ABSTRACT
Hypospadias is an uncommon sexual development disorder in cats, in which the urethral opening is not in its anatomical location on the penis. The purpose of this report is to describe two cases of hypospadias in the feline species. The first cat was asymptomatic, had a history of bacterial cystitis, and was diagnosed with perineal hypospadias at an appointment for preoperative evaluation of orchiectomy. The second cat had clinical signs of dysuria and pollakiuria for 30 days and had glandular hypospadias. Both cats showed abnormalities in the urinalysis which were suggestive of lower urinary tract disease. For both cases, clinical treatment with antibiotic therapy was performed. In the first patient, surgical treatment consisted of orchiectomy, while in the second animal a perineal urethrostomy and orchiectomy were performed. The cats had a satisfactory recovery after the treatments. Performing a thorough physical examination is essential to diagnose cases of hypospadias and choose the best treatment for each patient.
A hipospadia é uma desordem do desenvolvimento sexual pouco comum nos gatos, na qual a abertura uretral não está em sua localização anatômica do pênis. O objetivo do presente relato é descrever dois casos de hipospadia em felinos domésticos. O primeiro gato era assintomático, tinha histórico de cistite bacteriana prévio, e foi diagnosticado com hipospadia perineal em uma consulta para avaliação pré-cirúrgica de orquiectomia. O segundo gato apresentava sinais clínicos de disúria e polaquiúria há 30 dias e apresentava hipospadia glandular. A partir dos exames complementares, pôde-se observar que os animais, além do defeito anatômico, apresentavam alterações sugestivas de doença do trato urinário inferior. Para ambos os casos, foi realizado o tratamento clínico inicial com antibioticoterapia. No primeiro paciente, optou-se pelo procedimento de orquiectomia, enquanto no segundo animal foram realizadas as técnicas de uretrostomia perineal e orquiectomia. Os gatos mostraram recuperação satisfatória após os tratamentos instituídos. Dessa forma, pode-se observar a importância de se realizar um exame físico minucioso a fim de diagnosticar os casos de hipospadia e escolher o tratamento correto para cada paciente.
Subject(s)
Animals , Cats , Disorders of Sex Development/veterinary , Urethra/abnormalities , Urethral Diseases/veterinary , Cat Diseases , Hypospadias/veterinaryABSTRACT
Genetic determinants of human susceptibility to tuberculosis (TB) have not been completely elucidated. Interleukin-1 beta (IL-1beta) and the inhibitor of kB-like (IkBL) are important molecules that participate in the inflammatory response required for the immunological control of a broad spectrum of infectious agents. The transporter associated with antigen processing (TAP) is involved in the antigen processing via major histocompatibility complex class I molecules and in turn might regulate the T-cell response against Mycobacterium tuberculosis. To better characterize the host genetic factors determining the susceptibility to TB, we evaluated the influence of functional polymorphisms in IL1B, TAP and IKBL genes on the risk of developing pulmonary TB in a Northwestern Colombian population, an endemic area of M. tuberculosis infection. A total of 122 TB patients and 166 healthy controls (N = 166) negative for human immunodeficiency virus infection were examined for IL1B-511 and +3,953, TAP1 and TAP2 and IKBL+738 polymorphisms. Univariate analysis disclosed significant differences between patients and controls for IL1B+3,953 polymorphism. After unconditional logistic regression analysis, a strong protection conferred by IL1B+3,953 T-allele-carrying genotypes was observed. A trend between TAP2*0201 allele and disease was observed. Association between IL1B-511, TAP1 or IKBL polymorphisms and TB disease was not found. These results indicate that a functional polymorphism in the IL1B gene influences the susceptibility to TB and suggest a role for IL-1beta in the pathogenesis of mycobacterial infection.
Subject(s)
ATP-Binding Cassette Transporters/genetics , Histocompatibility Antigens Class II/genetics , Interleukin-1/genetics , Polymorphism, Single Nucleotide , Tuberculosis, Pulmonary/genetics , ATP Binding Cassette Transporter, Subfamily B, Member 2 , ATP Binding Cassette Transporter, Subfamily B, Member 3 , Adaptor Proteins, Signal Transducing , Adult , Case-Control Studies , Disease Susceptibility , Genetic Predisposition to Disease , Genotype , Haplotypes , Humans , Middle Aged , Mycobacterium tuberculosis/genetics , Tuberculosis, Pulmonary/microbiologyABSTRACT
Autoimmune rheumatic diseases (AIRD) are not uncommon in the general population and up to one third of hospitalized patients with AIRD may need admission to intensive care unit (ICU). This paper describes the causes of admission, the clinical features and outcome of 24 AIRD patients admitted to a medical ICU from a third level hospital. Thirteen patients had systemic lupus erythematosus (54.2%), three rheumatoid arthritis (12.5%), three pulmonary renal syndrome (12.5%), two dermatopolymyositis (8.3%), two scleroderma (8.3%) and one antiphospholipid syndrome (4.2%). The main causes for ICU admission were rheumatic disease flare-up (37.5%), infection (37.5%) and complications derived from rheumatic disease (29.1%). Mortality during ICU stay was 16.7% (four patients). Excluding shock requiring vasopressor support, no statistical difference was found between survivors and nonsurvivors; although there was a trend to higher test severity scores (APACHE II, ODIN) in nonsurvivors. Our results reveal a lower mortality rate in AIRD patients admitted to the ICU than reported previously. Severity scores such as APACHE II are predictors of mortality in patients with AIRD in the ICU.
Subject(s)
Autoimmune Diseases/therapy , Intensive Care Units , Rheumatic Diseases/therapy , Adolescent , Adult , Aged , Aged, 80 and over , Arthritis, Rheumatoid/mortality , Arthritis, Rheumatoid/therapy , Autoimmune Diseases/mortality , Colombia/epidemiology , Female , Hospitals, University , Humans , Lupus Erythematosus, Systemic/mortality , Lupus Erythematosus, Systemic/therapy , Male , Middle Aged , Patient Admission , Retrospective Studies , Rheumatic Diseases/mortalityABSTRACT
Interleukin-1 beta (IL-1beta) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1beta gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sjogren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1beta single-nucleotide polymorphisms (SNPs) at positions -511 (C/T) and + 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1beta were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1beta likely haplotypes, all belonging to the control group. Allele + 3953T was protective for SLE (odds ratio (OR) = 0.57, 95% confidence intervals (CI) = 0.34-0.88, P = 0.01) as was the haplotype -511C + 3953T (OR = 0.43, 95%CI = 0.25-0.74, pc = 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1beta secretion. Results suggest that IL-1beta polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1beta + 3953T allele on the secretion of IL-1beta under inflammatory circumstances.