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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
41

Efeito da insulina glargina sobre o controle glicêmico e risco de hipoglicemia em pacientes portadores de diabetes mellitus tipo 2 e doença renal crônica estágios 3 e 4: ensaio clínico, controlado e randomizado / Insulin glargine effect on glycemic control and hypoglycemia risk in patients with type 2 diabetes mellitus and chronic kidney disease stages 3 and 4: a randomized, open-label controlled clinical trial

Carolina de Castro Rocha Betonico 27 January 2017 (has links)
Diabetes mellitus (DM) é uma das principais causas de doença renal crônica terminal. Na doença renal diabética (DRD) observa-se um curso bifásico no padrão glicêmico, na fase inicial o aumento da resistência insulínica induz a hiperglicemia e, com perda progressiva da taxa de filtração glomerular, há redução na depuração dos medicamentos anti-hiperglicemiantes e insulina, aumentando o risco de hipoglicemias. Portanto, diante da perda da função renal, a reavaliação da terapia hipoglicemiante e ajustes constantes nas doses de insulina são necessários, com intuito de otimizar o controle glicêmico e minimizar seus efeitos colaterais. A revisão da literatura mostra diversos pontos sem resposta, principalmente relacionados à dose, ajuste da terapia insulínica, seguimento e monitoração do controle glicêmico em portadores de DM e DRC. O objetivo deste ensaio randomizado, cruzado, controlado foi comparar o controle glicêmico do tratamento com insulina glargina à insulina NPH em portadores de DM2 e DRD estágios 3 e 4. Pacientes e métodos: Trinta e quatro pacientes foram randomizados para receber insulina glargina uma vez ao dia ou insulina NPH em três aplicações diárias. Insulina lispro foi prescrita três vezes ao dia, em aplicações pré-prandiais nos dois grupos. Após 24 semanas de terapia, os pacientes tiveram seu esquema de insulina trocado para terapia insulínica oposta. Testes laboratoriais foram realizados após 12, 24, 36 e 48 semanas de estudo. O sistema de monitorização continua de glicose (CGMS) foi instalado ao término de cada terapia. Resultados: Dos 34 pacientes incluídos, 29 completaram as 48 semanas propostas no estudo, 2 pacientes perderam seguimento por má adesão e 3 pacientes não completaram o estudo em decorrência a eventos adversos (1 óbito, 1 ingresso em hemodiálise e 1 evento cardiovascular, todos em uso de insulina NPH). Após 24 semanas de tratamento com insulina glargina houve uma redução estatisticamente significante da média da HbA1c de 8,86 ± 1,4% para 7,95 ± 1,1% (p=0,0285), esta diferença não foi observada com a insulina NPH (8,21 ± 1,29% para 8,44 ± 1,32%). Durante o uso de insulina glargina o número de eventos noturnos de hipoglicemia foi menor comparado a insulina NPH (p=0,046); além disso, hipoglicemia grave ocorreu apenas na terapêutica com NPH. Conclusão: O tratamento com insulina glargina foi associado a melhor controle glicêmico e a redução do risco de hipoglicemia noturna quando comparada à insulina NPH,em pacientes portadores de DM e DRC estágios 3 e 4 / Diabetes mellitus is the leading cause of chronic kidney disease (CKD). Kidney disease diagnosis and its progression require re-evaluation of hypoglycemic therapy and constant dosing adjustments, to optimize glycemic control and minimize its side effects. Long acting insulin analogs and its pharmacokinetics have not been studied in different stages of kidney disease, nor is there consensus defining appropriate dose adjustment in patients with type 2 diabetes (T2DM) and CKD. The aim of this randomized, cross-over, open-label controlled clinical trial is to compare the glycemic response to intensive insulin treatment with NPH insulin or insulin glargine in T2DM patients and CKD stages 3 and 4. The primary efficacy end point was change in A1C from baseline. Thirty-four patients were randomized to receive insulin glargine once a day or NPH insulin, three times a day. Insulin lispro was prescribed as prandial insulin to both groups. After six months, patients switched to the other insulin therapy group. Laboratory tests were performed at baseline at 12, 24, 36 and 48 weeks. A continuous glucose monitoring system was implemented after 24 weeks and at the end of protocol. Results: Total of 29 subjects have completed the two branches of study, 2 patients dropped out due to low compliance and other 3 patients as a result of adverse events (1 death, 1 ingress on dialysis program, 1 cardiovascular event; all of them were on NPH therapy). After 24 weeks, average of A1c decreased on glargine group compared to baseline 8,86 ± 1,4% to 7,95 ± 1,1% (p=0,0285), but this difference was not observed on NPH group. There were no differences of insulin doses between both groups. Glargine group showed a tendency of lower risk of nocturnal hypoglycemia compared to NPH group (p=0,046). Conclusion: Insulin glargine improved glycemic control by reducing HbA1c without gain weight and with reduced tendency toward nocturnal hypoglycemic events compared with NPH insulin
42

Estudo comparativo entre duas insulinas humanas recombinantes NPH no tratamento do diabetes mellitus tipo 2 / Comparative study between two recombinant human insulins NPH in the treatment of type 2 diabetes mellitus

Rassi, Nelson 13 September 2014 (has links)
Submitted by Cláudia Bueno (claudiamoura18@gmail.com) on 2015-10-15T19:58:50Z No. of bitstreams: 2 Tese - NELSON RASSI - 2014.pdf: 2531801 bytes, checksum: 4a281a91c2ca563e8fead55207f00d61 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) / Approved for entry into archive by Cláudia Bueno (claudiamoura18@gmail.com) on 2015-10-15T20:31:04Z (GMT) No. of bitstreams: 2 Tese - NELSON RASSI - 2014.pdf: 2531801 bytes, checksum: 4a281a91c2ca563e8fead55207f00d61 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) / Made available in DSpace on 2015-10-15T20:31:04Z (GMT). No. of bitstreams: 2 Tese - NELSON RASSI - 2014.pdf: 2531801 bytes, checksum: 4a281a91c2ca563e8fead55207f00d61 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) Previous issue date: 2014-09-13 / Background: The number of patients with Type 2 Diabetes Mellitus (T2DM) in Brazil has, in recent decades, increased substantially and insulin therapy is often necessary in a large portion of this population in order to achieve appropriate glycemic control. Objective: To evaluate glycemic control achieved with recombinant human insulin NPH - Gansulin and compares it with human NPH insulin - Humulin N® in patients with Type 2 Diabetes Mellitus. Subjects and methods: A prospective, double-blind, randomized, parallel, single center with 37 individuals with type 2 diabetes using insulin NPH insulin. For statistical analyzes were used: the multiple comparison test of Tukey-Kramer test, Wilcoxon paired comparison test and Chi- Square. It was regarded level of significance value lower than 5% (p<0.05). Results: Insulins NPH and Humulin Gansulin showed similar reductions in HbA1c at the end of the study compared to baseline. Initial HbA1c 7.91% in the Humulin group was reduced to 6.56% (p<0.001) at the end of the study whereas in the Gansulin the glycated hemoglobin was reduced from 8.18% to 6.65% (p<0.001). At the end of the study there was no significant difference between the glycated hemoglobin levels (p=0.2410), fasting blood glucose (p=0.9257) and glucose at bedtime (p=0.3906) between the two types of insulin. Regarding the number of hypoglycemic events, there was no significant difference between the two insulins and no severe hypoglycemic episodes were recorded. Conclusion: The NPH Gansulin (Insuneo N®) presented glycemic control similar to that presented by human insulin Humulin N® in patients with DM2. It was considered level of significance value less than 5%. / Fundamento: O número de pacientes com Diabetes Mellitus Tipo 2 (DM2) no Brasil tem, nas últimas décadas, aumentado substancialmente e a terapia insulínica é necessária em uma grande parcela desta população com a finalidade de adquirir controle glicêmico adequado. Objetivo: Avaliar o controle glicêmico obtido com a insulina humana recombinante NPH – Gansulin e compará-la com o da insulina humana NPH – Humulin N® em pacientes com Diabetes Mellitus Tipo 2 (DM2). Sujeitos e métodos: Estudo prospectivo, duplo cego, randomizado, paralelo e monocêntrico com 37 indivíduos portadores de diabetes tipo 2, em uso de insulina NPH. Para as análises estatísticas foram utilizados: o teste de comparações múltiplas de Tukey-Kramer, o teste de comparação pareada de Wilcoxon e o teste Chi-Square. Foi considerado como nível de significância o valor inferior a 5% (p<0,05). Resultados: As insulinas NPH Humulin e Gansulin apresentaram reduções semelhantes da HbA1c ao final do estudo, quando comparadas aos valores iniciais. A HbA1c inicial de 7,91% do grupo Humulin foi reduzida para 6,56% (p<0,001), enquanto que na do Gansulin, a redução foi de 8,18% para 6,65% (p<0,001). Ao final do estudo não houve diferença significativa entre os valores de hemoglobina glicada (p=0,2410), glicemia jejum (p=0,9257) e glicemia ao deitar (p=0,3906) entre os dois tipos de insulina. Em relação ao número de eventos hipoglicêmicos, não se observou diferença significativa entre as duas insulinas e não foram registrados episódios hipoglicêmicos graves. Conclusão: A insulina NPH Gansulin apresentou controle glicêmico semelhante ao apresentado pela insulina humana Humulin N® em pacientes com DM2.
43

Development and Characterization of an Iridium-Modified Electrochemical Biosensor for Potential Diabetic Patient Management

Fang, Lei January 2009 (has links)
No description available.
44

Engineering the N-Glycosylation Pathway in Pichia Pastoris for the Expression of Glycoprotein Hormones

Manoharan, Simna January 2016 (has links) (PDF)
Proteins, participating in a myriad of biological function, are at the core of all cellular activities occurring within living organisms. Therapeutic proteins, hence constitute a major part of the pharmaceutical industry. The glycoprotein hormones follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH) and human chorionic gonadotropin (CG) regulate various reproductive and metabolic functions in humans and hence have high therapeutic potentials. The increasing demand of recombinant proteins for therapeutic uses drives the development of better expression systems. The methylotrophic yeast Pichia pastoris, has been termed as an industrial workhorse for heterologous protein expression. However, the N-glycosylation in yeast is of the high mannose type, resulting in a reduced serum half-life of the recombinant proteins. In the current work, we have re-engineered the Pichia N-glycosylation pathway to mimic the human type of N-glycosylation. Towards this end, we abolished the yeast native N-glycosylation and introduced enzymes from various eukaryotic sources into the system. These modifications resulted in the conversion of the yeast Man9-20GlcNAc2 glycan structure to a more human like GlcNAc2Man3GlcNAc2 form on over 70 % of the heterologous expressed proteins. In order to demonstrate the application of these strains as efficient protein expression hosts, the glycoengineerd Pichia was used for large scale expression of the glycoprotein hormones, hCG and FSH. The purified recombinant hormones were found to have binding affinities and structure similar to that of the natural hormones. These recombinant hormones were also able to elicit over two fold responses in animal models compared to buffer controls and the activity was comparable to the natural counterparts. Thus, we report the generation of a glycoengineered Pichia pastoris, which can be considered as a serious contender for the expression of glycosylated proteins of therapeutic importance.
45

BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE

Issa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
46

BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE

Issa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
47

BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE

Issa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.

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