Effect of high-voltage electrical stimulation on the albumin and histamine serum concentrations, edema, and pain in acute joint inflammation of rats

BACKGROUND: The mechanism by which high-voltage electrical stimulation (HVPC) acts on edema reduction is unknown. OBJECTIVE: To assess the effect of HVPC with negative polarity (-) applied to the ankle of rats with acute joint inflammation. METHOD: Sixty-four rats were divided into four groups (n=16): inflamed+HVPC(-), 0.03 mL application of ι-carrageenan (3%) to the tibiotarsal joint plus HVPC(-); inflamed+HVPC placebo, carrageenan application and HVPC placebo; normal+HVPC(-), HVPC application(-); and normal control, no intervention. The HVPC(-) 100 Hz at a submotor level was applied daily for 45 min on three consecutive days. The variables were pain, hind-foot volume, and serum histamine and albumin assessed before and during the 48 hours following inflammation. The variables were compared using the t test, one-way ANOVA, nested ANOVA for repeated measures, and the post hoc Bonferroni test. Analysis of covariance was applied to adjust the effects of HVPC(-) by measurements of pain, inflammation, albumin, and histamine at 24 h, and the final weight was compared to the other groups. The significance level was set at p<0.05. RESULTS: There were no differences between the inflamed+HVPC(-) and inflamed+HVPC placebo groups in terms of pain or edema (p>0.05). Albumin was reduced in the groups that received the intervention, but there was no differences between them. There was only a 24 hour increase in histamine with the normal+HVPC(-) (p=0.0001) and inflamed+HVPC placebo groups (p=0.01) compared to the normal control group. CONCLUSIONS: The results of the present study suggest that HVPC(-) with the parameters employed did not reduce pain or edema and did not change serum albumin or histamine levels,, which indicates the inability of this resource to have a positive effect when treating treat acute joint inflammation. .

Inhibition of carrageenan-induced expression of tissue and plasma prekallikreins mRNA by low level laser therapy in a rat paw edema model / Inibição da expressão de RNA mensageiro de pré-calicreínas tecidual e plasmática pela laserterapia em modelo de edema de pata induzido pela carragenina em ratos

BACKGROND: Low level laser therapy (LLLT) has been used clinically in order to treat inflammation, where tissue and plasma prekallikrein have crucial importance. Plasma prekallikrein (PPK) is synthesized by the hepatocytes and secreted into the bloodstream, where it participates in the surface-dependent activation of blood coagulation, fibrinolysis, kinin generation and inflammation. Tissue prekallikrein is associated with important disease states (including cancer, inflammation, and neurodegeneration) and has been utilized or proposed as clinically important biomarker or therapeutic target of interest. OBJECTIVE: To evaluate if LLLT modulates tissue and plasma prekallikreins mRNA expression in the carrageenan-induced rat paw edema. METHODS: Experimental groups were assigned as followed: A1 (Control-saline), A2 (Carrageenan-only), A3 (laser 660nm only) and A4 (Carrageenan + laser 660nm). Edema was measured by a plethysmometer. Subplantar tissue was collected for the quantification of prekallikreins mRNA by Real time-Polymerase Chain Reaction. RESULTS: A significantly decrease in the edema was observed after laser irradiation. Expression of prekallikreins increased after carrageenan injection. Tissue and plasma prekallikrein mRNA expression significantly decreased after LLLT's 660nm wavelength. CONCLUSION: These results suggest that expression of tissue and plasma prekallikreins is modulated by LLLT, which can be used in clinical practice due to its anti-inflammatory effects.

CONTEXTUALIZAÇÃO: A laserterapia de baixa potência tem sido usada para o tratamento de processos inflamatórios diversos em que a calicreína tecidual e a plasmática possuem participação ativa. A pré-calicreína plasmática (PPK) é sintetizada pelos hepatócitos e secretada na corrente sanguínea, onde participa da ativação da coagulação, fibrinólise, geração de cininas e inflamação. A pré-calicreína tecidual está associada com importantes doenças (incluindo câncer, inflamação e neurodegeneração) e tem sido utilizada ou sugerida clinicamente como importante biomarcador ou alvo terapêutico. OBJETIVO: Avaliar se a laserterapia altera a expressão gênica da pré-calicreína tecidual e da plasmática no modelo de inflamação aguda induzida pela carragenina. MÉTODOS: Quarenta ratos foram separados em quatro grupos experimentais: A1 (controle), A2 (carragenina, apenas), A3 (laser 660nm, apenas) e A4 (Carragenina + laser 660nm). O edema foi medido por um pletismômetro. Tecido subplantar foi coletado para a quantificação de RNA mensageiro (RNAm) de pré-calicreínas tecidual e plasmática por PCR em tempo real. RESULTADOS: Observou-se uma diminuição significativa no volume de edema após irradiação com laser 660nm. A expressão de RNAm de pré-calicreínas tecidual e plasmática aumentou após a inoculação de carragenina, entretanto a expressão gênica das pré-calicreínas diminuiu significantemente após laserterapia de baixa potência de 660nm. CONCLUSÃO: Os resultados sugerem que a expressão de RNAm das pré-calicreínas tecidual e plasmática é modulada pela laserterapia de baixa potência, podendo ser alvo terapêutico para tratamento de processos inflamatórios.

Síndrome de compresión de vena cava inferior secundario a fibrosis retroperitoneal / Inferior vena cava compression syndrome secondary to retroperitoneal fibrosis

Se estudió un paciente de 57 años de edad, de tez negra, con edemas en miembros inferiores relevantes por su volumen y extensión. Se realizó la discusión clínica la cual orientó hacia la búsqueda de una lesión o tumor retroperitoneal asociado a un síndrome de compresión u obstrucción de vena cava inferior y se comprobó imagenológicamente. La confirmación histológica se obtuvo por vía quirúrgica

We studied a 57 year-old patient of black complexion, with swelling of the lower limbs which was relevant due to its mass and extension. The clinical discussion guided us to search for a lesion or retroperitoneal tumor associated with a compression syndrome or obstruction of the inferior vena cava, which was determined radiologically. Histological confirmation was obtained through surgery

Epidemic dropsy--a clinical study of the Delhi outbreak.

BACKGROUND: A major outbreak of epidemic dropsy occurred in Delhi, India, in August-September 1998, due to the consumption of contaminated mustard oil. METHODS: The clinical data of 212 adult patients of epidemic dropsy who presented to our hospital is analysed. RESULTS: Pitting pedal oedema (100%), skin erythema (75%), limb tenderness (63%), diarrhea (51%) and hepatomegaly (34%) were the prominent clinical manifestations observed in the patients. Superficial retinal haemorrhages and retinal venous dilatation was observed on fundus examination and 9% of patients developed an open angle glaucoma over a three month follow up period. Cardiac failure was present in 14% of patients. Most patients had mild disease which responded to cessation of mustard oil consumption, bed rest, diuretics and antioxidants. There were six deaths, all of whom had intractable cardiac failure. A unique feature of this outbreak was the documentation of acute renal failure in three patients, a phenomenon never described previously. CONCLUSIONS: Strict law enforcement to prevent the contamination of edible oils is essential to avoid the occurrence of future similar outbreaks.

Presentacion de casos: deficiencia de la proteina inhibidora del primer factor del complemento / Case presentation: deficiency of protein inhibiting of the C1 complement

Se presenta una paciente de 33 anos con episodios subitos de edema facial y de miembros superiories desencadenados por traumatismos leves. Los episodios ceden espontaneamente y no son prevenidos por la administracion de corticoides o antihistaminicos. El nivel de C1 inh fue de 40% y el de C4 se encontro disminuido, indicando consumo de los factores de la via clasica. Se analizan las caracteristicas clinicas y de laboratorio, concluyendo que el cuadro corresponde a angioedema hereditario causado por deficiencia de C1 inh.