Recalcitrant Sterile Abscesses by Volux®: A New Therapeutic Approach.

The number of patients developing sterile abscesses because of hyaluronic acid (HA) filler procedures has increased for unknown reasons. We described this adverse reaction after filling with Juvederm Volux®, the latest innovative product in the Vycross range of technology. We presented five patients with recalcitrant sterile abscesses after filling with Juvederm Volux® who did not respond to the traditional therapy but whose lesions were resolved with the "Munhoz-Cavallieri lavage protocol" developed and recently published by the present authors. (SKINmed. 2023;21:27-33).

Rationale and Guidelines for the Use of Hyaluronidase: A Practical Guide for Complications Caused by Hyaluronic Acid.

The use of enzyme hyaluronidase to treat the complications of different brands of hyaluronic acid (HA) dermal fillers is increasing in the same proportion as the number of nonsurgical cosmetic procedures. Guidelines for diagnosing and treating complications remain controversial and are primarily based on anecdotal reports and small case series. We proposed approaching HA-related complications based on our clinical research and observations of treating more than 200 patients and providing a practical guide for the thoughtful use of hyaluronidase according to adverse events. Standardization of hyaluronidase dose and concentration is beneficial for better outcomes and future comparative analyses of the results of this treatment worldwide. The use of hyaluronidase is increasing for the reversal of the clinical manifestations of complications caused by HA fillers, although a consensus is lacking. We propose using different doses and concentrations of hyaluronidase to focus on selected anatomic areas considering properties of the product and pathogenesis of each complication.

Sterile abscess due to hyaluronic acid: A new diagnosis and a proposal for treatment-A series of eight cases.

BACKGROUND: In recent years, fillers procedures with hyaluronic acid (HA) have grown significantly. Despite HA relative safety, the number of cases of complications after injections has grown, and in many of which, we are not aware of or have little control over. AIMS: In this article, the authors describe a new adverse reaction after filling with HA injection, the sterile abscess. PATIENTS/METHODS: We present eight patients with similar clinical, laboratory, and ultrasound characteristics for sterile abscess and report a new therapeutic modality for it. RESULTS: All cases were treated with "Munhoz-Cavallieri Lavage Protocol" procedure with complete resolution. CONCLUSIONS: "Munhoz-Cavallieri Lavage Protocol" serves as a guideline in diagnosis and management of sterile abscess.

Immunomodulatory and anti-inflammatory effects of Kalanchoe brasiliensis.

The immunomodulatory effect of juice obtained from leaves of Kalanchoe brasiliensis (Kb) on zymosan-induced inflammation was investigated. C57B110 mice received a subcutaneous injection of 150 microg zymosan in the footpad. After 7 days, there was an increase in footpad thickness from 176 +/- 4 to 236 +/- 9 x 10(-2) mm and in blood flow in the footpad area, monitored by 99mTc, from 98 +/- 4 to 694 +/- 59 counts per minute (cpm). Zymosan induced a severe infiltration of leukocytes into the articular tissues and a 13-fold increase in the adjacent popliteal lymph node (PLN) weight. Beginning 2 days after the injection, mice were treated daily for 5 days with different concentrations of lyophilised Kb juice dissolved in water. Treatment with 480 mg/kg/day reduced footpad thickness to 193 +/- 5 x 10(-2) mm, leukocyte infiltration and blood flow to 150 +/- 18 cpm in the footpad area. PLN weight in zymosan-injected mice decreased from 6.5 +/- 0.5 to 1.5 +/- 0.4 mg, similarly to the decrease after treatment with indomethacin (3 mg/kg/day). Flow cytometric analysis of lymph node cells showed an important reduction in B cell number in Kb-treated mice. Treatment over a period of 10 days was also effective at reducing zymosan-induced inflammation, even when started 7 days after injection. These data suggest anti-inflammatory and immunosuppressive effects of K. brasiliensis that may account for its popularity in folk medicine against rheumatic diseases.

G-CSF suppresses allergic pulmonary inflammation, downmodulating cytokine, chemokine and eosinophil production.

AIMS: Granulocyte Colony-Stimulating Factor (G-CSF), which mobilizes hemopoietic stem cells (HSC), is believed to protect HSC graft recipients from graft-versus-host disease by enhancing Th2 cytokine secretion. Accordingly, G-CSF should aggravate Th2-dependent allergic pulmonary inflammation and the associated eosinophilia. We evaluated the effects of G-CSF in a model of allergic pulmonary inflammation. MAIN METHODS: Allergic pulmonary inflammation was induced by repeated aerosol allergen challenge in ovalbumin-sensitized C57BL/6J mice. The effects of allergen challenge and of G-CSF pretreatment were evaluated by monitoring: a) eosinophilia and cytokine/chemokine content of bronchoalveolar lavage fluid, pulmonary interstitium, and blood; b) changes in airway resistance; and c) changes in bone-marrow eosinophil production. KEY FINDINGS: Contrary to expectations, G-CSF pretreatment neither induced nor enhanced allergic pulmonary inflammation. Instead, G-CSF: a) suppressed accumulation of infiltrating eosinophils in bronchoalveolar, peribronchial and perivascular spaces of challenged lungs; and b) prevented ovalbumin challenge-induced rises in airway resistance. G-CSF had multiple regulatory effects on cytokine and chemokine production: in bronchoalveolar lavage fluid, levels of IL-1 and IL-12 (p40), eotaxin and MIP-1a were decreased; in plasma, KC, a neutrophil chemoattractant, was increased, while IL-5 was decreased and eotaxin was unaffected. In bone-marrow, G-CSF: a) prevented the increase in bone-marrow eosinophil production induced by ovalbumin challenge of sensitized mice; and b) selectively stimulated neutrophil colony formation. SIGNIFICANCE: These observations challenge the view that G-CSF deviates cytokine production towards a Th2 profile in vivo, and suggest that this neutrophil-selective hemopoietin affects eosinophilic inflammation by a combination of effects on lung cytokine production and bone-marrow hemopoiesis.

G-CSF-treated granulocytes inhibit acute graft-versus-host disease.

It has been shown that in vivo and in vitro treatment with G-CSF induces the generation of low-density granulocytes (LDGs), which copurify with PBMCs and inhibit IFN-gamma production by human T cells. These results prompted us to postulate an immunomodulatory role for LDGs in acute graft-versus-host disease (aGVHD). Here it is shown that in the mouse experimental model, in vivo and in vitro G-CSF treatment generates LDGs capable of inhibiting 80% of T-cell IFN-gamma production. To assess the role of these LDGs in aGVHD, lethally irradiated (C57BL/6 x BALB/c) F1 hosts were reconstituted with T cell-depleted bone marrow cells plus nylon wool-purified spleen cells from G-CSF-treated (G-NWS) or -nontreated (NWS) C57BL/6 donors. Recipients of G-NWS had a 75% survival rate in contrast to a rate of 25% in the NWS recipients. The protective effect was completely abolished, and the mortality rate was 100% if donor-cell infusion was treated with anti-Gr1. Moreover, if LDGs were infused with NWS, full protection of aGVHD was observed, and no signs of disease were evidenced by mortality rate, weight loss, or histopathology of target organs. These results revealed the unexpected immunosuppressive capacity of G-CSF based on the generation of LDGs, leading to the possibility of using these cells as inhibitors of aGVHD.

Aspectos imunopatológicos do vitiligo / Immunological aspects of vitiligo

Vitiligo é uma doença adquirida, hereditária, caracterizada por máculas acrômicas devido à ausência de melanócitos. Sem dúvida, é uma das dermatosescom efeito psicológico mais devastador. O fator que leva à destruição dos melanócitos permanece desconhecido. É uma doença multifatorial,onde estão envolvidos fatores genéticos, hereditários, imunológicos e ambientais.Inúmeras são as teorias para explicar o seu surgimento. Tradicionalmente temos a teoria neural, da autotoxicidade e a auto-imune. Evidências atuaisreforçam a hipótese da auto-imunidade, embora outras teorias como indução de apoptose dos melanócitos, descolamento melanocítico, melanocitorragia,defeito intrínseco do melanócito, teoria viral, alteração local das citocinas produzidas e teoria convergente tenham sido descritos.Dados da imunidade humoral são vastos. Entretanto evidências recentes têm enfatizado o papel da célula T citotóxica na eliminação dos melanócitosda epiderme. A questão sobre como a resposta imune é iniciada permanece. Persiste indefinido se as alterações imunológicas são a causa ou a conseqüênciada doença. Se elas representam um epifenômeno interessante, porém irrelevante, ou são, de fato, responsáveis pela injúria ao melanócito invivo. De qualquer forma, a descoberta e descrição dos fenômenos imunológicos são importantes para se entender o mecanismo de surgimento dovitiligo. Diferentes abordagens são sugeridas para o tratamento do vitiligo em todas as partes do mundo, desta forma torna-se fundamental aumentaro conhecimento sobre seu mecanismo de doença. Neste artigo, os autores reviram a patogênese do vitiligo enfatizando a destruição auto-imune (AU)

Vitiligo is an acquired disease, hereditary, characterized by achromic macules due to melanocytes abscence. Patients suffer from a huge psychologicalimpact. The factor that leads to destruction of melanocytes remais unknown. Genetic, hereditary, immunological and ambiental factors are related tothis disease. There are many theories to explain its occurrence. Traditionally neural, autotoxicity (autodestruction) and autoimmune theories are described.Actual evidence reinforces autoimmune hypothesis, although another hypothesis as melanocyte apoptosis, melanocyte detachment, melanocytorrhagy,intrinsic defects of melanocytes, viral theory, local alteration of production of cytokines have been postulated.Melanocyte death, evidenced in vitiligo patients, induces an humoral immunologic response and there are many data about this type of response.Although recent papers have showed the enrollment of cytotoxic T cell in the elimination of melanocytes in basal layer. The question about how theimmune response begins remains unsolved. Are the immunological alterations cause or consequence of this disease? To date, remains unknown if theimmunologic factors represent an interesting although irrelevant epiphenomena or they are, in fact, the cause of vitiligo. Different therapeutic approachesare suggested for vitiligo treatment all over the world, so it is essential to enhance knowledge about the mechanism of this disease. In this article,we reviewed pathogenesis of vitiligo enhancing autoimmunity destruction of melanocytes (AU)