Monoterapia com Laser na Fasceíte Plantar

Introdução: A fasceíte plantar (FP) constitui a causa mais frequente de dor no retropé. Está recomendada uma prova terapêutica inicial conservadora. Objetivos: Caraterizar fatores demográficos e sintomáticos, terapêutica prévia e resultados de monoterapia com laser. Material e Métodos: Estudo observacional retrospetivo (12 meses). O tratamento aplicado foi laser infravermelho (AsGa 904nm; densidade de energia 20J/cm2; potência de pico 200mW). Fez-se análise estatística descritiva e comparativa (nível de significância de 0,05). Resultados: Seguiram-se 32 doentes com FP, com idade média de 54,28 anos (24–86; DP 13,95), 66% mulheres, Índice de Massa Corporal (IMC) médio de 30,18Kg/m2 (17,91-41,13; DP 5,19), 75% unilaterais, tempo médio de evolução de 6,28 meses (0,2-24; DP 6,82), 21 tinham feito previamente farmacoterapia e 12 outros tratamentos de MFR. O nível de dor inicial (END) médio foi 7,31 (5-10; DP 1,38). Dos 26 doentes tratados (6 perdas), 24 (92,3%) reportaram melhoria. O número médio de sessões foi 28,5 (11– 60; DP 14,01). O nível médio de dor final foi 0,75 (0-5; DP 2,37), com melhoria média de 89,7% (28,6%-100%; DP 0,16) do nível de dor. A intensidade de dor inicial foi maior em doentes com IMC superior (p=0,002). Não se encontraram outras relações estatisticamente significativas. Conclusões: A FP caraterizou-se por um nível de dor significativo (moderado a grave). A obesidade pareceu ser um fator de risco. A taxa de melhoria com o tratamento com laser foi muito satisfatória. A terapia com laser de baixa intensidade IV constitui uma boa opção terapêutica, a justificar avaliação suplementar por ensaios prospetivos controlados e randomizados.

Enterocolite Necrosante com Perfuração e Drenagem Peritoneal no Recém-Nascido de Muito Baixo Peso: Um Caso Clínico de Evolução Favorável

A enterocolite necrosante (ECN) constitui o problema gastrointestinal mais grave e mais frequente no recém-nascido (RN) de baixo peso. A melhoria na taxa de sobrevivência tem sido atribuída ao diagnóstico mais precoce e à experiência adquirida no tratamento do recém-nascido pré-termo em estado crítico. Desde 1977 que a drenagem peritoneal como actuação prioritária nos quadros de ECN tem sido preconizada nos recém- -nascidos de peso inferior a 1500 g com perfuração intestinal, e nos de peso superior a 1500 g com instabilidade hemodinâmica. Neste artigo relata-se o caso de um recém-nascido, com 1473 g de peso e 30 semanas de idade gestacional, ECN, sinais de perfuração intestinal e de instabilidade hemodinâmica, o qual foi submetido a drenagem peritoneal com evolução favorável e sem sequelas. Na discussão faz-se referência especial, de acordo com dados de literatura, aos mecanismos que explicam os bons resultados do procedimento em cerca de 2/3 dos casos de ECN com perfuração, os quais estão relacionados com as características particulares da cicatrização nos tecidos imaturos. Em conclusão, admite-se que a drenagem peritoneal deverá constituir a forma de actuação prioritária nos casos de ECN com perfuração e instabilidade hemodinâmica em RN pré-termo de muito baixo peso.

Course of infection and histopathological lesions in mice infected with seventeen Trypanosoma cruzi strains isolated from chronic patients

Mice were infected with blood forms of 17 Trypanosoma cruzi strains recently isolated from chronic patients, which were dassified as of low, medium or high virulence on grounds of the prepatent period, parasitemia and mortality at the acute phase. A total of 212 mice were studied after 3, 6, 9 and 12 months of infection. In the chronic phase, intracellular parasites were detected in 11.0%,27.9%and 54.0,% of mice inoculated, respectively, with the low, medium and high virulent strains (r= 0.98, p < 0.005). Heart fibrosis was also related to virulence, affecting 5.7%, 11.6%and30.8% (r = 0.98, p < 0.001) of the mice inoculated with the above strains; a similar relationship was observed between intensity and frequency of the heart inflammatory reaction and the severity of infection at its early stage. Necrotizing arteritis was detected in 12.2% of the inoculated animals and this lesion was related to the infection duration rather than to strain characteristics. Inflammatory lesions and tissue parasitism were stable within the period of observation, whereas fibrosis was Progressive. The findings suggest that mice may reproduce heart lesions resembling human pathology and that organ damage apparently depends on the parasite virulence.

Clinical Epidemiology of Buruli ulcer from Benin (2005-2013): effect of time-delay to diagnosis on clinical forms and severe phenotypes

Buruli Ulcer (BU) is a neglected infectious disease caused by Mycobacterium ulcerans that is responsible for severe necrotizing cutaneous lesions that may be associated with bone involvement. Clinical presentations of BU lesions are classically classified as papules, nodules, plaques and edematous infiltration, ulcer or osteomyelitis. Within these different clinical forms, lesions can be further classified as severe forms based on focality (multiple lesions), lesions' size (>15 cm diameter) or WHO Category (WHO Category 3 lesions). There are studies reporting an association between delay in seeking medical care and the development of ulcerative forms of BU or osteomyelitis, but the effect of time-delay on the emergence of lesions classified as severe has not been addressed. To address both issues, and in a cohort of laboratory-confirmed BU cases, 476 patients from a medical center in Allada, Benin, were studied. In this laboratory-confirmed cohort, we validated previous observations, demonstrating that time-delay is statistically related to the clinical form of BU. Indeed, for non-ulcerated forms (nodule, edema, and plaque) the median time-delay was 32.5 days (IQR 30.0-67.5), while for ulcerated forms it was 60 days (IQR 20.0-120.0) (p = 0.009), and for bone lesions, 365 days (IQR 228.0-548.0). On the other hand, we show here that time-delay is not associated with the more severe phenotypes of BU, such as multi-focal lesions (median 90 days; IQR 56-217.5; p = 0.09), larger lesions (diameter >15 cm) (median 60 days; IQR 30-120; p = 0.92) or category 3 WHO classification (median 60 days; IQR 30-150; p = 0.20), when compared with unifocal (median 60 days; IQR 30-90), small lesions (diameter =15 cm) (median 60 days; IQR 30-90), or WHO category 1+2 lesions (median 60 days; IQR 30-90), respectively. Our results demonstrate that after an initial period of progression towards ulceration or bone involvement, BU lesions become stable regarding size and focal/multi-focal progression. Therefore, in future studies on BU epidemiology, severe clinical forms should be systematically considered as distinct phenotypes of the same disease and thus subjected to specific risk factor investigation.

Spontaneous healing of Mycobacterium ulcerans lesions in the guinea pig model

Buruli Ulcer (BU) is a necrotizing skin disease caused by Mycobacterium ulcerans infection. BU is characterized by a wide range of clinical forms, including non-ulcerative cutaneous lesions that can evolve into severe ulcers if left untreated. Nevertheless, spontaneous healing has been reported to occur, although knowledge on this process is scarce both in naturally infected humans and experimental models of infection. Animal models are useful since they mimic different spectrums of human BU disease and have the potential to elucidate the pathogenic/protective pathway(s) involved in disease/healing. In this time-lapsed study, we characterized the guinea pig, an animal model of resistance to M. ulcerans, focusing on the macroscopic, microbiological and histological evolution throughout the entire experimental infectious process. Subcutaneous infection of guinea pigs with a virulent strain of M. ulcerans led to early localized swelling, which evolved into small well defined ulcers. These macroscopic observations correlated with the presence of necrosis, acute inflammatory infiltrate and an abundant bacterial load. By the end of the infectious process when ulcerative lesions healed, M. ulcerans viability decreased and the subcutaneous tissue organization returned to its normal state after a process of continuous healing characterized by tissue granulation and reepethelialization. In conclusion, we show that the experimental M. ulcerans infection of the guinea pig mimics the process of spontaneous healing described in BU patients, displaying the potential to uncover correlates of protection against BU, which can ultimately contribute to the development of new prophylactic and therapeutic strategies.

Lack of the transcription factor hypoxia-inducible factor (HIF)-1α in macrophages accelerates the necrosis of Mycobacterium avium-induced granulomas

Accepted Manuscript

Pédiatrie [Pediatrics].

Several preliminary studies suggest that prophylactic administration of probiotics reduces the incidence of necrotizing enterocolitis (NEC) in preterm infants, and several neonatology units have introduced this treatment under strict surveillance. Nonetheless, breast milk feeding remains the mainstay of NEC prevention. The beta-blocker propranolol, known for its effectiveness on cutaneous hemangiomas, is also proving useful for the treatment of subglottic or visceral hemangiomas. Following the decrease in severe bacterial infections thanks to widespread vaccinations, the McCarthy clinical score has regained importance in the prediction of the risk of bacterial infection in febrile infants. It is easy to use, economical, and has a diagnostic value comparable to laboratory tests. The new WHO growth charts have been introduced in Switzerland in 2011 to take into account the increasing regional and ethnic variations in our country. Any significant change in growth velocity should prompt an evaluation of the need of further investigations.

Estudio de la patogenia de clostridium perfringens tipo b y d en pequeños rumiantes

Proyecto de investigación realizado a partir de una estancia en la University of California, Davis, Estados Unidos, entre octubre y desembre del 2007. Clostridium perfringens (C. perfringens) tipo C causa enteritis necrotizante en humanos y enterotoxemias en animales domésticos. Esta bacteria produce beta toxina (CPB), alfa toxina (CPA) y perfringolisina (PFO) durante la fase logarítimca de crecimiento. En nuestro estudio se evaluó la relación entre CPB y la virulencia del aislamiento CN3685 de Cl. perfringens tipo C en un modelo caprino con inoculación intraduodenal. De manera similar a la infección natural por C. perfringens tipo C, el cultivo vegetativo del tipo salvaje de CN3685 provocó dolor abdominal, diarrea hemorrágica, enteritis necrotizante, colitis, edema pulmonar, hidropericardio y muerte en 2 cabritos, a las 24 horas postinoculación. Por otro lado, mediante tecnología Targe Tron® se prepararon mutantes isogénicos carentes de toxina CPB, los cuales fueron inoculados siguiendo el modelo anteriormente descrito. Los resultados mostraron que estos mutantes carecían de todo tipo de virulencia, ya que no se observaron signos clínicos durante las primeras 24 h postinoculación ni tampoco lesiones macroscópicas ni histopatológicas. Posteriormente se desarrolló un modelo experimental similar a los anteriores, en los que se había repuesto la capacidad de producción de CPB en los mutantes. Los dos animales inoculados con estos mutantes complementarios presentaron signos clínicos y lesiones similares a las observadas en el caso del tipo salvaje. Estos resultados muestran que la toxina CPB es necesaria y suficiente para inducir la enfermedad causada por CN3685. Esto a su vez, demuestra la importancia de este tipo de toxina en la patogénesis de C. perfringems tìpo C.

Macrophage activation and histopathological findings in Calomys callosus and Swiss mice infected with several strains of Trypanosoma cruzi

Peritoneal macrophage activation as measured by H2O2 release and histopathology was compared between Swiss mice and Calomys callosus, a wild rodent, reservoir of Trypanosoma cruzi, during the course of infection with four strains of this parasite. In mice F and Y strain infections result in high parasitemia and mortality while with silvatic strains Costalimai and M226 parasitemia is sub-patent, with very low mortality. H2O2 release peaked at 33,6 and 59 nM/2 x 10(elevado a sexta potência) cells for strains Y and F, respectively, 48 and 50 nM/2 x 10 (elevado a sexta potência) for strains Costalimai and M226, at different days after infection. Histopathological findings of myositis, myocarditis, necrotizing artheritis and abscence of macrophage parasitism were foud for strains F and Costalimai. Y strain infection presented moderate myocarditis and myositis, with parasites multiplying within macrophages. In C. callosus all four strains resulted in patent parasitemia wich was eventually overcome, with scarce mortality. H2O2 release for strains Y or F was comparable to that of mice-peaks of 27 and 53 nM/2 x 10 (elevado a sexta potência) cells, with lower values for strains Costalimai and M226 - 16.5 and 4.6 nM/2 x 10(elevado a sexta potência)cells, respectively. Histopathological lesions with Y and F strain injected animals were comparable to those of mice at the onset of infections; they subsided completely at the later stages with Y strain and partially with F strain infected C. callosus. In Costalimai infected C. callosus practically no histopathological alterations were observed.

Imaging of cavitary necrosis in complicated childhood pneumonia.

The aim of this study was to illustrate the chest radiographs (CR) and CT imaging features and sequential findings of cavitary necrosis in complicated childhood pneumonia. Among 30 children admitted in the Pediatric Intensive Care Unit for persistent or progressive pneumonia, respiratory distress or sepsis despite adequate antibiotic therapy, a study group of 9 children (5 girls and 4 boys; mean age 4 years) who had the radiographic features and CT criteria for cavitary necrosis complicated pneumonia was identified. The pathogens identified were Streptococcus pneumoniae( n=4), Aspergillus( n=2), Legionella( n=1), and Staphylococcus aureus( n=1). Sequential CR and CT scans were retrospectively reviewed. Follow-up CR and CT were evaluated for persistent abnormalities. Chest radiographs showed consolidations in 8 of the 9 patients. On CT examination, cavitary necrosis was localized to 1 lobe in 2 patients and 7 patients showed multilobar or bilateral areas of cavitary necrosis. In 3 patients of 9, the cavitary necrosis was initially shown on CT and visualization by CR was delayed by a time span varying from 5 to 9 days. In all patients with cavities, a mean number of five cavities were seen on antero-posterior CR, contrasting with the multiple cavities seen on CT. Parapneumonic effusions were shown by CR in 3 patients and in 5 patients by CT. Bronchopleural fistulae were demonstrated by CT alone ( n=3). No purulent pericarditis was demonstrated. The CT scan displayed persistent residual pneumatoceles of the left lower lobe in 2 patients. Computed tomography is able to define a more specific pattern of abnormalities than conventional CR in children with necrotizing pneumonia and allows an earlier diagnosis of this rapidly progressing condition. Lung necrosis and cavitation may also be associated with Aspergillus or Legionella pneumonia in the pediatric population.

Multifocal nodular episcleritis and scleritis with undiagnosed Hodgkin's lymphoma.

PURPOSE: To report the case of a patient with undiagnosed Hodgkin's lymphoma who presented with coexistent unilateral nodular episcleritis and scleritis. DESIGN: Interventional case report and literature review METHODS: Review of clinical history, laboratory findings, histology of episcleral and cervical lymph node biopsies, and follow-up. RESULTS: A 20-year-old female presented with a 5-month history of redness and pain in her left eye, with associated symptoms of dyspnea, malaise, and fever. The patient was found to have multifocal nodular episcleritis and scleritis that was not responsive to topical steroids or systemic nonsteroidal anti-inflammatory treatment. Laboratory tests subsequently revealed evidence of systemic inflammation, and radiologic studies showed extensive mediastinal and cervical adenopathy. A cervical lymph node biopsy showed Reed-Sternberg cells and a chronic lymphocytic infiltrate consistent with nodular sclerosing Hodgkin's lymphoma. Histopathologic analysis of an episcleral nodule revealed a necrotizing granuloma with vasculitis. Systemic chemotherapy was instituted for the Hodgkin's disease; this therapy abolished the nodular scleritis. CONCLUSIONS: This case raises the possibility of concurrent undiagnosed systemic vasculitis with only an ocular manifestation with Hodgkin's lymphoma, either as a coincidence or as a paraneoplastic syndrome. Moreover, it emphasizes the important role of tissue biopsy in establishing diagnosis and directing treatment.

Indocyanine Green Angiography Findings in Acute Retinal Necrosis Syndrome.

BACKGROUND: Acute retinal necrosis syndrome is clinically defined by the presence of peripheral necrotizing retinitis associated with severe occlusive vasculitis caused primarily by herpes simplex virus and varicella zoster virus. Previously considered as an exclusively retinal pathology, choroidal involvement, as demonstrated by indocyanine green angiography, has not been extensively studied. HISTORY AND SIGNS: Indocyanine green angiography was performed in 4 patients with ARN. Observed angiographic patterns included: 1. a characteristic triangular area of hypo-perfusion, 2. hypofluorescent lobular patches and areas of fuzzy choroidal vascular hyperfluorescence, and 3. isolated hypofluorescent lobular patches of the contralateral eye. THERAPY AND OUTCOME: Marked choroidal hypo-perfusion on indocyanine green angiography was associated with extensive retinal ischemia. Treatment included a combination of antiviral agents and corticosteroids complemented by prophylactic acetylsalicylate. CONCLUSION: Indocyanine green angiography may provide important information regarding choroidal vascular involvement in ARN. It may also permit the timely identification of sub-clinical contralateral eye involvement.

Boerhaave Syndrom: an unusual complication of acute vomiting in a child

Introduction: Boerhaave syndrome (BS) is a spontaneous esophageal perforation, described in aged, alcoholic males, secondary to forceful vomiting. BS has rarely been described in children. Case presentation: The patient is a 7-year-old Nigerian girl. She has a past history of clinical gastro-esophageal reflux (treated conservatively with prokinetics and good evolution), malaria at the age of 3 months and an episode of acute pancreatitis at 5 years. One week prior admission, she had stopped atovaquone-proguanil (AP) prophylaxis after a trip in an endemic area. Two days prior admission, she presented several bouts of isolated acute vomiting, without fever or diarrhea. On admission, she complained of chest pain. Cardiac auscultation revealed crepitus. No subcutaneous emphysema nor respiratory distress was present. Chest radiography and CT-scan confirmed a pneumomediastinum extending to the neck. Esophageal perforation was suspected. An upper gastrointestinal endoscopy was performed and showed a small esophageal tear, grade II-III esophagitis and a single gastric ulcer without any sign of H. Pylori infection. Enteral feeds were stopped and a nasogastric sucking tube inserted. The patient made a full recovery on intravenous antibiotics and conservative treatment. Of note a second episode of subclinical acute pancreatitis, treated conservatively, probably drug-induced. Discussion: BS is a complete rupture of all layers of the esophagus, secondary to an increased intra-abdominal pressure due to incomplete opening of the cricophayngeal sphincter occurring during vomiting or cough. Rarer causes include eosinophilic or Barrett's esophagitis, HIV and caustic ingestion. Esophageal perforation in children is rare, most of time secondary to necrotizing esophagitis in the newborn, medical intervention (endoscopy, sucking, or intubation) or trauma in the older child. Our patient had none of those risk factors and it is still unclear what predisposed her to this complication. However, we believe that preceding forceful vomiting with increased abdominal pressure acting on a weakened oesophagus due to esophagitis might be responsible. We could not find any association in the literature between AP and BS nor between BS and acute pancreatitis. The origin of her recurrent pancreatitis remains unclear, reason for which genetic testing for mutations in the trypsinogen, trypsin inhibitor and CFTR genes will be performed in case of a third episode.