Hospital Universitario del Valle ESE
Hospital / health systemSantiago de Cali, Colombia
Research output, citation impact, and the most-cited recent papers from Hospital Universitario del Valle ESE (Colombia). Aggregated across the NobleBlocks index of 300M+ scholarly works.
Top-cited papers from Hospital Universitario del Valle ESE
BACKGROUND: Zika virus (ZIKV) infection has been linked to the Guillain-Barré syndrome. From November 2015 through March 2016, clusters of cases of the Guillain-Barré syndrome were observed during the outbreak of ZIKV infection in Colombia. We characterized the clinical features of cases of Guillain-Barré syndrome in the context of this ZIKV infection outbreak and investigated their relationship with ZIKV infection. METHODS: A total of 68 patients with the Guillain-Barré syndrome at six Colombian hospitals were evaluated clinically, and virologic studies were completed for 42 of the patients. We performed reverse-transcriptase-polymerase-chain-reaction (RT-PCR) assays for ZIKV in blood, cerebrospinal fluid, and urine, as well as antiflavivirus antibody assays. RESULTS: A total of 66 patients (97%) had symptoms compatible with ZIKV infection before the onset of the Guillain-Barré syndrome. The median period between the onset of symptoms of ZIKV infection and symptoms of the Guillain-Barré syndrome was 7 days (interquartile range, 3 to 10). Among the 68 patients with the Guillain-Barré syndrome, 50% were found to have bilateral facial paralysis on examination. Among 46 patients in whom nerve-conduction studies and electromyography were performed, the results in 36 patients (78%) were consistent with the acute inflammatory demyelinating polyneuropathy subtype of the Guillain-Barré syndrome. Among the 42 patients who had samples tested for ZIKV by RT-PCR, the results were positive in 17 patients (40%). Most of the positive RT-PCR results were in urine samples (in 16 of the 17 patients with positive RT-PCR results), although 3 samples of cerebrospinal fluid were also positive. In 18 of 42 patients (43%) with the Guillain-Barré syndrome who underwent laboratory testing, the presence of ZIKV infection was supported by clinical and immunologic findings. In 20 of these 42 patients (48%), the Guillain-Barré syndrome had a parainfectious onset. All patients tested were negative for dengue virus infection as assessed by RT-PCR. CONCLUSIONS: The evidence of ZIKV infection documented by RT-PCR among patients with the Guillain-Barré syndrome during the outbreak of ZIKV infection in Colombia lends support to the role of the infection in the development of the Guillain-Barré syndrome. (Funded by the Bart McLean Fund for Neuroimmunology Research and others.).
BACKGROUND: To validate a new practical Sepsis Severity Score for patients with complicated intra-abdominal infections (cIAIs) including the clinical conditions at the admission (severe sepsis/septic shock), the origin of the cIAIs, the delay in source control, the setting of acquisition and any risk factors such as age and immunosuppression. METHODS: The WISS study (WSES cIAIs Score Study) is a multicenter observational study underwent in 132 medical institutions worldwide during a four-month study period (October 2014-February 2015). Four thousand five hundred thirty-three patients with a mean age of 51.2 years (range 18-99) were enrolled in the WISS study. RESULTS: Univariate analysis has shown that all factors that were previously included in the WSES Sepsis Severity Score were highly statistically significant between those who died and those who survived (p < 0.0001). The multivariate logistic regression model was highly significant (p < 0.0001, R2 = 0.54) and showed that all these factors were independent in predicting mortality of sepsis. Receiver Operator Curve has shown that the WSES Severity Sepsis Score had an excellent prediction for mortality. A score above 5.5 was the best predictor of mortality having a sensitivity of 89.2 %, a specificity of 83.5 % and a positive likelihood ratio of 5.4. CONCLUSIONS: WSES Sepsis Severity Score for patients with complicated Intra-abdominal infections can be used on global level. It has shown high sensitivity, specificity, and likelihood ratio that may help us in making clinical decisions.
Treatment for vitiligo is difficult and prolonged. Nevertheless, at present considerable knowledge accumulated during several decades on the pathogenic mechanisms, revealed important clues for designing new strategies to improve vitiligo depigmentation. With available medical therapies, high repigmentation percentages mostly on facial and neck lesions are achieved, although they are less effective on trunk and limbs and poor on the acral parts of the extremities. Narrow band UVB and psoralens and UVA are the two most important treatments for generalized vitiligo affecting more than 10-20% of the cutaneous surface, and topical corticosteroids, or calcineurin inhibitors are the most valuable treatments for localized vitiligo. Persistence of achieved regimentation is variable and an undefined percentage of patients may have variable recurrence. When vitiligo becomes refractory, surgical methods may improve depigmentation as effectively as with medical therapy; in segmental (unilateral) or long standing, non-segmental (bilateral) stable vitiligo, repigmentation with surgical methods is usually permanent.
Autologous minigrafting has been reported as an effective method for repigmenting diverse types of stable leukoderma. A group of 22 patients with localized vitiligo, 17 segmental and five focal, who are under treatment with this method, are described. Thirteen patients attained a 90% to 100% repigmentation, two others achieved a partial improvement, and five patients had a positive test area indicating the possibility of repigmentation by means of this procedure. Only two patients had a negative test with minigrafts and, consequently, they were left untreated. Autologous minigrafting is suggested as an alternative for treating localized vitiligo, particularly when other medical therapeutic attempts have failed in repigmenting this often refractory condition.
In an open study, 17 patients (16 women, 1 man) with refractory or severe rheumatoid arthritis were treated with thalidomide. Two withdrew from the study in the first weeks. Thirteen patients received 531 +/- 63 mg/day of thalidomide for 18.8 +/- 8.8 weeks; in 2 the dose was 300 mg/day during 62 and 65 weeks. Seven patients attained complete remission, 5 partial remission, and the last 3 no improvement at all. Remissions lasted 6 years in 1 patient, 2 years in 3, 1 year in one, and varied between 8 months and 8 weeks in 7. After relapse, 5 patients received a 2nd course of treatment and attained remission again. This lasted 24, 10, and 9 months in 3; two are taking 100 mg/day of thalidomide as a maintenance dose and remain asymptomatic after 36 and 30 months. The side effects were drowsiness, constipation, hard swelling of the lower limbs, erythema of the face and limbs with local pruritus or burning sensation, hair loss, cough, nasal obstruction, fever, and skin and mucosal dryness. In 8 patients there was mild eosinophilia (less than 10%) and in 2 leukopenia. A 33-year-old woman showed amenorrhea up to 2 months after stopping treatment. After a 2nd course of treatment, 2 patients developed peripheral sensory neuropathy, which resolved spontaneously in 6 months. We believe these findings justify controlled trials with this agent.
A retrovirus involvement in the etiology of certain neurological diseases is currently an area of intense interest. Tropical spastic paraparesis and other chronic progressive myelopathies have been clearly associated with increased serum and cerebrospinal fluid antibody titers to human T-lymphotropic virus type I; however, little is known about the cellular immune response. In the present study, activated T-lymphocytes were found in the peripheral blood of patients with this disorder. There were increased numbers of large CD3-positive cells that also expressed histocompatibility leukocyte Class II (DR) and interleukin 2-receptor molecules. In addition, a significantly elevated spontaneous lymphoproliferative response was demonstrated in all patients. This is consistent with the known in vitro effects of human T-lymphotropic virus type I. In one patient, a defect in the generation of measles virus-specific cytotoxic T cells was identified. These observations indicate abnormalities of the cellular immune response in tropical spastic paraparesis.
INTRODUCTION: Infections caused by carbapenem-resistant Enterobacteriaceae are a public health problem associated with higher mortality rates, longer hospitalization and increased healthcare costs. We carried out a study to describe the characteristics of patients with carbapenemase-producing Enterobacteriaceae (CPE) and non-CPE bloodstream infection (BSI) from Latin American hospitals and to determine the clinical impact in terms of mortality and antibiotic therapy. METHODS: Between July 2013 and November 2014, we conducted a multicenter observational study in 11 hospitals from 7 Latin American countries (Argentina, Colombia, Ecuador, Guatemala, Mexico, Peru, Venezuela). Patients with BSI caused by Enterobacteriaceae were included and classified either as CPE or non-CPE based on detection of blaKPC, blaVIM, blaIMP, blaNDM and blaOXA-48 by polymerase chain reaction. Enrolled subjects were followed until discharge or death. Demographic, microbiological and clinical characteristics were collected from medical records. Both descriptive and inferential statistics were used to analyze the information. RESULTS: A total of 255 patients with Enterobacteriaceae BSI were included; CPE were identified in 53 of them. In vitro non-susceptibility to all screened antibiotics was higher in the patients with CPE BSI, remaining colistin, tigecycline and amikacin as the most active drugs. Combination therapy was significantly more frequent in the CPE BSI group (p < 0.001). The most common regimen was carbapenem + colistin or polymyxin B. The overall mortality was 37% (94/255). Overall and attributable mortality were significantly higher in patients with CPE BSI (p < 0.001); however, we found that patients with CPE BSI who received combination therapy and those who received monotherapy had similar mortality. After multivariate adjustment, CPE BSI (adjusted odds ratio [aOR] 4; 95% confidence interval [CI] 1.7-9.5; p = 0.002) and critical illness (aOR 6.5; 95% CI 3.1-13.7; p < 0.001) were independently associated with in-hospital mortality. CONCLUSIONS: This study provides valuable data on the clinical characteristics and mortality risk factors in patients with CPE BSI. We determined that CPE infection is an independent mortality predictor and thus Latin American hospitals should perform campaigns on prevention and control of CPE BSI.
Fragile X Syndrome (FXS) is a genetic disease due to a CGG trinucleotide expansion, named full mutation (greater than 200 CGG repeats), in the fragile X mental retardation 1 gene locus Xq27.3; which leads to an hypermethylated region in the gene promoter therefore silencing it and lowering the expression levels of the fragile X mental retardation 1, a protein involved in synaptic plasticity and maturation. Individuals with FXS present with intellectual disability, autism, hyperactivity, long face, large or prominent ears and macroorchidism at puberty and thereafter. Most of the young children with FXS will present with language delay, sensory hyper arousal and anxiety. Girls are less affected than boys, only 25% have intellectual disability. Given the genomic features of the syndrome, there are patients with a number of triplet repeats between 55 and 200, known as premutation carriers. Most carriers have a normal IQ but some have developmental problems. The diagnosis of FXS has evolved from karyotype with special culture medium, to molecular techniques that are more sensitive and specific including PCR and Southern Blot. During the last decade, the advances in the knowledge of FXS, has led to the development of investigations on pharmaceutical management or targeted treatments for FXS. Minocycline and sertraline have shown efficacy in children.
In an open study, oral administration of thalidomide to 7 female patients with classic or definite rheumatoid arthritis, in doses ranging from 6.9 to 15 mg/kg/day, led to clinical improvement within several weeks. In 4 women, remission lasted long after discontinuation of the drug. All patients showed normalization or marked reduction of the erythrocyte sedimentation rate, and several showed a significant decrease in rheumatoid factor titer. Adverse side effects included drowsiness, constipation, and edema of the lower limbs, which disappeared after discontinuation of the drug.
Advanced stages of mycobacterial diseases such as leprosy and tuberculosis are characterized by a loss of T-cell function. The basis of this T-cell dysfunction is not well understood. The present report demonstrates major alterations in the expression of signal transduction molecules in T cells of leprosy patients. These alterations were most frequently observed in lepromatous leprosy (LL) patients. Of 29 LL patients, 69% had decreased T-cell receptor zeta-chain expression, 48% had decreased p56(lck) tyrosine kinase, and 63% had a loss of nuclear transcription factor NF-kappaB p65. An electrophoretic mobility shift assay with the gamma interferon core promoter region revealed a loss of the Th1 DNA-binding pattern in LL patients. In contrast, tuberculoid leprosy patients had only minor signal transduction alterations. These novel findings might improve our understanding of the T-cell dysfunction observed in leprosy and other infectious diseases and consequently might lead to better immunologic evaluation of patients.
The masticatory system is a complex and highly organized group of structures, including craniofacial bones (maxillae and mandible), muscles, teeth, joints, and neurovascular elements. While the musculoskeletal structures of the head and neck are known to have a different embryonic origin, morphology, biomechanical demands, and biochemical characteristics than the trunk and limbs, their particular molecular basis and cell biology have been much less explored. In the last decade, the concept of muscle-bone crosstalk has emerged, comprising both the loads generated during muscle contraction and a biochemical component through soluble molecules. Bone cells embedded in the mineralized tissue respond to the biomechanical input by releasing molecular factors that impact the homeostasis of the attaching skeletal muscle. In the same way, muscle-derived factors act as soluble signals that modulate the remodeling process of the underlying bones. This concept of muscle-bone crosstalk at a molecular level is particularly interesting in the mandible, due to its tight anatomical relationship with one of the biggest and strongest masticatory muscles, the masseter. However, despite the close physical and physiological interaction of both tissues for proper functioning, this topic has been poorly addressed. Here we present one of the most detailed reviews of the literature to date regarding the biomechanical and biochemical interaction between muscles and bones of the masticatory system, both during development and in physiological or pathological remodeling processes. Evidence related to how masticatory function shapes the craniofacial bones is discussed, and a proposal presented that the masticatory muscles and craniofacial bones serve as secretory tissues. We furthermore discuss our current findings of myokines-release from masseter muscle in physiological conditions, during functional adaptation or pathology, and their putative role as bone-modulators in the craniofacial system. Finally, we address the physiological implications of the crosstalk between muscles and bones in the masticatory system, analyzing pathologies or clinical procedures in which the alteration of one of them affects the homeostasis of the other. Unveiling the mechanisms of muscle-bone crosstalk in the masticatory system opens broad possibilities for understanding and treating temporomandibular disorders, which severely impair the quality of life, with a high cost for diagnosis and management.
Two patients with Adams-Oliver syndrome and congenital cardiac malformations are described. A literature review revealed at 13.4% occurrence of congenital cardiac malformations in individuals with Adams-Oliver syndrome, suggesting that cardiac anomalies are a frequent manifestation of this syndrome. All patients with Adams-Oliver syndrome (aplasia cutis congenita and terminal digital anomalies) should be evaluated for cardiac anomalies.
Abstract A multi‐national, hospital‐based, case‐control study was conducted to evaluate the possible relationships of steroid contraceptives to 6 neoplasms. Based on data from 122 newly diagnosed cases of primary liver cancer and 802 matched controls, the relative risk of liver cancer in women who had ever used combined oral contraceptives was estimated to be 0.71 (95% Cl 0.4–1.2). No consistent trend in risk with months of use or time since first or last use was observed. Separate analyses also revealed no association between use of combined oral contraceptives and hepatocellular carcinoma (RR = 0.60) or cholangiocarcinoma (RR = 1.22). Most women in this study came from areas in which hepatitis B is endemic and rates of liver cancer are relatively high, and in most cases use of oral contraceptives was of short duration. These results provide no evidence that short‐term use of oral contraceptives enhances risk of liver cancer in countries where the determinants of this disease are similar to those observed in the countries where this study was conducted.
BACKGROUND: Dopa-negative, inactive melanocytes, present in the middle portion of the hair follicle, but also in hair bulbs, have been reported as a source of pigment cells, when repopulation of epidermal melanocytes occurs. A melanocyte reservoir in these anatomical sites has been suggested. Our objective was to investigate the ability of the lower third of the hair follicle (hair bulb) to repigment achromic skin in vitiligo. METHODS: Scalp hair bulbs were transplanted within leukodermic areas in 10 patients with vitiligo. RESULTS: Repigmentation around the grafts was suitable for evaluation in four cases. Dopa-positive (+) cells were seen in the epidermal basal cell layer of the repigmented areas. CONCLUSIONS: Although these findings were observed only in a few patients, they suggest that melanocytes from the implanted lower third portion of the hair follicle (hair bulb) act as a reservoir in this anatomic location and are able to migrate and repigment achromic areas in vitiligo.
The technique known as autologous minigrafting is reviewed. This procedure has proven useful and reliable for repigmenting diverse types of leukoderma. A few refinements of this technique are described. These refinements were used in six patients who were successfully repigmented. Causes of pigment loss in these cases included thermal burns, contact with monobenzyl ether of hydroquinone, chronic discoid lupus erythematosus, and segmental vitiligo.
BACKGROUND: Vitiligo therapy is difficult. Depending on its clinical presentation, unilateral or bilateral vitiligo lesions respond well with different repigmentation rates, according to age, affected anatomic area, extension of lesions, time at onset, timing of depigmentation spread, and other associated factors. When stable and refractory to medical treatment, vitiligo lesions may be treated by implanting pigment cells on depigmented areas. OBJECTIVE: To describe the main events of depigmentation and the fundamentals of surgical techniques for repigmenting vitiligo by implanting noncultured cellular or tissue grafts, in vitro cultured epidermis-bearing pigment cells, or melanocyte suspensions. METHODS: A description of the available techniques for repigmentation of vitiligo is done, emphasizing the most important details of each procedure to obtain the best repigmentation and minimize side effects. RESULTS: With most of these techniques, adequate repigmentation is obtained, although there are limitations when applying some methods to clinical practice. CONCLUSIONS: Restoration of pigmentation may be accomplished with all available surgical procedures in most anatomic locations, but they are of little value for acral areas. Unilateral vitiligo responds well in a high proportion of patients, and bilateral disease may also respond when stable. Appropriate patient selection is important to achieve the best results.
To the Editor: In the United States, the dissemination of a major clone of community-associated methicillin-resistant Staphylococcus aureus (MRSA), designated USA300, and outbreaks of vancomycin-resistant Enterococcus faecalis (VREF) have been described.1,2 Community-associated MRSA infections emerged in Colombia in 2005,3 and a total of 15 community-associated MRSA infections were documented in four cities in 2006 and 2007. All the patients presented with severe skin and soft-tissue infections, which were often complicated by necrotizing fasciitis, bacteremia, paraspinal abscess, arthritis, or meningitis, with a mortality rate of 20%. The first known Colombian VREF isolate was recovered in a hospital in Bogota in . . .
Contribution over time of human papillomavirus (HPV) types in human cancers has been poorly documented. Such data is fundamental to measure current HPV vaccines impact in the years to come. We estimated the HPV type-specific distribution in a large international series of invasive cervical cancer (ICC) over 70 years prior to vaccination. Paraffin embedded ICC cases diagnosed between 1940 and 2007 were retrieved from eleven countries in Central-South America, Asia and Europe. Included countries reported to have low-medium cervical cancer screening uptake. Information on age at and year of diagnosis was collected from medical records. After histological confirmation, HPV DNA detection was performed by SPF-10/DEIA/LiPA25 (version1). Logistic regression models were used for estimating the adjusted relative contributions (RC) of HPV16 and of HPV18 over time. Among 4,771 HPV DNA positive ICC cases, HPV16 and HPV18 were the two most common HPVs in all the decades with no statistically significant variations of their adjusted-RC from 1940-59 to 2000-07 (HPV16-from 61.5 to 62.1%, and HPV18-from 6.9 to 7.2%). As well, the RC of other HPV types did not varied over time. In the stratified analysis by histology, HPV16 adjusted-RC significantly increased across decades in adenocarcinomas. Regarding age, cases associated to either HPV16, 18 or 45 were younger than those with other HPV types in all the evaluated decades. The observed stability on the HPV type distribution predicts a high and stable impact of HPV vaccination in reducing the cervical cancer burden in future vaccinated generations.
OBJECTIVE: To characterize the epidemiological, clinical, and histopathological features of patients with cancer who develop widespread polymorphic and pruritic skin lesions following radiotherapy. PATIENTS, DESIGN, AND INTERVENTIONS: During phase 1, epidemiological and clinical features of 103 patients with cancer, 83 treated with radiotherapy (71 women and 12 men) and 20 controls who did not undergo radiotherapy (16 women and 4 men), were explored during 3 months (October 1995 to January 1996). During phase 2, in 30 additional patients with cancer who were treated with telecobalt or linear accelerator, 18 with skin lesions (15 women and 3 men) and 12 without lesions (10 women and 2 men), the following were investigated: (1) hematoxylin-eosin-stained sections for routine histopathological examination and direct immunofluorescence, and lymphocytic markers; (2) blood, skin, and primary tumor eosinophilia; and (3) the presence of antiepidermal autoantibodies. Patients were examined during 5 months (February 1996 to June 1996). SETTING: A dermatology department at a university hospital. RESULTS: During phase 1, 14 (17%) of the 83 patients undergoing radiotherapy developed an eruption. Acral excoriations, erythematous papules, vesicles, and bullae were the most frequent lesions. During phase 2, in 18 patients, a superficial and deep lymphocytic perivascular infiltrate with numerous eosinophils, intraepidermal and interstitial eosinophilic infiltrates, eosinophilic panniculitis, IgM and C3 perivascular deposits, and slightly predominant CD4+ cells were observed. No antiepidermal autoantibodies were found. CONCLUSIONS: The clinical, histopathological, and immunopathologic features in patients with cancer undergoing radiotherapy are described. To our knowledge, this condition has not been well characterized. Because of its unique presentation, the denomination "eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy" is suggested.
A method of repigmenting some leukodermas by transplantation of minigrafts of normally pigmented, autologous skin into them is described. Such grafts in addition to retaining their pigment stimulate repigmentation around them by migration of melanocytes and spread of pigment from the grafts. Three patients, one with piebaldism, another with leukoderma from monobenzyl ether of hydroguinone, and a third with depigmentation following healing of a burn enjoyed successful and cosmetically acceptable repigmentation from practice of the method.