Gastrointestinal colonization by OXA-48-producing Enterobacterales: risk factors for persistent carriage.

Carbapenem-resistant Enterobacterales (CRE) infections are a major health problem. Intestinal colonization is a key factor in developing infection. However, factors associated with persistent colonization by CRE are unknown. The aim of the study was to identify factors associated with persistent CRE gut colonization. This is a retrospective, single-centre, observational study of adult patients with CRE gut colonization between January 2015 and January 2020. Epidemiologic characteristics, comorbidities, infectious events, duration of hospitalization and antimicrobial treatment received in the follow-up period were collected. Colonization was defined as isolation in at least 2 rectal swab culture samples of CRE. Decolonization was defined as 3 negative rectal swab cultures or 2 negative cultures and a negative molecular test. A cohort of 86 patients with CRE gut colonization was selected: 44 patients with spontaneous decolonization (DC) and 42 patients with persistent colonization (PC). The mean follow-up period was 24 months (IQR 14-33) in the DC group vs. 25 months (IQR 16-36) in the PC group (p = 0.478). Patient characteristics were similar between both groups. Colonization by other MDR microorganisms was high (44 patients, 51%) and slightly more common in the PC group (PC 60% vs. DC 43%, p = 0.139). The use of ceftazidime-avibactam was more common among the PC group (PC 33% vs. DC 14%, p = 0.041). We observed a higher percentage of antimicrobial therapy in the previous 30 days (PC 68% vs. DC 57%, p = 0.371) and 90 days (PC 81% vs. DC 82%, p = 0.353) in the PC group. Multivariable analysis showed that patients that have received ceftazidime-avibactam therapy (OR 4.9 95% CI [1.45-16.39], p = 0.010), and those colonized by other MDR microorganisms (OR 2.5, 95% CI [0.96-6.25], p = 0.060) presented a higher risk of PC. Ceftazidime-avibactam use and colonization by other MDR microorganisms might be associated with CRE persistent gut colonization.

Ceftazidime-avibactam treatment in bacteremia caused by OXA-48 carbapenemase-producing Klebsiella pneumoniae.

Therapeutic options for bacteremia caused by carbapenem-resistant Enterobacterales (CRE) OXA-48-type are limited. The objective of this study was to analyze clinical success of CAZ-AVI compared with best available therapy (BAT) in patients with Klebsiella pneumoniae carbapenemase-producing OXA-48-type bacteremia (CRKp-OXA-48). We conducted a retrospective, single-center observational study in adult patients with CRKp-OXA-48 between December 2015 and May 2019. We collected the patients' clinical and epidemiological characteristics, antibiotic treatment (CAZ-AVI vs. BAT), and evolution. Factors associated with clinical success were analyzed using binary logistic regression. The study included 76 patients with CRKp-OXA-48-type bacteremia 33 received CAZ-AVI and 43 BAT. CAZ-AVI was mainly used in monotherapy (91%). Clinical success was more common in patients < 70-year-old (OR 4.79, 95% CI [1.435-16.002], p = 0.011) and CAZ-AVI treatment (OR 6.69, 95% CI [1.68-26.604], p = 0.007). Kaplan-Meier survival curve of 14-day mortality showed a lower mortality in patients who received CAZ-AVI (log rank 0.013). However, CAZ-AVI did not achieve statistical difference in IPTW for 14- and 30-day mortality (aOR 0.1, 95% CI [0.02-1.22], p = 0.076 and aOR 1.7, 95% CI [0.48-5.98], p = 0.413, respectively). CAZ-AVI treatment might be associated with a greater clinical success in CRKp-OXA-48 bacteremia.

Home treatment of venous thromboembolism disease. / Tratamiento domiciliario de la enfermedad tromboembólica venosa.

Despite the potential benefits of outpatient care, most patients with pulmonary embolisms are treated in hospitals for fear of possible adverse events. However, there is a wealth of scientific evidence from studies covering more than 4000 outpatients, which has led the current clinical practice guidelines to recommend early discharge or outpatient treatment when a low risk of death or complications has been confirmed, when there are no comorbidities or aggravating processes present to warrant hospitalisation and when appropriate monitoring and treatment are observed. This approach minimises the complications that can arise in hospitals and represents considerable cost savings. When selecting these patients, the use of prognostic tools such as the Pulmonary Embolism Severity Index (PESI), its simplified version (sPESI) and the Hestia Criteria are of paramount importance. Using these tools, the short-term outcomes (30-90days) show low mortality (in general <3%) and a low incidence of other complications (rate of recurrence and major bleeding <2%). Based on the available evidence, outpatient treatment can be considered the most appropriate strategy at this time for most hemodynamically stable patients with pulmonary embolisms.

Forma de presentación "prono-doloroso-like" del síndrome de Parsonage-Turner / Parsonage-Turne síndrome "pulled elbow-like" presentation form

Introducción: El síndrome de Parsonage-Turner es una neuritis del plexo braquial de etiología desconocida. Se ha des-crito su aparición tras procesos infecciosos, por lo que se sospecha un mecanismo autoinmune. Su descripción en la edad pediátrica se limita a casos aislados. En los adultos, la sintomatología típica es un dolor súbito e intenso, localizado en el hombro y la región proximal de la extremidad superior, seguido de parálisis flácida y amiotrofia. Caso clínico: Lactante de 14 meses de edad que consulta por presentar una impotencia funcional de los miembros superiores de 48 horas de evolución. Los días previos mostró una infección respiratoria de las vías altas. Presentaba el brazo derecho en posición de prono, debilidad de la musculatura proximal de ambas extremidades superiores, sobre todo la derecha, e incapacidad para la movilización. Se detectó rhinovirus en la reacción en cadena de la polimerasa de moco nasal. El electromiogra-ma (EMG) del deltoides demostró una denervación aguda intensa de los músculos proximales de ambas extremidades superiores, sobre todo la derecha, compatible con una plexitis braquial bilateral. Conclusiones: El espectro clínico de presentación de la neuralgia amiotrófica puede ser distinto en la edad pediátrica. El dolor, característico de la forma adulta, puede no estar presente. Su forma de presentación puede asemejarse a un prono doloroso, por lo que deberemos incluirlo en su diagnóstico diferencial. El diagnóstico se basa en hallazgos clínicos; son de utilidad la resonancia magnética y el EMG, que debe realizarse 2-3 semanas tras el inicio del cuadro. El conocimiento de esta entidad permite establecer un diagnóstico precoz, lo que evita tratamientos potencialmente yatrogénicos, y anticipar el pronóstico

Introduction: Parsonage-Turner syndrome is a brachial plexus neuritis of unknow etiology. An autoinmune mecha-nism is suspected because of its appearance after infections. It predominantly affects proximal muscles of upper ex-tremities, with a first painful phase, which evolves to paresis and atrophy of the affected muscles. His description in pediatric patients is limited to isolated cases. Case report: 14 months infant consulting for weakness of upper limbs. He had an upper respiratory tract infection the previous days. Examination revealed weakness of the proximal muscles of the both arms, more marked on the right side and inability to active mobility simulating a pulled elbow. Magnetic resonance imaging of neck and shoulder showed no structural pathology. The electromyogram performed at 3 weeks of the onset of symptoms demonstrated acute denervation of the proximal arm muscles compatible with bilateral brachial plexitis. Rhinovirus was detected in polimerasa chain reaction in nasopharyngeal aspirate. Conclusions: Parsonage-Turner syndrome is an entity to consider in painful shoulder or upper limb functional impo-tence, as pulled elbow. Diagnosis is based on clinical findings. It's useful to rule one MRI and EMG (which must be per-formed 2-3 weeks after onset). It has spontaneous evolution partially favorable to rehabilitation and anti-inflammatory treatment. Knowledge of this entity allows proper handling, avoiding iatrogenic treatments, and allows anticipate the outcome

GABAergic drug use and global, cognitive, and motor functional outcomes after stroke.

BACKGROUND: In animal models and healthy volunteers, the use of GABA A receptor agonists (GABA-AGs) seem deleterious for functional recovery. The agents are widely used for subacute stroke, but their effect on functional recovery remains unclear. OBJECTIVES: We aimed to evaluate the association between GABA-AG use and functional recovery after stroke. METHODS: We retrospectively recruited 434 survivors of subacute stroke admitted for inpatient rehabilitation between 2000 and 2013 in our institution (107 with and 327 without GABA-AG use). We used multivariate regression to assess the association of GABA-AG use and successful functional recovery, defined as reaching, between admission and discharge, the minimal clinically important difference (MCID) of 22 points on the global Functional Independence Measure (FIM). Secondary analyses were the associations of GABA-AG with cognitive and motor FIM MCID and constant GABA-AG exposure (24h/24 GABA-AG) with global, cognitive and motor FIM MCID. A new estimation of the MCID was performed with the standard error of measurement. RESULTS: Reaching the global FIM MCID was associated with GABA-AG use (adjusted odds ratio [aOR] 0.54 [95% CI 0.31-0.91], P=0.02) as well as 24h/24 GABA-AG use (aOR 0.25 [0.08-0.83]; P=0.02). Furthermore, GABA-AG and 24h/24 GABA-AG use was inversely but not always significantly associated with reaching the cognitive FIM MCID (aOR 0.56, P=0.07; aOR 0.26, P=0.06, respectively) and motor FIM MCID (aOR 0.51, P=0.07; aOR 0.13, P=0.01, respectively). The estimated MCID was 19 for global FIM, 4 for cognitive FIM, and 16 for motor FIM. CONCLUSIONS: GABA-AG use is associated with not reaching successful functional recovery during stroke rehabilitation. Randomised trials are needed to formally establish the potential deleterious effect of GABA-AG use on functional recovery.

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)

Psoriasis vulgaris and human leukocyte antigens.

BACKGROUND: Psoriasis vulgaris is a skin disease with a complex immunological and genetic background, triggered by environmental factors. The association of human leukocyte antigens (HLA) and psoriasis has long been reported on population and familial studies. OBJECTIVES: To review and discuss studies on psoriasis vulgaris and HLA, in Caucasian and non-Caucasian populations. METHODS: The major population studies on psoriasis vulgaris and the associated HLA antigens and alleles are described and discussed based on a review of the current literature. RESULTS: Population studies demonstrate the presence of different HLA specificities as well as extended haplotypes in patients with psoriasis, when compared to controls. Some alleles occur in a lower frequency in patients with psoriasis, indicating they could be protection alleles. In all studies which HLA class I was typed, Cw6 or Cw*0602 was present in a significant frequency in patients with psoriasis, mainly when early onset and positive family history were considered. HLA-DRB1*0701 was also present in a higher frequency in patients in different populations. CONCLUSIONS: Different antigens and alleles from both HLA classes I and II were seen in a significantly higher frequency in patients with psoriasis vulgaris. HLA Cw*0602 and DRB1*0701 were represented in different reports, and the former was related mainly to psoriasis type I.

Clinical and serological follow-up studies of endemic pemphigus foliaceus (fogo selvagem) in Western Parana, Brazil (2001-2002).

BACKGROUND: Fogo selvagem (FS) has been described in several regions of Brazil, including the Western regions of the state of Parana. In 1990, Empinotti et al. reported case studies of 213 patients with FS that were collected from 1976 to 1988. The same author (J.C.E.) has observed that the frequency of cases in these regions of Parana has decreased. OBJECTIVES: The purpose of this study was to clinically and serologically evaluate a small group of the patients originally reported in 1990 and compare data with a group of control individuals. These patients were treated at the onset of the disease with systemic steroids. PATIENTS AND METHODS: Patients with FS, their unaffected relatives (n = 80) and genetically unrelated controls (n = 15) were identified during a field study from 1 May 2001 to 30 June 2002. Sera from nine patients with FS and six normal controls that were collected in the 1976-1988 evaluation were available for this study. The sera were tested by indirect immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and immunoprecipitation using recombinant human desmoglein 1 (Dsg1). RESULTS: Only 16 of the originally identified 213 patients with FS were found during the field studies. Thirteen of the 16 patients were in clinical and serological remission; 20% of normal controls (19 of 95) were positive in the Dsg1 ELISA. The majority of these subjects (17 of 19) were genetically related to FS patients. Six normal controls that were positive in the Dsg1 ELISA in the original survey were found to be negative or weakly positive in this evaluation. CONCLUSION: The reduced frequency of positive serological markers of disease in patients and normal controls from Western Parana, as well as the absence of recurrent disease in previously identified patients, suggest that environmental antigenic stimulation of the population at risk may have decreased in recent years.

Pseudoaneurisma de arteria esplénica como complicación de pancreatitis / Pseudoaneurysm of splenic artery as complication of pancreatitis

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Hematoma retroperitoneal con neuropatía del femoral, ¿actitud conservadora o quirúrgica? / Retroperitoneal hematoma with femoral neuropathy, conservative or surgical posture?

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Correlation between HLA and pityriasis rosea susceptibility in Brazilian blacks.

OBJECTIVES: The human leucocyte antigen (HLA) has been related to susceptibility factors in several diseases. This study aimed to determine the potential genetic susceptibility of patients with pityriasis rosea (PR) through HLA molecular typing analysis. METHODS: The method of choice was polymerase chain reaction with sequence-specific primers (PCR-SSP) using low-resolution typing kits, with determination of the alleles class I (HLA-A, HLA-B and HLA-C) and class II (HLA-DRB1, DRB3, DRB4, DRB5 and DQB1) performed in 30 Afro-Brazilian PR-diagnosed patients and 45 healthy individuals as the control group (PR-C). RESULTS: Analysis of the HLA typing results showed that the relative risk (RR) of 4.00 [95% confidence interval (95% CI) 1.20-13.28, two-tailed P = 0.018] for allele HLA-DQB1*04 class II, detected in 33.3% of PR patients, was significant. By contrast, in the control group only 11.1% of subjects had that allele. Three out of six B*51 alleles and three out of six B*53 alleles detected in PR patients were found, together with the allele DQB1*04. CONCLUSION: We suggest that alleles DQB1*04 may be involved in the genetic susceptibility of PR based on the significant predominance of those alleles observed in the black PR patients. We also recommend that more studies are conducted on populations of other ethnic origins, preferentially with higher resolution techniques of DNA typing.

Comparative biochemistry of human skin: glycosaminoglycans from different body sites in normal subjects and in patients with localized scleroderma.

OBJECTIVES: The aim of this investigation is to compare the relative proportions of disaccharides of chondroitinase-digestible glycosaminoglycans (GAGs) among the different body sites in control human skin and in the skin lesions of patients with localized scleroderma. METHODS: The disaccharide relative proportions were determined using high-performance liquid chromatography (HPLC). RESULTS: DeltaDi-4S, the main disaccharide unit of dermatan sulphate (DS), was the major skin GAG disaccharide (approximately 70% of the total) in control skin among all different body sites studied here. In scleroderma there was an increase in the relative proportion of both deltaDi-HA, the main disaccharide unit of hyaluronic acid (HA), and deltaDi-diS(B) (alpha-deltaUA(2SO4)-1-->3-GalNAc(4SO4)), derived from DS, and a decrease in deltaDi-4S, as compared with the uninvolved skin or the site-matched control skin. CONCLUSION: DS is the major GAG species in normal skin from different body sites. In addition, our results suggest a decrease and also a structural change in DS and an increase in the proportion of HA in scleroderma skin.

Type I and type III collagens in cutaneous mucinosis.

Cutaneous mucinoses are a heterogeneous group of diseases characterized by the focal or diffuse dermal deposition of glycosaminoglycans. The histopathologic examination of many cutaneous mucinoses reveals that the collagen fibers are fragmented. We wanted to characterize the type I (COL1) and type III (COL3) collagen distribution in skin biopsy specimens of patients with cutaneous mucinosis. The diagnosis of mucinosis was based on a modification of the classification by Rongioletti and Rebora: four patients had familial papulonodular mucinosis: four had papular mucinosis, one of which was associated with myxedema and one had scleromyxedema; and one had focal mucinosis. We performed anti-type I and type III collagens immunolabeling on frozen sections. Immunofluorescence for COL1 was increased in the superficial dermis of 2/4 familial papulonodular mucinosis, in 5/5 of papular mucinosis, and in scleromyxedema and focal mucinosis cases. The mid-dermis showed intense staining for COL1 at the periphery of collagen bundles and, in three cases of familial papulonodular mucinosis and two cases of papular mucinosis, a lacy appearance. The superficial dermis of familial papulonodular mucinosis specimens and of papular mucinosis + myxedema, scleromyxedema, and focal mucinosis specimens had decreased COL3 staining. The mid-dermis showed a more prominent fibrillar staining at the periphery of the collagen bundles, and two cases of papular mucinosis showed intense labeling for COL3. Both COL1 and COL3 distributions are altered in cutaneous mucinosis. An intense labeling with COL1 is predominantly found in the superficial layer of cutaneous mucinosis. Cases of FTP revealed decreased COL3 reactivity at the superficial layer.

Alloantibody from a patient with severe von Willebrand disease inhibits von Willebrand factor-FVIII interaction.

The aim of this study was to analyze the ability of an alloantibody from a patient with severe von Willebrand disease (vWD) to interfere with the vWF domain for FVIII, to inhibit factor VIII (FVIII), and to compare it with a rabbit polyclonal antibody. The vWF domain for binding to FVIII was assayed by a method previously described but using recombinant FVIII (r-FVIII, Kogenate), which contains no vWF, instead of Hemofil M (HM). Rabbit or human antibodies towards FVIII (FVIII-Ab) were analyzed using microtiter wells with immobilized r-FVIII through a monoclonal anti-FVIII antibody and an ELISA method. IgG from plasma of a patient with hemophilia A and FVIII inhibitor was used as a positive control. Normal human and rabbit IgGs were included as negative controls. Human vWD alloantibody IgG and the rabbit anti-vWF antibody IgG reacted with immobilized normal vWF, inhibiting its binding to r-FVIII in a dose-dependent manner, which suggests that it is specific. Normal human IgG fraction, as well as nonspecific rabbit IgG, did not interfere with this binding at all. The monoclonal antibody used in this assay to immobilize vWF did not alter this interaction at all. Human vWD alloantibody IgG and the rabbit antibody against vWF showed a partial inhibitory activity to plasma FVIII as well as r-FVIII. The inhibition reached a plateau with residual FVIII activity. FVIII-Ab were not detected in human alloantibody or in rabbit antibody preparations. In contrast, hemophiliac FVIII inhibitor showed FVIII-AB. This human vWD alloantibody behaves like polyclonal heterologous antibodies, and their inhibition of FVIII seems to be nonspecific due to a steric hindrance mechanism provided that both have no FVIII antibodies.