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1.
Molecules ; 29(4)2024 Feb 06.
Article in English | MEDLINE | ID: mdl-38398500

ABSTRACT

Systemic lupus erythematosus (SLE) is an idiopathic chronic autoimmune disease that can affect any organ in the body, including the neurological system. Multiple factors, such as environmental (infections), genetic (many HLA alleles including DR2 and DR3, and genes including C4), and immunological influences on self-antigens, such as nuclear antigens, lead to the formation of multiple autoantibodies that cause deleterious damage to bodily tissues and organs. The production of autoantibodies, such as anti-dsDNA, anti-SS(A), anti-SS(B), anti-Smith, and anti-neuronal DNA are characteristic features of this disease. This autoimmune disease results from a failure of the mechanisms responsible for maintaining self-tolerance in T cells, B cells, or both. Immune complexes, circulating antibodies, cytokines, and autoreactive T lymphocytes are responsible for tissue injury in this autoimmune disease. The diagnosis of SLE is a rheumatological challenge despite the availability of clinical criteria. NPSLE was previously referred to as lupus cerebritis or lupus sclerosis. However, these terms are no longer recommended because there is no definitive pathological cause for the neuropsychiatric manifestations of SLE. Currently, the treatment options are primarily based on symptomatic presentations. These include the use of antipsychotics, antidepressants, and anxiolytic medications for the treatment of psychiatric and mood disorders. Antiepileptic drugs to treat seizures, and immunosuppressants (e.g., corticosteroids, azathioprine, and mycophenolate mofetil), are directed against inflammatory responses along with non-pharmacological interventions.


Subject(s)
Lupus Erythematosus, Systemic , Lupus Vasculitis, Central Nervous System , Humans , Lupus Vasculitis, Central Nervous System/diagnosis , Lupus Vasculitis, Central Nervous System/drug therapy , Lupus Erythematosus, Systemic/drug therapy , Lupus Erythematosus, Systemic/genetics , Autoantibodies , Immunosuppressive Agents/therapeutic use , Seizures/drug therapy
2.
Microorganisms ; 11(9)2023 Sep 05.
Article in English | MEDLINE | ID: mdl-37764077

ABSTRACT

Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by a defect in the phagocytic function of the innate immune system owing to mutations in genes encoding the five subunits of the nicotinamide adenine dinucleotide phosphatase (NADPH) oxidase enzyme complex. This review aimed to provide a comprehensive approach to the pathogens associated with chronic granulomatous disease (CGD) and its management. Patients with CGD, often children, have recurrent life-threatening infections and may develop infectious or inflammatory complications. The most common microorganisms observed in the patients with CGD are Staphylococcus aureus, Aspergillus spp., Candida spp., Nocardia spp., Burkholderia spp., Serratia spp., and Salmonella spp. Antibacterial prophylaxis with trimethoprim-sulfamethoxazole, antifungal prophylaxis usually with itraconazole, and interferon gamma immunotherapy have been successfully used in reducing infection in CGD. Haematopoietic stem cell transplantation (HCT) have been successfully proven to be the treatment of choice in patients with CGD.

3.
IJID Reg ; 3: 96-100, 2022 Jun.
Article in English | MEDLINE | ID: mdl-35755456

ABSTRACT

Objective: To assess colonization of Streptococcus agalactiae [group B streptococcus (GBS)], and delineate capsular serotype distribution and antibiotic susceptibility profiles among pregnant women in Trinidad and Tobago. Methods: Vaginal swabs were collected from 248 pregnant women attending antenatal clinics in northern Trinidad, and processed using standard microbiological laboratory tests to confirm GBS. Polymerase chain reaction detected atr and cps serotype genes. Antimicrobial susceptibility tests were performed using the Kirby-Bauer method, and SPSS Version 25 was used for statistical analysis. Prevalence ratio measured the risk, and P≤0.05 was considered to indicate significance. Results: The GBS carriage rate was 29% (72/248, 95% confidence interval 23.3-34.8), and carriage was significantly associated with variables including gestational diabetes (P=0.042), age 25-35 years (P=0.006), multiparity (P=0.035) and marital status (P=0.006). The most common serotype was type II [47.2% (34/72)], and serotypes V, VI, VII and VIII were not encountered. GBS showed high resistance to amoxicillin-clavulanic acid (37.5%), erythromycin (30.6%), trimethoprim-sulphamethoxazole (58.3%) and tetracycline (97.2%). Conclusion: GBS colonization among pregnant women and resistance to commonly used antibiotics are high in Trinidad and Tobago. A population-based study is required to obtain accurate figures in order to improve maternal healthcare services.

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