Invasive squamous-cell carcinoma and arsenical keratoses.

A 42-year-old man presented with a six-month history of a slowly-enlarging ulcer on his right sole, a 30-year history of altered pigmentation of the trunk and extremities, and hyperkeratotic papules of the palms and soles. Histopathologic examination showed an invasive squamous-cell carcinoma of the right sole and hyperkeratosis with keratinocyte atypia of the left finger and left lateral foot. The clinical and histopathologic findings are consistent with chronic arsenicism, which most commonly occurs in the setting of drinking contaminated water or after occupational exposure. Evaluation should include a physical examination, basic laboratory work-up, and measurement of a 24-hour urine arsenic concentration. Vigilant surveillance for the development of cutaneous malignancies is required. Oral retinoids may be helpful in reducing hyperkeratosis secondary to chronic arsenicism.

Influência da heparina sódica na ocorrência de laminite eqüina induzida por sobrecarga de carboidratos / Influence of heparin in occurrence of carbohydrate overload-induced equine laminitis

Avaliou-se a eficiência da infusão intravenosa de heparina sódica (100UI/kg/8h, a partir de 24h após o fornecimento de carboidrato, até completar 48h) no controle da laminite eqüina experimentalmente induzida por sobrecarga de carboidrato (17,6g de amido de milho/kg de peso corpóreo). Foram utilizados 15 eqüinos adultos, distribuídos em três grupos experimentais: GI (grupo-controle); GII (grupo laminite) e GIII (grupo laminite+heparina). Posteriormente ao fornecimento de carboidrato, os animais foram submetidos a exames físicos e laboratoriais durante um período de 48 horas. Ao final do experimento, os animais foram submetidos à eutanásia pela aplicação intravenosa de 5ml de maleato de acepromazina seguida de 1g de tiopental sódico e 1 litro de solução saturada de KCl para a obtenção de amostras de tecidos dos cascos, necessárias ao exame histológico. Os animais de GII e GIII, submetidos à sobrecarga de carboidratos, desenvolveram laminite, exibindo claudicação 12 e 24h após o fornecimento de carboidrato, respectivamente, bem como aumentos da freqüência cardíaca e do tempo de preenchimento capilar. As alterações histológicas, semelhantes em GII e GIII, eram do tipo degenerativo, como adelgaçamento de lâminas epidérmicas, retração, achatamento e deslocamento de lâminas dérmicas, vacuolização epidérmica e desorganização do tecido epidérmico. A infusão da heparina sódica não preveniu ou atenuou a degeneração laminar.(AU)

The efficacy of intravenous heparin administration (100UI/kg/8h, from 24 to 48h after carbohydrate administration) in the control of carbohydrate overload-induced equine laminitis (17.6g of corn starch/kg live weight) was evaluated. Fifteen horses were allocated into three experimental groups: GI (control group), GII (laminitis group), and GIII (laminitis+heparin group). These animals were submitted to physical and laboratorial examination during 48h. After that time, they were euthanized with intravenous administration of 5ml of acepromazine followed by 1g of thiopental sodium and 1 liter of saturated solution of KCl to obtain hoof tissues samples for histological examination. GII and GIII horses developed laminitis, showing lameness 12 and 24h after carbohydrate administration, respectively, as well increased heart rate and capillary refill time. The histological alterations, similar in GII and GIII, were degenerative lesions, as thinness of epidermal lamina, retraction, flattening and dislocation of the dermal lamina, epidermal vacuolization, and disruption of the epidermal tissues. The occurrence of laminar degeneration was not prevented or attenuated with intravenous heparin administration.(AU)

Influência da heparina sódica na ocorrência de laminite eqüina induzida por sobrecarga de carboidratos / Influence of heparin in occurrence of carbohydrate overload-induced equine laminitis

Avaliou-se a eficiência da infusão intravenosa de heparina sódica (100UI/kg/8h, a partir de 24h após o fornecimento de carboidrato, até completar 48h) no controle da laminite eqüina experimentalmente induzida por sobrecarga de carboidrato (17,6g de amido de milho/kg de peso corpóreo). Foram utilizados 15 eqüinos adultos, distribuídos em três grupos experimentais: GI (grupo-controle); GII (grupo laminite) e GIII (grupo laminite+heparina). Posteriormente ao fornecimento de carboidrato, os animais foram submetidos a exames físicos e laboratoriais durante um período de 48 horas. Ao final do experimento, os animais foram submetidos à eutanásia pela aplicação intravenosa de 5ml de maleato de acepromazina seguida de 1g de tiopental sódico e 1 litro de solução saturada de KCl para a obtenção de amostras de tecidos dos cascos, necessárias ao exame histológico. Os animais de GII e GIII, submetidos à sobrecarga de carboidratos, desenvolveram laminite, exibindo claudicação 12 e 24h após o fornecimento de carboidrato, respectivamente, bem como aumentos da freqüência cardíaca e do tempo de preenchimento capilar. As alterações histológicas, semelhantes em GII e GIII, eram do tipo degenerativo, como adelgaçamento de lâminas epidérmicas, retração, achatamento e deslocamento de lâminas dérmicas, vacuolização epidérmica e desorganização do tecido epidérmico. A infusão da heparina sódica não preveniu ou atenuou a degeneração laminar.

The efficacy of intravenous heparin administration (100UI/kg/8h, from 24 to 48h after carbohydrate administration) in the control of carbohydrate overload-induced equine laminitis (17.6g of corn starch/kg live weight) was evaluated. Fifteen horses were allocated into three experimental groups: GI (control group), GII (laminitis group), and GIII (laminitis+heparin group). These animals were submitted to physical and laboratorial examination during 48h. After that time, they were euthanized with intravenous administration of 5ml of acepromazine followed by 1g of thiopental sodium and 1 liter of saturated solution of KCl to obtain hoof tissues samples for histological examination. GII and GIII horses developed laminitis, showing lameness 12 and 24h after carbohydrate administration, respectively, as well increased heart rate and capillary refill time. The histological alterations, similar in GII and GIII, were degenerative lesions, as thinness of epidermal lamina, retraction, flattening and dislocation of the dermal lamina, epidermal vacuolization, and disruption of the epidermal tissues. The occurrence of laminar degeneration was not prevented or attenuated with intravenous heparin administration.

Anti-inflammatory effects of low-level laser therapy (LLLT) with two different red wavelengths (660 nm and 684 nm) in carrageenan-induced rat paw edema.

It has been suggested that low-level laser therapy (LLLT) can modulate inflammatory processes. The aim of this experiment was to investigate what effects red laser irradiation with two different wavelengths (660 nm and 684 nm) on carrageenan-induced rat paw edema and histology. Thirty two male Wistar rats were randomly divided into four groups. One group received a sterile saline injection, while inflammation was induced by a sub-plantar injection of carrageenan (1 mg/paw) in the three other groups. After 1 h, LLLT was administered to the paw in two of the carrageenan-injected groups. Continuous wave 660 nm and 684 nm red lasers respectively with mean optical outputs of 30 mW and doses of 7.5 J/cm(2) were used. The 660 nm and 684 nm laser groups developed significantly (p<0.01) less edema (0.58 ml [SE+/-0.17] ml and 0.76 ml [SE+/-0.10] respectively) than the control group (1.67 ml [SE+/-0.19]) at 4h after injections. Similarly, both laser groups showed a significantly lower number of inflammatory cells in the muscular and conjunctive sub-plantar tissues than the control group. We conclude that both 660 nm and 684 nm red wavelengths of LLLT are effective in reducing edema formation and inflammatory cell migration when a dose of 7.5 J/cm(2) is used.

In vivo study of the anti-inflammatory effect of Rhus toxicodendron.

BACKGROUND: Homeopathic Rhus toxicodendron (Rhus tox) is used in various inflammatory conditions. We screened its effect compared to succussed ethanol controls and appropriate active controls. METHOD: We initially experimented with Rhus tox 6, 12, 30 and 200 cH, using carrageenan-induced paw oedema in rats. The 6 cH dilution appeared most effective and was used in subsequent assays. We used pre-treatment and single treatment regimes in Wistar rats, and mice. RESULTS: We found significant reductions compared to control in carrageenan-induced paw oedema, vascular permeability, writhing induced by intraperitoneal acetic acid and stress induced gastric lesions. CONCLUSIONS: Rhus tox in homeopathic dilution appears to interfere with inflammatory processes involving histamine, prostaglandins and other inflammatory mediators.

Anti-inflammatory effect of bioflora probiotic administered orally or subcutaneously with live or dead bacteria.

The anti-inflammatory effect of Bioflora probiotic administered orally or subcutaneously with viable or nonviable bacteria was analyzed in two experimental models of randomly selected female Wistar rats. The use of indomethacin at a dose of 50 mg/kg was associated with gastric necrotic lesions and multiple erosions of the small intestine, with marked mucosal neutrophil infiltrate measured by myeloperoxidase (MPO). Probiotics prevented both gastrointestinal lesions and neutrophil infiltrate (p < 0.001). In the model of carrageenin-induced plantar edema in the rat, the oral or subcutaneous administration of Bioflora with live or dead bacteria proved to prevent plantar edema (p < 0.001). We concluded that Bioflora probiotic given orally or subcutaneously with live or dead bacteria has an anti-inflammatory effect.

Relevance of tumour necrosis factor-alpha for the inflammatory and nociceptive responses evoked by carrageenan in the mouse paw.

1. The present study evaluated the participation of tumour necrosis factor-alpha (TNF-alpha) in the inflammatory and nociceptive responses evoked by carrageenan in the mouse paw. 2. The intraplantar injection of carrageenan (300 microg paw-1) induced a marked and biphasic paw oedema formation (peaks at 6 and 72 h), which was accompanied by a long-lasting mechanical allodynia (that remained elevated for up to 72 h) and a significant increase of myeloperoxidase (MPO) activity (peak at 6 h) in both Swiss and C57/BL6 mice. 3. The paw oedema, the elevation of MPO activity and to a lesser extent the mechanical allodynia elicited by carrageenan were found to be significantly reduced in TNF-alpha p55 receptor knockout mice. 4. Of interest, the systemic administration of an anti-TNF-alpha antibody produced a significant inhibition of paw oedema, mechanical allodynia and MPO activity. A noteworthy decrease in inflammatory and nociceptive responses caused by carrageenan was also observed when mice were previously treated with the preferential inhibitor of TNF-alpha synthesis, thalidomide. 5. The present results clearly indicate that the proinflammatory cytokine TNF-alpha plays a critical role in the oedema formation, as well as in the mechanical allodynia and the neutrophil migration, following carrageenan administration into the mouse paw. Intraplantar injection of carrageenan in mice could constitute a useful model for assessment of the in vivo effects of potential inhibitors of TNF-alpha-related pathways.

Anti-inflammatory activity of Arnica montana 6cH: preclinical study in animals.

The anti-inflammatory effect of Arnica montana 6cH was evaluated using acute and chronic inflammation models. In the acute, model, carrageenin-induced rat paw oedema, the group treated with Arnica montana 6cH showed 30% inhibition compared to control (P < 0.05). Treatment with Arnica 6cH, 30 min prior to carrageenin, did not produce any inhibition of the inflammatory process. In the chronic model, Nystatin-induced oedema, the group treated 3 days previously with Arnica montana 6cH had reduced inflammation 6 h after the inflammatory agent was applied (P < 0.05). When treatment was given 6 h after Nystatin treatment, there was no significant inhibitory effect. In a model based on histamine-induced increase of vascular permeability, pretreatment with Arnica montana 6cH blocked the action of histamine in increasing vascular permeability.

Action of Causticum in inflammatory models.

The anti-inflammatory effect of Causticum was evaluated using acute and chronic inflammatory models in vivo. The administration of concentrated Causticum solution into the hind paw of rats produced an inflammatory reaction with oedema formation within the first hour, showing that Causticum acts as an oedematogenic agent. Carrageenin induced rat paw oedema was significantly inhibited (P<0.05) in the group treated with Causticum 30cH solution compared to control. Groups treated with potentized Causticum (6cH, 12cH, 30cH and 200cH), showed significant inhibition (P<0.05) of the inflammation pre-induced by carrageenin. However pre-treatment with Causticum 30cH for 6 days (0.5 ml, daily) did not significantly inhibit granulation using an implantation method.

Role of nitric oxide on the increased vascular permeability and neutrophil accumulation induced by staphylococcal enterotoxin B into the mouse paw.

The role of nitric oxide (NO) on the increase in vascular permeability and neutrophil migration induced by staphylococcal enterotoxin B (SEB; 25 microgram/paw) in the mouse was investigated in this study. The NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) [but not its inactive enantiomer N(omega)-nitro-D-arginine methyl ester (D-NAME)], given intravenously (25-100 micromol/kg) or subplantarly (0.25-1.0 micromol/paw), reduced SEB-induced paw oedema significantly. A similar response was observed with aminoguanidine, given either intravenously (200-600 micromol/kg) or subplantarly (2 micromol/paw). In contrast to paw oedema, the plasma exudation in response to SEB was not affected by the subplantar injection of L-NAME or aminoguanidine. The inhibition of oedema and plasma exudation by systemic treatment with L-NAME or aminoguanidine was reversed by co-injection of the vasodilator iloprost (0.3 nmol/paw). Subplantar injection of SEB (25 microgram/paw) increased by 69% the myeloperoxidase (MPO) activity of SEB-treated paws, indicating the presence of neutrophils. Intravenous (12.5-50 micromol/kg) or subplantar (0.125-0.5 micromol/paw) administration of L-NAME (but not of its inactive enantiomer, D-NAME) largely reduced the MPO activity in SEB-treated paws. Similarly, intravenous (200-600 micromol/kg) or subplantar (2 micromol/paw) administration of aminoguanidine significantly reduced the MPO values of the SEB-injected paws. The vasodilator iloprost (0.3 nmol/paw) completely reversed the inhibition by L-NAME or aminoguanidine of the MPO activity in SEB-injected paws. Our results show that the increased vascular permeability and neutrophil accumulation in response to subplantar injection of SEB in the mouse are inhibited by L-NAME and aminoguanidine by mechanisms probably involving reduction of local microvascular blood flow.

[Dupuytren's and Ledderhose's diseases associated with chronic use of anticonvulsants. Case report]. / Doenças de Dupuytren e de Ledderhose associadas ao uso crônico de anticonvulsivantes. Relato de caso.

We present the case of a patient that after chronic use of anticonvulsant drugs without proven epilepsy, developed Dupuytren's and Ledderhose's diseases. We discuss the most frequent predisposing factors, and their relationship with chronic use of anticonvulsants, particularly phenobarbitone.

Further studies on anti-inflammatory activity of phycocyanin in some animal models of inflammation.

OBJECTIVE: To examine the effects of C-phycocyanin, a pigment found in blue-green algae which acts as an antioxidant in vitro and in vivo, in different animal models of inflammation. MATERIAL: Male Sprague Dawley rats and OF1 mice were used. TREATMENTS: Oedema was induced by: a) AA (0.5 mg/ear) or TPA (4 microg/ear) in the mouse ear b) carrageenan injection (0.1 mL of 1% suspension) in the rat paw (+/-adrenalectomy) and c) cotton pellet implantation in the rat axilla. Phycocyanin (50-300mg/kg, p.o.) or indomethacin (1 mg/ear or 3-10mg/kg, p.o.) as control were tested in the four animal models. METHODS: Measurement of the increase in the weight (mg) of 6 mm ear punch biopsies from treated ears were made in comparison to control ears, together with myeloperoxidase (MPO) activity as an index of neutrophil infiltration. The increase in the paw thickness (mm) was measured with a dial caliper. Cotton pellet was implanted and seven days afterwards the granuloma was removed and the dry weight was determined. Acute toxicity was studied in mice and rats. Statistics were performed using one-way analysis of variance with the Duncan Multirange test. RESULTS: Phycocyanin reduced significantly (p < 0.05) and in a dose-dependent manner ear oedema induced by AA and TPA in mice as well as carrageenan-induced rat paw oedema (both in intact and adrenalectomized animals). In the TPA test, phycocyanin also reduced MPO content. Phycocyanin also exerted an inhibitory effect in the cotton pellet granuloma test. In the acute toxicity test in rats and mice, even at the highest dose tested (3000 mg/kg, p.o.), no toxicity was found. CONCLUSIONS: Phycocyanin shows anti-inflammatory activity in four experimental models of inflammation. Its antioxidative and oxygen free radical scavenging properties may contribute, at least in part, to its anti-inflammatory activity.

Mouse paw edema. A new model for inflammation?

1. Injection of carrageenan into the mouse paw produced a biphasic edema. During the first phase, which developed up to 24 h, edema was of low intensity and unrelated to the dose of carrageenan given. During the second phase, after 24 h, edema was more pronounced, presented a clear dose-response relationship and peaked at 72 h after injection. 2. Histological analysis of the subplantar area 4 h after carrageenan injection revealed a diffuse cellular infiltrate with predominance of polymorphonuclear neutrophils. Between 48 and 72 h, an intense accumulation of macrophages, eosinophils and lymphocytes was observed, together with a great increase in the number of circulating leukocytes and platelets. 3. Pretreatment with the anti-inflammatory drugs indomethacin and dexamethasone reduced both phases of edema in a dose-dependent fashion. 4. The present study shows that carrageenan-induced mouse paw edema constitutes a new and interesting model for the study of the mediators of inflammation and for the screening of new anti-inflammatory drugs.