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1.
Diabetes Educ ; 39(3): 354-64, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23610182

RESUMO

PURPOSE: The purpose of this pilot study was to evaluate the safety and preliminary efficacy of a treatment algorithm and education intervention for the management of patients with type 2 diabetes and hyperglycemia presenting to the emergency department (ED) and stable enough to be discharged home. METHODS: Urban hospital ED patients (n = 86) with BG ≥ 200 mg/dL were enrolled in a 4-week prospective, nonrandomized pilot intervention with historic self-controls. Follow-up visits occurred at 12 to 72 hours, 2 and 4 weeks, and 6 months. T2DM medications were initiated or adjusted at each visit using a guideline-based diabetes medication management algorithm. Survival skills diabetes self-management education and navigation to outpatient services were provided. RESULTS: Participants were 51.8% male and 92% black, and 87.3% had private or public insurance. The top reasons for presenting to the ED were no provider appointment available (41.7%) and no primary care provider (14.6%). No hypoglycemia occurred in the first 24 hours following ED T2DM medication initiation or titration and overall hypoglycemia rates were low. BG was reduced from 356 ± 110 mg/dL at baseline to 183 ± 103 mg/dL at 4 weeks (P < .001). CONCLUSION: Diabetes medication management and survival skills education for uncontrolled diabetes may be safely initiated in the ED, as demonstrated by the multidisciplinary STEP-DC intervention, which effectively enabled glycemic control in this pilot study.


Assuntos
Glicemia/efeitos dos fármacos , Diabetes Mellitus Tipo 2/tratamento farmacológico , Serviço Hospitalar de Emergência/estatística & dados numéricos , Hiperglicemia/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Insulina/uso terapêutico , Autocuidado , Adolescente , Adulto , Algoritmos , Diabetes Mellitus Tipo 2/economia , Diabetes Mellitus Tipo 2/epidemiologia , District of Columbia/epidemiologia , Serviço Hospitalar de Emergência/economia , Estudos de Viabilidade , Feminino , Humanos , Hiperglicemia/economia , Hiperglicemia/epidemiologia , Masculino , Pessoa de Meia-Idade , Alta do Paciente , Educação de Pacientes como Assunto , Projetos Piloto , Guias de Prática Clínica como Assunto , Estudos Prospectivos , Autocuidado/métodos , População Urbana
2.
Diabetes Technol Ther ; 13(2): 121-6, 2011 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-21284478

RESUMO

BACKGROUND: No study of transition from intravenous to subcutaneous insulin after cardiac surgery with dose based on percentage of intravenous total daily insulin (TDI) has reported a clearly superior regimen for achieving target blood glucose. We compared three first-dose transition strategies for insulin glargine: two based on TDI alone and one that also took body weight into account. METHODS: Mostly obese, type 1 and type 2 diabetes patients (n = 223) undergoing cardiac surgery were randomized to receive insulin glargine subcutaneously at 60% or 80% of TDI or in a dose based on TDI and body weight. RESULTS: Transition to subcutaneous insulin occurred 27.4 ± 6.6 h after surgery. Over the study period, mean proportion of blood glucose values within target range (80-140 mg/dL) were 0.34 ± 0.24, 0.35 ± 0.24, and 0.36 ± 0.22 in the 60% TDI, 80% TDI, and weight-based groups, respectively. This difference was not significant. Significantly more insulin corrections were needed in the 60% TDI group than in the weight-based group. There was only one incidence of hypoglycemia (blood glucose < 40 mg/dL). CONCLUSIONS: No subcutaneous insulin regimen implemented approximately 1 day after cardiac surgery showed significantly better control of blood glucose over the 3-day study period. Further studies are needed to determine optimal formulae for effecting an early transition to subcutaneous insulin after cardiac surgery or whether it is preferable and/or necessary to continue intravenous insulin therapy for an additional period of time.


Assuntos
Glicemia/análise , Doenças Cardiovasculares/cirurgia , Diabetes Mellitus Tipo 1/tratamento farmacológico , Diabetes Mellitus Tipo 2/tratamento farmacológico , Hipoglicemiantes/administração & dosagem , Insulina/análogos & derivados , Cuidados Pós-Operatórios/métodos , Idoso , Índice de Massa Corporal , Doenças Cardiovasculares/complicações , Diabetes Mellitus Tipo 1/sangue , Diabetes Mellitus Tipo 1/complicações , Diabetes Mellitus Tipo 2/sangue , Diabetes Mellitus Tipo 2/complicações , Cálculos da Dosagem de Medicamento , Monitoramento de Medicamentos , Feminino , Hemoglobinas Glicadas/análise , Humanos , Hipoglicemia/induzido quimicamente , Hipoglicemia/prevenção & controle , Hipoglicemiantes/efeitos adversos , Hipoglicemiantes/uso terapêutico , Injeções Subcutâneas , Insulina/administração & dosagem , Insulina/efeitos adversos , Insulina/uso terapêutico , Insulina Glargina , Insulina de Ação Prolongada , Masculino , Pessoa de Meia-Idade , Obesidade/complicações , Cuidados Pós-Operatórios/efeitos adversos
3.
Semin Oncol ; 37(6): 580-90, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21167377

RESUMO

Parathyroid cancer is an uncommon malignancy and rare cause of primary hyperparathyroidism (HPT) with a high morbidity and patient death in advanced cases usually resulting from intractable hypercalcemia. Inactivation of the HRPT2/CDC73 gene, encoding the putative tumor-suppressor protein parafibromin and discovered in the context of the hyperparathyroidism-jaw tumor (HPT-JT) syndrome, is a common, somatic event in most parathyroid cancers. Approximately 25% of patients with apparently sporadic parathyroid cancer carry germline HRPT2/CDC73 mutation. Germline DNA analysis for HRPT2/CDC73 mutation is recommended in all patients with parathyroid cancer because of the potential benefit for first-degree relatives, who should nevertheless undergo serum calcium screening. The histopathologic diagnosis of parathyroid cancer is nonspecific unless vascular, lymphatic, capsular, or soft tissue invasion is seen, or metastases are clinically evident. Immunohistochemical analysis of parathyroid tumors for loss of parafibromin expression offers promise as a diagnostic tool. En bloc tumor resection offers the highest chance of cure in patients with suspected parathyroid carcinoma. No adjuvant chemotherapy regimen has yet proven effective, and the role of local adjuvant radiotherapy is being evaluated. Metastatic disease can be palliated with surgical debulking. Medical therapy with the calcimimetic cinacalcet and bisphosphonates can ameliorate hypercalcemia in patients with inoperable disease.


Assuntos
Neoplasias das Paratireoides/patologia , Neoplasias das Paratireoides/terapia , Biomarcadores Tumorais , Progressão da Doença , Humanos , Hipercalcemia/etiologia , Mutação , Neoplasias das Paratireoides/complicações , Neoplasias das Paratireoides/genética , Paratireoidectomia , Prognóstico , Proteínas Supressoras de Tumor/análise , Proteínas Supressoras de Tumor/genética
4.
Best Pract Res Clin Endocrinol Metab ; 24(3): 491-502, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20833339

RESUMO

Primary hyperparathyroidism (HPT) results from the excessive secretion of parathyroid hormone from parathyroid tumours. While most HPT is sporadic, it is associated with a familial syndrome in a minority of cases. The study of these syndromes has helped define the pathophysiology of both familial and sporadic parathyroid neoplasms. Investigation of kindred with multiple endocrine neoplasia type 1 (MEN1) and the hyperparathyroidism-jaw tumour syndrome (HPT-JT) led to the discovery of the tumour suppressor genes MEN1 and HRPT2. We now recognise that somatic mutations in MEN1 and HRPT2 tumour suppressor genes are frequent events in sporadic parathyroid adenomas and carcinomas, respectively. Parathyroid tumours in the MEN2A syndrome result from mutational activation of the RET oncogene. The CCND1/PRAD1 oncogene was discovered by analysis of sporadic parathyroid tumours. Studies of familial isolated HPT and analysis of chromosomal loss and gain in parathyroid tumours suggest that other genes relevant to parathyroid neoplasia await identification.


Assuntos
Hiperparatireoidismo Primário/genética , Neoplasias das Paratireoides/genética , Feminino , Humanos , Hiperparatireoidismo Primário/patologia , Masculino , Neoplasia Endócrina Múltipla Tipo 1/genética , Neoplasia Endócrina Múltipla Tipo 1/patologia , Hormônio Paratireóideo/genética , Neoplasias das Paratireoides/patologia , Proteínas Proto-Oncogênicas c-ret/genética , Proteínas Supressoras de Tumor/genética
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