Hormonal Control of Metabolism in Trauma and Sepsis

Frayn, Keith N.

doi:10.1111/j.1365-2265.1986.tb03288.x

Cited by 244 publications

(123 citation statements)

References 105 publications

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“…Increased beta-cell activity, leading to release of immature granules with a higher proinsulin-to-insulin ratio most likely explain these findings. The observation of a high insulin level and a modest increase in plasma glucose concentration is characteristic for the flow phase of the response to injury [27,28,29]. Burn patients, and experimental animals exhibit an exaggerated insulin response to exogenous glucose [28,30,3 11.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic beta‐cell function and interleukin‐1β in plasma during the acute phase response in patients with major burn injuries

Wogensen¹,

Jensen²,

Svensson³

et al. 1993

Eur J Clin Investigation

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Abstract. Animal experiments demonstrate that interleukin-lfl (IL-Ib) is beta-cell cytotoxic in vitro and inhibits insulin secretion in vivo. However, it is unknown if IL-ID affects beta-cell function in man. Since IL-Ip and other cytokines are main mediators of the acute phase response, the objectives of the present study were to examine beta-cell function in patients with major burn injuries, and to test if changes in betacell function correlated to systemic levels of IL-IS and tumour necrosis factor ci (TNFol). We established and validated an IL-lB assay measuring free and protein bound IL-Ip; protein bound IL-lP was detached from the IL-Ip specific binding protein by acidification, rendering it accessible for the employed antibody. The IL-1 p specific binding protein (43-60 kDa) was found in serum and plasma from all tested patients and normal subjects. Survivors of burn injuries had a stimulated beta-cell function, whereas non-survivors had an impaired beta-cell function as indicated by an increased plasma concentration of proinsulin, and an increased proinsulin/insulin ratio. In addition, nonsurvivors had significantly increased plasma levels of TL-I/?. However, we could not demonstrate any correlation between C-peptide, proinsulin, insulin or proinsulin/insulin ratio and plasma concentration of IL-1fi.In conclusion, beta-cell function abnormalities are evident in patients with major burn injuries, and a high plasma level of IL-Ip correlates with a fatal outcome. However, the present study did not provide evidence for the hypothesis that beta-cell function is influenced by circulating IL-IB or TNFci during the acute phase response.

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Section: Discussionmentioning

confidence: 99%

Pancreatic beta‐cell function and interleukin‐1β in plasma during the acute phase response in patients with major burn injuries

Wogensen¹,

Jensen²,

Svensson³

et al. 1993

Eur J Clin Investigation

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“…88 The different lymphocyte populations seem to be affected by malnutrition differently: in thymus-dependant areas, there is a reduction in the number of T-lymphocytes, especially the CD4 + population, whereas the number of Blymphocytes in the spleen, lymph nodes and blood remain normal. 89 According to Frayn (1986), lymphopenia is a result of the reduction in cell proliferation which in turn can be a direct consequence of the lack of protein or elements like iron, zinc and copper or due to hormonal imbalance involving adrenaline, insulin, thyroxin or cortisol. 90 Existing data on humoral response are conflicting, which makes definitive conclusions hard to reach.…”

Section: 57mentioning

confidence: 99%

“…89 According to Frayn (1986), lymphopenia is a result of the reduction in cell proliferation which in turn can be a direct consequence of the lack of protein or elements like iron, zinc and copper or due to hormonal imbalance involving adrenaline, insulin, thyroxin or cortisol. 90 Existing data on humoral response are conflicting, which makes definitive conclusions hard to reach. 2 The concentrations of IgA, IgG and IgM can be, according to some authors, increased, 3,91 or normal or decreased.…”

Section: 57mentioning

confidence: 99%

Haematological alterations in protein malnutrition

Borelli¹,

Blatt²,

Rogero³

et al. 2004

Rev. Bras. Hematol. Hemoter.

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“…A exceção é encontrada naqueles pacientes com lesões muito severas que evoluem para óbito 30 . É possível pressupor também que, uma eventual persistência da hiperglicemia , relatada por vários autores 28,35 , esteja ligada não só aos níveis plasmáticos de cortisol 36 , mas também à ação das interleucinas e prostaglandinas 37,38. A demonstração de que a infusão combinada de cortisol, insulina e glucagon, por período superior a 3 dias 24 , falha na manutenção da resistência insulínica, é mais uma evidência do papel das citoquinas na gênese da proteólise observada nas primeiras semanas após o TCE. A queda da glicemia ocorre somente após o final da fase de fluxo, hipercatabólica, que se prolonga, por vezes, além do 10º dia após o trauma 19,39 .…”

Section: Análise Dos Dados Bioquímicos E Metabólicos E Evolução Dos Punclassified

A resposta metabólica ao trauma cranioencefálico é autolimitada? Análise das proteínas de fase aguda e glicemia

Schelp

Angeleli

Zanini

et al. 1998

Arq. Neuro-Psiquiatr.

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RESUMO -Nos últimos anos tem havido referências à limitação da resposta metabólica nas duas primeiras semanas após trauma cranioencefálico (TCE). Foi feita proposta de estudo a partir de experimento clínico em pacientes com trauma encefálico grave, que foram avaliados por volta de 7 dias após a lesão (M1). A segunda avaliação ocorreu 4 dias após (M2), e a terceira 3 a 4 dias após (M3). Em um período de 2 anos, foram selecionados 28 pacientes do sexo masculino, com trauma encefálico grave, escala de gravidade de Glasgow entre 4 e 6. Dentre os 28 pacientes, 6 completaram o estudo proposto. Os pacientes foram acompanhados clinicamente durante toda a fase do experimento. Em cada um dos momentos de análise, foram feitas análises da excreção nitrogenada e proteínas de fase aguda. Da mesma forma foram feitas determinações da glicemia plasmática, N-amínico e triglicerídeos. Os resultados do estudo demonstraram não haver modificações no balanço nitrogenado, normalização da proteína-C-reativa e redução relativa da glicemia ao final do experimento. Os autores tecem considerações sobre os possíveis mecanismos envolvidos na modulação da resposta metabólica e concluem que o hipermetabolismo, a basear-se na análise da glicemia e das proteínas de fase aguda, não persiste além do 13°d ia do período de recuperação pós-trauma. São feitas sugestões de estudos futuros que possam elucidar os mecanismos envolvidos na normalização do hipercatabolismo e hipermetabolismo observados nas duas primeiras semanas após TCE. PALAVRAS-CHAVE: trauma cranioencefálico, proteínas de fase aguda, metabolismo protéico. Is the metabolic response self-limited in head trauma? Analysis of acute phase proteins and glycemiaABSTRACT -There are many reports supporting a self-limitation mechanism involved with hypermetabolic response after severe cranial injury. It was proposed a study with severe head injury patients, in three stages of the evolution. The first 7 days after admission (moment 1-M1), the second three days latter (M2) and the last 7 days after the first (M3). Among male patients with severe head injury, attended between January 1992 and December 1993 in University Hospital of Botucatu, UNESP, were selected 28 male patients, with Glasgow severity scale between 4 and 6, with pO 2 < 70 mm Hg, weighting 60 kg or more. Among these patients, 6 finished the study, including analysis of the excretion of N, acute phase proteins, glycemia, triglycerides and amine nitrogen. During the study there were no changes in nitrogen balance and there was a decrease in protein Creative. Glycemia tends to fall within two weeks after injury. The authors make some considerations about possible mechanisms involved in brain modulation associated with the period of dependence of hypermetabolism and hypercatabolism after closed brain injury. There are some evidences that the brain responds to head trauma with a gobal non specific way, which tends to be reorganized beyond the first two weeks after lesion. The study does not show any influence of the type and severity of head...

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Hormonal Control of Metabolism in Trauma and Sepsis

Cited by 244 publications

References 105 publications

Pancreatic beta‐cell function and interleukin‐1β in plasma during the acute phase response in patients with major burn injuries

Pancreatic beta‐cell function and interleukin‐1β in plasma during the acute phase response in patients with major burn injuries

Haematological alterations in protein malnutrition

A resposta metabólica ao trauma cranioencefálico é autolimitada? Análise das proteínas de fase aguda e glicemia

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