Assuntos
Humanos , Pé Diabético/epidemiologia , Saúde Global , Custos de Cuidados de Saúde , Difosfonatos , Efeitos Psicossociais da Doença , Fator de Crescimento Derivado de Plaquetas , Neuropatias Diabéticas/fisiopatologia , Pé Diabético/economia , Pé Diabético/terapia , Transplante de Pele , Úlcera/fisiopatologiaAssuntos
Pé Diabético/epidemiologia , Saúde Global , Efeitos Psicossociais da Doença , Pé Diabético/economia , Pé Diabético/terapia , Neuropatias Diabéticas/fisiopatologia , Difosfonatos , Custos de Cuidados de Saúde , Humanos , Pamidronato , Fator de Crescimento Derivado de Plaquetas , Transplante de Pele , Úlcera/fisiopatologiaRESUMO
We examined the records of 2576 patients with non-insulin-dependent diabetes mellitus (NIDDM) and categorised them according to race and family history of diabetes. Family history of diabetes is known to play an important role in the development of NIDDM, and a maternal history is thought to be most influential. We found that a maternal history of diabetes was present in 60% of Caucasian and West Indian patients with a parental history of diabetes, whereas in Asian patients the figure was only 34%. Asian men were also more likely to have a father with diabetes. This anomaly may be due to cultural differences in the reporting of the disease. Our data support the dominant maternal role in the development of NIDDM in their offspring and suggest an under-reporting of NIDDM in Asian females.
Assuntos
População Negra/genética , Diabetes Mellitus Tipo 2/genética , Mães , População Branca/genética , África/etnologia , Comparação Transcultural , Diabetes Mellitus Tipo 2/epidemiologia , Família , Pai , Feminino , Humanos , Incidência , Masculino , Prontuários Médicos , Estudos Retrospectivos , Caracteres Sexuais , Fatores Sexuais , Reino Unido , Índias Ocidentais/etnologiaRESUMO
Diabetic neuropathy (DN) is chronic complication which occurs in 50% of long standing diabetes mellitus. DN is a consequence of hyperglycemia probably through the following mechanisms: a) activation of aldose-reductase, intracellular sorbitol accumulation and myoinositol depletion, reduced activity of Na+/K+ATPase, loss of Na+ channels and demyelination; b) proteins glycation; c) microangiopathy; the first mechanism being the best known and the most reliable. DN may be subclinical or clinical. The main clinical picture is a peripheral, bilateral, symmetric polyneuropathy with a "socks and gloves" sensory impairment, muscular weakness, hyporeflexia, plantar ulcers and arthropathy. Less frequent syndromes are proximal motor neuropathy and mononeuropathy of cranial nerves or thoraco-abdominal roots. Diagnosis is based on clinical data, and may be sustained on impaired nerve conduction velocity, abnormal evoked somatosensory potentials, or sural nerve biopsy. These methods are highly sensitive but unspecific. Etiopathogenic treatment is based on glycemic control and aldose reductase inhibitors. Improvement in clinical, electrophysiologic and histopathologic data have been obtained with the latter. Symptomatic treatment includes carbamazepin, phenytoin, tricyclic antidepressives and a phenotiazin. Mononeuropathies tend to complete recovery in less than 6 months. Polyneuropathy is thought to be irreversible and progressive; however, with excellent glycemic control or with aldose reductase inhibitors nerve damage may be stabilized or even reversed.