Depression and Anxiety after Stroke in Young Adult Filipinos.

BACKGROUND AND OBJECTIVES: Young adult patients may suffer from poststroke depression (PSD) and anxiety. Few studies have evaluated these important psychiatric conditions that may lead to adverse outcomes in young adults. We aimed to determine the prevalence of PSD and anxiety as well as to identify their predictors in a population of young Filipino adults (18-49 years old). METHODS: We performed a cross-sectional epidemiologic study in the largest tertiary hospital in the Philippines. The study involved the administration of a structured survey tool and review of medical records. The Hospital Anxiety and Depression Score - Pilipino version (HADS-P) was used to screen for anxiety and depression. Multivariable logistic regression analysis was performed to determine significant socio-economic and clinical risk factors of PSD and anxiety. RESULTS: 114 young adult stroke patients were included. The prevalence of depression was 20.2% while that of anxiety was 34.2%. Significant predictors of PSD were the presence of anxiety (OR 1.84; CI 1.05-3.22), lower mRS scores (mRS 3-5 OR 5.52; 95% CI 1.09-8.03) and diabetes (OR 2.09; 95% CI 1.67-6.26). Meanwhile, significant predictors of poststroke anxiety included depression (OR 7.5; 95% CI 5.02-21.94) and dependency (Barthel Index scores 95-100; OR 0.94; 95% CI 0.89-0.99). Relationship status, educational attainment, stroke subtype and location were not found to be significant predictors of PSD and anxiety. CONCLUSION: A significant proportion of young adults suffered from depression and anxiety after stroke. Clinicians should be aware of these psychiatric conditions that influence outcomes and quality of life of young adults with stroke.

Angiogenic mechanisms of human dental pulp and their relationship with substance P expression in response to occlusal trauma.

Angiogenesis is the formation of new blood vessels based on a pre-existing vasculature. It comprises two processes, sprouting of endothelial cells and the division of vessels due to abnormal growth of the microvasculature. It has been demonstrated that substance P (SP) can induce angiogenesis either by modulating endothelial cell growth (direct mechanism) or by attracting cells with angiogenic potential to the injury site (indirect mechanism). Therefore, the purpose of this article is to review the angiogenic mechanisms that regulate mineralized tissue formation in human dental pulp tissue and their relationship with SP expression as a defence response to stimuli such as the masticatory function and occlusal trauma. Articles included in this review were searched in PubMed, Scopus and ISI Web of Science databases, combining the following keywords: human dentine pulp, angiogenesis, angiogenic growth factors, neuropeptides, substance P, neurogenic inflammation, dentine matrix, dentinogenesis, occlusal trauma and dental occlusion. It is concluded that human dental pulp tissue responds to occlusal trauma and masticatory function with a neurogenic inflammatory phenomenon in which SP plays an important role in the direct and indirect mechanisms of angiogenesis by the action evoked via NK1 receptors at different cells, such as fibroblasts, endothelial and inflammatory cells, leading to new blood vessel formation which are needed to stimulate mineralized tissue formation as a defence mechanism.

Bloodstream infections caused by Escherichia coli producing AmpC ß-lactamases: epidemiology and clinical features.

The aim of the study was to investigate the epidemiology and clinical features of bloodstream infections due to Escherichia coli producing AmpC ß-lactamases (AmpC-Ec-BSI). In a multi-centre case-control study, all third-generation-cephalosporin-resistant Escherichia coli BSI (3GC-Ec-BSI) isolates were analysed. Acquired bla AmpC (bla ac-AmpC) detection was done by polymerase chain reaction (PCR) and sequencing. Chromosomal bla AmpC (bla c-AmpC) expression was quantified by real-time PCR. Cases were patients with AmpC-Ec-BSI. Controls were patients with cephalosporin-susceptible E. coli BSI, matched 1:1 by sex and age. Demographics, comorbidities, intrinsic and extrinsic risk factors for antimicrobial resistance, clinical presentation and outcomes were investigated. Among 841 E. coli BSI, 17 were caused by AmpC-Ec (2 %). Eleven isolates (58.8 %) had bla ac-AmpC and six were bla c-AmpC overproducers. The mean age of cases was 66.2 years and 71 % were men. Cases were more frequently healthcare-related (82 vs. 52 % controls, p < 0.05) and presented more intrinsic and extrinsic risk factors. At least one risk factor was present in 94.1 % of cases vs. 41.7 % of controls (p = 0.002). Severity and length of stay (LOS) were higher among cases (mean Pitt Score 2.6 vs. 0.38 in controls, p = 0.03; LOS 17.5 days vs. 6 in controls, p = 0.02). Inappropriate empirical therapy (IET) was administered to 70.6 % of cases and 23.5 % of controls (p < 0.003). No differences were found in terms of cure rate at the 14th day and mortality. Bloodstream infections due to AmpC-Ec (mostly plasmid-mediated) are infrequent in our area. AmpC-Ec-BSI affects mainly patients with intrinsic risk factors and those with previous antibiotic exposure. A high proportion received IET.

Ex vivo construction of a novel model of bioengineered bladder mucosa: A preliminary study.

OBJECTIVE: To generate and to evaluate ex vivo a novel model of bioengineered human bladder mucosa based on fibrin-agarose biomaterials. METHODS: We first established primary cultures of stromal and epithelial cells from small biopsies of the human bladder using enzymatic digestion and selective cell culture media. Then, a bioengineered substitute of the bladder lamina propria was generated using cultured stromal cells and fibrin-agarose scaffolds, and the epithelial cells were then subcultured on top to generate a complete bladder mucosa substitute. Evaluation of this substitute was carried out by cell viability and histological analyses, immunohistochemistry for key epithelial markers and transmission electron microscopy. RESULTS: The results show a well-configured stroma substitute with a single-layer epithelium on top. This substitute was equivalent to the control bladder mucosa. After 7 days of ex vivo development, the epithelial layer expressed pancytokeratin, and cytokeratins CK7, CK8 and CK13, as well as filaggrin and ZO-2, with negative expression of CK4 and uroplakin III. A reduction of the expression of CK8, filaggrin and ZO-2 was found at day 14 of development. An immature basement membrane was detected at the transition between the epithelium and the lamina propria, with the presence of epithelial hemidesmosomes, interdigitations and immature desmosomes. CONCLUSIONS: The present results suggest that this model of bioengineered human bladder mucosa shared structural and functional similarities with the native bladder mucosa, although the epithelial cells were not fully differentiated ex vivo. We hypothesize that this bladder mucosa substitute could have potential clinical usefulness after in vivo implantation.

Aetiology of community-acquired pneumonia among adults in an H1N1 pandemic year: the role of respiratory viruses.

This study aimed to determine the aetiology of community-acquired pneumonia (CAP) by adding polymerase chain reaction (PCR) to conventional methods and to describe the clinical and laboratory features between patients with bacterial pneumonia (BP) and viral pneumonia (VP). Adults with CAP admitted from November 2009 to October 2010 were included. Demographics, comorbidities, severity and clinical features were recorded. Conventional microbiological methods included blood and sputum cultures, acute and convalescent serologic samples, and antigen urinary detection. New methods included multiplex PCR for Mycoplasma pneumoniae, Legionella pneumophila, Chlamydophila pneumoniae, Bordetella pertussis and 15 respiratory viruses. A total of 169 patients were included. Using conventional methods, we identified a pathogen in 51 % of cases. With PCR, up to 70 % of cases had an aetiological diagnosis. Forty-five patients had BP (34 %), 22 had VP (17 %) and 25 (19 %) had co-infection (BP and VP). Pneumococci and respiratory syncytial virus (RSV) were the most frequently identified pathogens. Procalcitonin (PCT) and C-reactive protein (CRP) median values were significantly higher in BP than in VP patients. Shaking chills, higher CURB score and shock were significantly more frequent in BP. A viral infection was identified in more than one-third of patients with CAP. Clinical and laboratory features could help to differentiate between VP and BP and to guide empirical therapy.

SEA 2022 Standards for Global Control of Cardiovascular Risk. / Estándares SEA 2022 para el control global del riesgo cardiovascular.

One of the objectives of the Spanish Society of Arteriosclerosis is to contribute to better knowledge of vascular disease, its prevention and treatment. It is well known that cardiovascular diseases are the leading cause of death in our country and entail a high degree of disability and health care costs. Arteriosclerosis is a multifactorial disease and therefore its prevention requires a global approach that takes into account the different risk factors with which it is associated. Therefore, this document summarizes the current level of knowledge and includes recommendations and procedures to be followed in patients with established cardiovascular disease or at high vascular risk. Specifically, this document reviews the main symptoms and signs to be evaluated during the clinical visit, the laboratory and imaging procedures to be routinely requested or requested for those in special situations. It also includes vascular risk estimation, the diagnostic criteria of the different entities that are cardiovascular risk factors, and makes general and specific recommendations for the treatment of the different cardiovascular risk factors and their final objectives. Finally, the document includes aspects that are not usually referenced in the literature, such as the organization of a vascular risk consultation.

Biomedical image classification made easier thanks to transfer and semi-supervised learning.

BACKGROUND AND OBJECTIVES: Deep learning techniques are the state-of-the-art approach to solve image classification problems in biomedicine; however, they require the acquisition and annotation of a considerable volume of images. In addition, using deep learning libraries and tuning the hyperparameters of the networks trained with them might be challenging for several users. These drawbacks prevent the adoption of these techniques outside the machine-learning community. In this work, we present an Automated Machine Learning (AutoML) method to deal with these problems. METHODS: Our AutoML method combines transfer learning with a new semi-supervised learning procedure to train models when few annotated images are available. In order to facilitate the dissemination of our method, we have implemented it as an open-source tool called ATLASS. Finally, we have evaluated our method with two benchmarks of biomedical image classification datasets. RESULTS: Our method has been thoroughly tested both with small datasets and partially annotated biomedical datasets; and, it outperforms, both in terms of speed and accuracy, the existing AutoML tools when working with small datasets; and, might improve the accuracy of models up to a 10% when working with partially annotated datasets. CONCLUSIONS: The work presented in this paper allows the use of deep learning techniques to solve an image classification problem with few resources. Namely, it is possible to train deep models with small, and partially annotated datasets of images. In addition, we have proven that our AutoML method outperforms other AutoML tools both in terms of accuracy and speed when working with small datasets.

Cost of hospitalization for stroke in a low-middle-income country: Findings from a public tertiary hospital in the Philippines.

BACKGROUND: Determining the cost of hospitalization for acute stroke is important in the appropriate allocation of resources for public health facilities and in the cost effectiveness analysis of interventions. Despite being the second leading cause of mortality in the Philippines, there are no published data on the cost of stroke in the country. AIM: The study aims to determine the in-hospitalization cost for stroke (IHCS) in a tertiary public hospital in the Philippines and identify the factors influencing IHCS. METHODS: The study was a retrospective review of the medical and billing records of the hospital. Adult patients admitted for acute stroke between 1 June 2017 and 31 May 2018 were included in the analysis. After the mean cost of stroke was determined, multivariate logistic regression analysis was done to determine demographic and clinical characteristics that were predictive of stroke cost. RESULTS: A total of 863 patient records were analyzed. The median in-hospitalization cost for stroke was PHP 17,141.50 or US$329.52. Independent determinants of higher cost include male sex (p = 0.021), stroke type (hemorrhagic stroke, p = 0.001; subarachnoid hemorrhage, p < 0.001), lower GCS on admission (p = 0.023), surgical intervention (p < 0.001), intravenous thrombolysis (p < 0.001), infection (p < 0.001), length of hospital stay (p < 0.001), and mechanical ventilation (p = 0.008). CONCLUSION: The study provided current data on the in-hospitalization cost of acute stroke in a public tertiary hospital in the Philippines. Male sex, stroke type, lower GCS on admission, surgical intervention, intravenous thrombolysis, infection, length of hospital stay, and mechanical ventilation were independent predictors of cost.

Autoimmune encephalitis in a tertiary hospital in the Philippines.

BACKGROUND: Autoimmune encephalitis (AE) is an emerging disorder in adults and children. Due to its potentially reversible nature, prompt recognition and intervention are of utmost importance. OBJECTIVE: To describe the clinical and paraclinical features, as well as treatment outcomes of patients with AE admitted in a Philippine tertiary hospital. METHODS: Retrospective case series of patients with definite AE. RESULTS: Eighteen (18) patients were included (12 adults, 6 children), majority of whom had anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis. The median age of onset was 32 (IQR: 10.8) years old and 13 (IQR: 4.8) years old in the adult and pediatric population, respectively. In both age groups, most presented with psychiatric symptoms and normal imaging findings. Cerebrospinal fluid (CSF) pleocytosis was detected in 8/12 (66.7%) adults and 2/6 (33.3%) children, while CSF protein elevation was only seen in 6/12 (50%) adults. Most patients presented with seizures, and the most frequent electroencephalography (EEG) abnormality detected was slow activity (70.5%). A high proportion of patients received high dose steroids, alone (35.3%) or in combination with intravenous immunoglobulin (IVIG, 52.9%). Overall, 66.7% had improved outcomes, mostly seen in the pediatric population. CONCLUSION: This study highlighted the broad clinical phenotype, as well as the similarities and differences of AE manifestations in adults and children. It demonstrated the limited but supportive role of laboratory investigations in the diagnosis of AE. It also underscored the importance of early intervention in AE and highlighted factors influencing treatment practices and discharge outcomes in the local setting.

Analysis of somatic mutation in five B cell subsets of human tonsil.

Using a series of phenotypic markers that include immunoglobulin (Ig)D, IgM, IgG, CD23, CD44, Bcl-2, CD38, CD10, CD77, and Ki67, human tonsillar B cells were separated into five fractions representing different stages of B cell differentiation that included sIgD+ (Bm1 and Bm2), germinal center (Bm3 and Bm4), and memory (Bm5) B cells. To establish whether the initiation of somatic mutation correlated with this phenotypic characterization, we performed polymerase chain reaction and subsequent sequence analysis of the Ig heavy chain variable region genes from each of the B cell subsets. We studied the genes from the smallest VH families (VH4, VH5, and VH6) in order to facilitate the mutational analysis. In agreement with previous reports, we found that the somatic mutation machinery is activated only after B cells reach the germinal center and become centroblasts (Bm3). Whereas 47 independently rearranged IgM transcripts from the Bm1 and Bm2 subsets were nearly germline encoded, 57 Bm3-, and Bm4-, and Bm5-derived IgM transcripts had accumulated an average of 5.7 point mutations within the VH gene segment. gamma transcripts corresponding to the same VH gene families were isolated from subsets Bm3, Bm4, and Bm5, and had accumulated an average of 9.5 somatic mutations. We conclude that the molecular events underlying the process of somatic mutation takes place during the transition from IgD+, CD23+ B cells (Bm2) to the IgD-, CD23-, germinal center centroblast (Bm3). Furthermore, the analysis of Ig variable region transcripts from the different subpopulations confirms that the pathway of B cell differentiation from virgin B cell throughout the germinal center up to the memory compartment can be traced with phenotypic markers. The availability of these subpopulations should permit the identification of the functional molecules relevant to each stage of B cell differentiation.

Receptor revision of immunoglobulin heavy chain variable region genes in normal human B lymphocytes.

Contrary to the general precepts of the clonal selection theory, several recent studies have provided evidence for the secondary rearrangement of immunoglobulin (Ig) genes in peripheral lymphoid tissues. These analyses typically used transgenic mouse models and have only detected secondary recombination of Ig light chain genes. Although Ig heavy chain variable region (V(H)) genes encode a substantial element of antibody combining site specificity, there is scant evidence for V(H) gene rearrangement in the periphery, leaving the physiological importance of peripheral recombination questionable. The extensive somatic mutations and clonality of the IgD(+)Strictly-IgM(-)CD38(+) human tonsillar B cell subpopulation have now allowed detection of the first clear examples of receptor revision of human V(H) genes. The revised VDJ genes contain "hybrid" V(H) gene segments consisting of portions from two separate germline V(H) genes, a phenomenon previously only detected due to the pressures of a transgenic system.

Molecular characterization of a cross-reactive idiotope on human immunoglobulins utilizing the VH4-21 gene segment.

The anti-idiotypic (anti-Id) antibody (Ab) 9G4 binds a cross-reactive idiotope (CRI) present in a select group of human autoantibodies. This Id has been localized to the portion of immunoglobulin (Ig) heavy (H) chains encoded by the VH4-21 gene segment, a member of the human VH4 family. This gene segment is utilized by essentially all cold agglutinin (CA) Abs with I/i specificity isolated from patients with CA disease stemming from chronic lymphoproliferative disorders. In this study, mutational analysis of a CA has been used to determine the structural basis for 9G4 binding to Abs utilizing the VH4-21 gene segment. Recombinant CA H chain mutants were produced and their 9G4 reactivity determined. Mutants were generated by exchanging VH4-21 sequences in the FR1, CDR1, and CDR2 with corresponding sequences from a closely related gene segment V71-2, a VH4 family member that is associated neither with Abs having CA activity nor with Abs that react with 9G4. The results indicate that the motif AVY at amino acid positions 23-25 in FR1 defines the 9G4 idiotope. Reaction of these recombinant Abs with a polyclonal rabbit anti-CA antiserum absorbed to render it specific for a CA CRI also maps predominantly to FR1. These findings indicate that the solvent-exposed FR1 plays an important role in eliciting an immune response to Igs.

Somatic hypermutation introduces insertions and deletions into immunoglobulin V genes.

During a germinal center reaction, random mutations are introduced into immunoglobulin V genes to increase the affinity of antibody molecules and to further diversify the B cell repertoire. Antigen-directed selection of B cell clones that generate high affinity surface Ig results in the affinity maturation of the antibody response. The mutations of Ig genes are typically basepair substitutions, although DNA insertions and deletions have been reported to occur at a low frequency. In this study, we describe five insertion and four deletion events in otherwise somatically mutated VH gene cDNA molecules. Two of these insertions and all four deletions were obtained through the sequencing of 395 cDNA clones (approximately 110,000 nucleotides) from CD38+IgD- germinal center, and CD38-IgD- memory B cell populations from a single human tonsil. No germline genes that could have encoded these six cDNA clones were found after an extensive characterization of the genomic VH4 repertoire of the tonsil donor. These six insertions or deletions and three additional insertion events isolated from other sources occurred as triplets or multiples thereof, leaving the transcripts in frame. Additionally, 8 of 9 of these events occurred in the CDR1 or CDR2, following a pattern consistent with selection, and making it unlikely that these events were artifacts of the experimental system. The lack of similar instances in unmutated IgD+CD38- follicular mantle cDNA clones statistically associates these events to the somatic hypermutation process (P = 0.014). Close scrutiny of the 9 insertion/deletion events reported here, and of 25 additional insertions or deletions collected from the literature, suggest that secondary structural elements in the DNA sequences capable of producing loop intermediates may be a prerequisite in most instances. Furthermore, these events most frequently involve sequence motifs resembling known intrinsic hotspots of somatic hypermutation. These insertion/deletion events are consistent with models of somatic hypermutation involving an unstable polymerase enzyme complex lacking proofreading capabilities, and suggest a downregulation or alteration of DNA repair at the V locus during the hypermutation process.

The interferon-alpha signature of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease's unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production of autoantibodies have long been recognized as major pathogenic events in this disease. Over the past decade the type I interferon cytokine family has been postulated to play a central role in SLE pathogenesis, by promoting feedback loops progressively disrupting peripheral immune tolerance and driving disease activity. The identification of key molecules involved in the pathogenesis of SLE will not only improve our understanding of this complex disease, but also help to identify novel targets for biological intervention.

[Scientific Presentations at the meetings of the Spanish Pediatric Nephrology Association (AENP), 1988-2007]. / Comunicaciones científicas en los congresos de la Asociación Española de Nefrología Pediátrica (AENP), 1988-2007.

UNLABELLED: OBJECTIVES AND STUDY: To find out that characteristics of the scientific presentations given at the AENP's meetings in the past 20 years. METHODS: We reviewed in the scientific programs of the AENP's meetings of the past 20 years: number of presentations, number of participating institutions, institutions that provided the majority of the presentations, presentation format, number of studies involving experimental nephrology, topics most commonly presented. RESULTS: There have been 1,119 presentations in the past 20 years, 45/year between 88-92 and 67/year between 03-07. Ninety-one institutions participated in the meetings, 17/year between 88-92 and 34/year between 03-07. Pediatric Nephrology unit from the H. La Paz (Madrid) contributed the most presentations. Poster presentations were accepted at the ANEP meetings after 1995. Since then, 369 of the 815 presentations followed this format. Between 88-07 only 16 presentations dealt with experimental nephrology. The most common topics of presentation were glomerular disease (203) and urinary tract infection/VUR (132). Fifty-one presentations dealt with dialysis (almost 2/3 peritoneal). Transplantation was the topic of 123 presentations. Of the 21 presentations on molecular genetics only one happened before 1998. CONCLUSIONS: The poster is a useful alternative in scientific presentations which has allowed an increase in presentations, authors and institutions participating in the ANEP meetings. The main topic of presentation was glomerular disease. The frequency of presentations dealing with transplantation has increased in the last years. The past decade has seen more presentations on molecular genetics, but presentations dealing with experimental nephrology are still infrequent.

Induction of dendritic cell differentiation by IFN-alpha in systemic lupus erythematosus.

Dendritic cells (DCs) are important in regulating both immunity and tolerance. Hence, we hypothesized that systemic lupus erythematosus (SLE), an autoimmune disease characterized by autoreactive B and T cells, may be caused by alterations in the functions of DCs. Consistent with this, monocytes from SLE patients' blood were found to function as antigen-presenting cells, in vitro. Furthermore, serum from SLE patients induced normal monocytes to differentiate into DCs. These DCs could capture antigens from dying cells and present them to CD4-positive T cells. The capacity of SLE patients' serum to induce DC differentiation correlated with disease activity and depended on the actions of interferon-alpha (IFN-alpha). Thus, unabated induction of DCs by IFN-alpha may drive the autoimmune response in SLE.

DeepClas4Bio: Connecting bioimaging tools with deep learning frameworks for image classification.

BACKGROUND AND OBJECTIVE: Deep learning techniques have been successfully applied to tackle several image classification problems in bioimaging. However, the models created from deep learning frameworks cannot be easily accessed from bioimaging tools such as ImageJ or Icy; this means that life scientists are not able to take advantage of the results obtained with those models from their usual tools. In this paper, we aim to facilitate the interoperability of bioimaging tools with deep learning frameworks. METHODS: In this project, called DeepClas4Bio, we have developed an extensible API that provides a common access point for classification models of several deep learning frameworks. In addition, this API might be employed to compare deep learning models, and to extend the functionality of bioimaging programs by creating plugins. RESULTS: Using the DeepClas4Bio API, we have developed a metagenerator to easily create ImageJ plugins. In addition, we have implemented a Java application that allows users to compare several deep learning models in a simple way using the DeepClas4Bio API. Moreover, we present three examples where we show how to work with different models and frameworks included in the DeepClas4Bio API using several bioimaging tools - namely, ImageJ, Icy and ImagePy. CONCLUSIONS: This project brings to the table benefits from several perspectives. Developers of deep learning models can disseminate those models using well-known tools widely employed by life-scientists. Developers of bioimaging programs can easily create plugins that use models from deep learning frameworks. Finally, users of bioimaging tools have access to powerful tools in a known environment for them.

Acute hemorrhagic leukoencephalitis of Weston Hurst secondary to herpes encephalitis presenting as status epilepticus: A case report and review of literature.

Acute hemorrhagic leukoencephalitis (AHL) is a rare and mostly fatal fulminant demyelinating disease. This case describes a 63-year old male in status epilepticus associated with an intracerebral hemorrhage following a one week viral prodrome with rapid decline to coma. He exhibited peripheral leukocytosis, neutrophilic pleocytosis with normal glucose and high protein in cerebrospinal fluid (CSF). Additionally, CSF was positive for herpes simplex virus (HSV) polymerase chain reaction (PCR). Medical decompression, low-dose dexamethasone, antibiotics and acyclovir were initially given. Magnetic resonance imaging (MRI) was suggestive of AHL, thus he was treated with methylprednisolone 1 g/day for 5 days. The patient improved and was discharged with significant neurologic morbidity. This is the first reported case of AHL in the Philippines presenting as a diagnostic dilemma with a protracted clinical course who responded to high dose intravenous steroids.

Neuromyelitis optica spectrum disorder in a tertiary hospital in the Philippines: a case series.

Neuromyelitis optica spectrum disorder (NMOSD) is a rare disease that commonly presents with optic nerve and spinal cord inflammation, and it is associated with the presence of aquaporin-4 immunoglobulin G antibody (AQP4-IgG). Information on the clinical profile and occurrence of NMOSD among Filipino patients, however, is not sufficiently documented. In this series, we presented eighteen (18) patients with NMOSD consecutively seen in the Philippine General Hospital, a major tertiary referral center. Demographic data showed a female-to-male ratio of 2.6:1. Median age of onset of symptoms was 26 years. Eight patients (53.3%) were positive for AQP4-IgG. Most patients initially presented with myelitis (56.6%) and followed by optic neuritis (16.7%) and area postrema syndrome (16.7%). All patients had longitudinally extensive transverse myelitis on magnetic resonance imaging (MRI). Cranial MRI rarely demonstrated lesions in the optic nerves (18.2%). CSF pleocytosis (33%) and increased protein (8.3%) were infrequent. These results demonstrated that the profile of Filipino patients with NMOSD seen in our institution strengthens those described in other populations with this disorder. Large scale cross-sectional studies are necessary to fully define the profile of these patients and to determine with accuracy the prevalence and incidence of this disorder in the Philippines. Further investigation regarding the utility of ancillary tests as diagnostic and prognostic indicators in patients with NMOSD are also suggested by the authors.

Analysis of human antitopoisomerase-I idiotypes.

Antibodies to topoisomerase-I are present in approximately 26% of patients with scleroderma and are rarely found in patients with other diseases. In the current study, the expression of the antitopoisomerase-I (antitopo-I) idiotype from two scleroderma patients (E.M. and S.G.) and from a healthy individual (N.M.) were studied. Idiotype EM-SCL was restricted to the three classes of antitopo-I, whereas idiotypes SG-SCL and NM were found in all classes of antitopo-I as well as in their non-antitopo-I Igs. Sera from 9 of 10 antitopo-I-positive unrelated scleroderma patients expressed idiotype SG-SCL and some also expressed idiotype NM. Sera from N.M.'s 3 daughters and from 7 of 18 nonrelated normals expressed idiotype NM in the three immunoglobulin classes of non-antitopo-I. Two of the antitopo-I antibodies expressed a cross-reacting idiotype (CRI) that is present in non-antitopo-I antibodies from the same donor. Contrary to the natural CRI, SG-SCL's CRI is closely associated with the antigen binding site. Antitopo-I idiotypes are on the heavy chains. Like many other autoantibodies, Id-SG-SCL use VH4.2-1, DXP1, and JH4 in germline configuration.