical application of DMSO daily for 7 days tended to decrease the maximal diameter and accelerate healing of skin ulcers produced by intradermal doxorubicin. alpha-Tocopherol appeared to worsen the ulceration. None of the 11 agents studied prevented the development of ulcerations completely.
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Skin ulcers on fish are one of the most well-recognized indicators of polluted or otherwise stressed aquatic environments. In recent years, skin ulcer epidemics have been either experimentally or epidemiologically linked to exposure to a number of xenobiotic chemicals as well as to biotoxins. Some of these agents, such as toxins produced by the dinoflagellate alga Pfiesteria, have led to serious concerns about the health of aquatic ecosystems, such as estuaries along the east coast of the United States. However, a number of other risk factors besides Pfiesteria have been shown to damage epithelium and may also play important roles in skin ulcer pathogenesis. In addition, increasing evidence indicates that not only may skin damage occur via direct contact with toxins, but it may also be induced indirectly from physiological changes that result from exposure not only to toxins but also to other environmental stressors, such as pH and temperature extremes. The multifactorial pathways that operate at both the ecological and the organismal levels as well as the nonspecific response of the skin to insults make it very challenging to link epidemic skin ulcers to any single cause in natural aquatic populations. Consequently, using pathology to unequivocally identify the specific cause of a lesion (eg. Pfiesteria exposure) is not a valid approach. Only with an increased understanding of the basic mechanisms leading to skin damage (including development of specific biomarkers for specific toxins), along with a better understanding of ecological processes operating in these environments, will we be able to discern the relative importance of various risk factors in skin ulcer development.
Skin ulcers by Leishmania (Viannia) braziliensis are often deep and irregular and are difficult to measure by just the skin surface transverse and longitudinal diameters. The proposal is to mould the cavity, after local asepsis with fresh water plus soap, with a gelatinous plastic which contains silence, potassium alginate, calcium sulphate, magnesium oxide commercialized under the name of jeltrate (Dentsply Laboratory), by solving 9.5g of jeltrate in 20ml of fresh water and applying the gel on the ulcer which solidifies in 5 minutes. This mould is then filled with a self polymerising acrylic and its volume measured either by weight (by using an analytical balance)-technique 1-or by water displacement by applying Archimeds'principle-technique 2. We show data in a field trial before and after 20 days treatment in 20 patients using three different schedules as follows: 7 received pentamidine isethionate, 7 patients received aminosidine sulphate and 6 received meglumine antimoniate. The results point out that there was a uniform reduction of ulcer volume occurred during this period in the three groups, in both technique. Regarding the therapeutic schedules we are sure that there was a significant statistical difference between the three schedules using the T Student Test, which showed that aminostdine sulphate produced a better volume reduction of the ulcer than the other drugs. Serial moulds reflect clinical billing and are a permanent record. We conclude that the measure of the volume of the skin ulceration can be useful in the therapeutic evaluation, as a practical and cheap procedure, and may be used in field trials.
UNLABELLED: Clinical, physiological and biochemical studies of PGE1 were done in a series of collagen disease patients with skin ulcer, in a foot varix patient with skin ulcer as a non-inflammatory skin ulcer control, and in two diabetics without skin ulcer as no skin ulcer controls. Intravenous infusions of prostaglandin E1 (PGE1) were given continuously at the dose of 1 ng/kg/min for 72 hours. Blood samples were collected from the cubital vein, before, during, immediately after and at seven days after PGE1 therapy. Platelet aggregations were studied by light transmittance (PRP: modified by Born's method; whole blood: modified by Tohjima's method). Platelet iPGE (immunoreactive PGE-like material) levels were assayed by radio-immunoassay. Essential fatty acid compositions of plasma, platelet and red cells, were analysed by gas chromatography. Results were as follows: (1) in all cases, complete healing of skin ulcers was observed; (2) In most cases, skin temperature increased during PGE1 treatment; (3) Platelet aggregation was higher during PGE1 treatment than before and was higher in PRP than in whole blood during PGE1 treatment; (4) The platelet basal iPGE levels were significantly decreased by PGE1 (P less than 0.025); (5) The plasma and platelet linoleic acid levels were significantly higher than before PGE1 treatment (plasma: P less than 0.05, platelets: P less than 0.025); (6) Thrombocytosis of one case of MRA was healed by the second PGE1 treatment. CONCLUSION: The inflammatory skin ulcers in collagen diseases were healed completely by continuous intravenous infusion of PGE1. This effect might be brought about by the suppression of PG metabolism, especially in platelets.
BACKGROUND: THe antimitotic agent paclitaxel is highly active in the therapy of several tumor types, including ovarian and breast cancer. The commercial formulation (Taxol) is supplied in a vehicle containing alcohol and the surfactant Cremophor EL (polyethoxylated castor oil). Whereas Phase I studies did not describe extravasation necrosis, more recent case reports have suggested that paclitaxel can cause soft tissue necrosis if inadvertently extravasated. The efficacy of various antidotal maneuvers, if any, was not known. METHODS: Dehaired, BALB/c mice were given intradermal (ID) injections of paclitaxel 0.3 mg, 0.6 mg, or 1.2 mg, or Cremophor EL, 0.1 mL, into the dorsal skin. The sites were observed thrice weekly for evidence of ulceration. Perpendicular widths of skin ulcers were measured by caliper and multiplied to yield a lesion area in cm2. The lesion area multiplied by time in days was integrated by computer to yield cumulative ulceration areas in (cm2 x days). Potential pharmacologic adjuvants were injected ID after paclitaxel. These included saline (0.05 mL), albumin (0.05 mL), hyaluronidase (15 Units), and hydrocortisone (2.5 mg). Topical adjuvants included dimethylsulfoxide solution, (0.1 mL), cooling to 8-10 degrees C or heating to 43-44 degrees C for 30 minutes after ID paclitaxel. RESULTS: Dose-dependent skin ulcers that lasted 12-17 days were created with the 3 ID paclitaxel doses. The two higher paclitaxel dose levels, 0.6 mg and 1.2 mg, were selected for antidote studies. Hyaluronidase and saline were effective ID antidotes for lesions induced by the 0.6-mg paclitaxel dose, but not for the higher paclitaxel dose of 1.2 mg (P<0.05 by analysis of variance). None of the topical adjuvants or other ID adjuvants significantly reduced paclitaxel-induced skin ulcers in the mice. CONCLUSIONS: Paclitaxel has experimental vesicant potential in the ID mouse skin model. Clinical extravasations of paclitaxel may be treated by subcutaneous injections of hyaluronidase diluted in saline.
OBJECTIVE: To report a case of skin ulceration as a result of treatment with leflunomide for rheumatoid arthritis. CASE SUMMARY: A 78-year-old white woman developed bilateral leg ulcers after 6 months of treatment with leflunomide for rheumatoid arthritis. A history of leg ulcers after methotrexate therapy had been documented. Serologic and diagnostic tests did not support an alternate process. Other medications prescribed were oral ethinyl estradiol 0.05 mg/d, felodipine 5 mg/d, and paroxetine 20 mg/d, for which no documented correlation with the skin breakdown could be made. DISCUSSION: This is the first published case describing a possible relationship between the use of the immunosuppressant agent leflunomide and skin ulceration. CONCLUSIONS: Skin breakdown and ulceration is a recognized adverse effect of drugs with immunosuppressant activity such as methotrexate. Leflunomide, a newer agent prescribed in the treatment of rheumatoid arthritis, may now be listed among the drugs in this category associated with this adverse drug effect.
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Doxorubicin (DOX)-induced skin ulceration in rats and pigs has been reported to be reduced when treated with topical DMSO and/or vitamin E. In the present study using a mouse model, neither intradermal nor topical DMSO with or without vitamin E, administered up to 7 days, reduced intradermal DOX-induced skin ulceration. Intradermal DMSO with or without vitamin E caused skin ulceration and significantly increased DOX-induced ulcerations. Topical DMSO-containing solutions were not toxic to mouse skin. To test for a systemic effect of topical DMSO, two groups of mice received an additional 0.05-mg intradermal injection of DOX above a DMSO-treated lesion. There was no apparent effect of topical DMSO with or without vitamin E on this proximal but untreated DOX lesion. The results suggest either a major difference in DOX ulceration characteristics between rats and pigs on the one hand and mice on the other hand or a lack of significant efficacy for DMSO and vitamin E as DOX extravasation antidotes.
We report the case of a boy with low expression of HLA class I molecules on peripheral blood mononuclear cells, which is associated with immunodeficiency. The patient, who had a Marfan-like phenotype, had chronic deep skin ulcers and sinobronchiectasis. Immunohistologic examination of the ulcerated skin showed a dense perivascular infiltrate composed of normal mature lymphocytes and macrophages. All cells in the infiltrate showed an apparently normal expression of HLA class I molecules, but intraepidermal dendritic Langerhans' cells were negative for CD1a, an antigen that is a highly specific marker for these cells and is abundantly expressed in some self-healing forms of cutaneous lesions. It is therefore speculated that a defective expression of CD1a molecules can contribute to the chronic persistence of deep skin ulcers, which have already been reported in association with defective expression of HLA class I molecules.
Radiation skin ulcer is a common adverse complication after radiotherapy. Currently, there is no efficient therapy for this complication. In this study, we searched for the potential pathological targets of radiation skin ulcer and the potential pharmacological targets of quercetin, respectively, and obtained the potential therapeutic targets after intersection. Subsequently, an array of bioinformatics assessments on possible therapeutic targets was conducted, encompassing functional enrichment studies, analysis of protein interaction networks, identification of key targets, and validation through molecular docking. The enrichment analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways shows that the therapeutic effect of quercetin on radiation skin ulcer may be through targeting aging cells. In addition, we identified 5 core targets, including AKT1, EGFR, MAPK3, SRC, and TP53. They are significantly enriched in EGFR tyrosine kinase inhibitors (SRC, AKT1, EGFR, and MAPK3) and epidermal growth factor receptor signaling pathways (SRC, EGFR, and AKT1), indicating the importance of EGFR signaling. Quercetin may have a therapeutic effect on radiation skin ulcer by targeting aging cells. Specifically, it may act through 4 core targets, including AKT1, EGFR, SRC, and TP53.
BACKGROUND: Skin ulcerations are rarely reported in dermatomyositis of the adult. We report on a case of perforating ulcers resistant to classical treatments in a woman with dermatomyositis. CASE REPORT: A 34 year-old woman, treated for typical dermatomyositis, developed a few weeks after starting her treatment, multiple perforating skin ulcers on her shoulders, elbows and wrists though general signs had completely disappeared. In spite of the increase in oral steroids, the patient presented again with worsened lesions and a new perforating ulcer on the hand which lead to the breaking of a tendon. She underwent hand surgery and was also treated with a bolus of steroids IV (1 g daily during 3 days), followed by oral steroids, IM methotrexate and antimalarial drugs. The lesions healed completely after one month, with no atrophy. DISCUSSION: Skin ulcers are rarely described in dermatomyosites of the adult and are associated with underlying vasculitis and bad prognosis. Our case is remarkable by the absence of vasculitis, a very slow cure requiring aggressive treatment and excellent prognosis after three years of follow-up.
Skin necrosis was produced in 24 male Fischer 344 rats by intradermal injection of 0.5 ml of doxorubicin (Adriamycin) at a concentration of 2 mg/ml. The resulting wounds healed slowly over 6 to 7 weeks with the reduced contraction rate paralleling the prolonged morbidity of doxorubicin ulcers in humans. Electron microscopy showed bizarre rough endoplasmic reticulum, double-walled vacuoles, and swollen mitochondria from 1 through 12 weeks after injury. Myofibroblasts with 60- to 80-A microfilaments with electron-dense bodies, intercellular connections, and prominent microtubules were seen from 4 through 12 weeks after injury. Although the appearance of myofibroblasts was delayed, their structure was normal. The delayed contraction of doxorubicin-induced skin ulcers thus appears due to persistent nonspecific cellular damage at the nuclear level rather than to specific derangement of myofibroblast function.