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Biomedical subjects

R D Griffiths

Publications and source records attributed to R D Griffiths.

At least 37 records · Page 2Linked to original sources
PubMed1999

Randomized clinical outcome study of critically ill patients given glutamine-supplemented enteral nutrition.

Glutamine is normally an abundant amino acid in the body. It has many important metabolic roles, which may protect or promote tissue integrity and enhance the immune system. Low plasma and tissue levels of glutamine in the critically ill suggest that demand may exceed endogenous supply. A relative deficiency of glutamine could compromise recovery, resulting in prolonged illness and an increase in late mortality, morbidity, and consequently hospital costs. Using a prospective block-randomized, double-blind treatment study design, we tested whether a glutamine-containing enteral feed compared with an isonitrogenous, isoenergetic control feed would influence outcome. The study endpoints were morbidity, mortality, and hospital cost at 6 mo postintervention. In one general intensive care unit (ICU), to ensure consistency of management policies, 78 critically ill adult patients with Acute Physiological and Chronic Health Evaluation (APACHE) II score of 11 and greater and who were considered able to tolerate introduction of enteral nutrition were studied. Fifty patients successfully received enteral nutrition (26 glutamine, 24 control). There was no mortality difference between those patients receiving glutamine-containing enteral feed and the controls. However, there was a significant reduction in the median postintervention ICU and hospital patient costs in the glutamine recipients $23,000 versus $30,900 in the control patients (P = 0.036). For patients given glutamine there was a reduced cost per survivor of 30%. We conclude that in critically ill ICU patients enteral feeds containing glutamine have significant hospital cost benefits.

Adult↗
PubMed1999

Glutamine: establishing clinical indications.

Glutamine, a non-essential amino acid, is abundant in the human body and in the food we eat; it is mainly produced in skeletal muscle and acts as a major inter-organ nitrogen and carbon transporter. Its importance to the metabolism is evident during stress, when it becomes a conditionally essential amino acid when endogenous supply fails to meet increased demands. During the past 2 years, an increased understanding has been gained into the role of glutamine in metabolism. A number of new clinical studies of glutamine supplementation have shown interesting outcomes that should be influencing clinical decision-making.

Arginine↗
PubMed1999

Hypokalaemic paralysis revealing Sjögren syndrome in an elderly man.

A 73 year old white man presented with life threatening hypokalaemic paralysis requiring admission to an intensive care unit. Biochemical investigations showed severe hypokalaemia with hyperchloraemic metabolic acidosis, a spot urine pH of 6.5, and a positive urinary anion gap, establishing the diagnosis of distal renal tubular acidosis. Autoimmune tests revealed Sjögren syndrome as the underlying cause of the distal renal tubular acidosis. Full recovery followed potassium and alkali replacement. This dramatic presentation of Sjögren syndrome has not previously been reported in an elderly man.

Acidosis, Renal Tubular↗
PubMed1999

Manipulating the metabolic response to injury.

In this short review we will concentrate on just one of the features of the metabolic response to injury (classified as accidental trauma, injury or sepsis) which are collectively known as the 'flow' phase. These include an increase in energy expenditure (hypermetabolism), changes in substrate utilisation (insulin resistance) and the focus of this chapter muscle wasting or catabolism. It is recognised that the three features are interrelated, for example insulin is believed to be an important factor in controlling amino acid flux in skeletal muscle and increasing environmental temperature which may reduce flow phase hypermetabolism has been shown to reduce postoperative nitrogen excretion (a marker of protein catabolism). However, we will concentrate on muscle wasting and refer the reader to other reviews on insulin resistance and metabolic rate.

Glutamine↗
PubMed1998

Microvascular endothelial activation in the skeletal muscles of patients with multiple organ failure.

The relationship between microvascular damage and the presence of muscle fibre atrophy and necrosis has been investigated in skeletal muscle biopsies taken from 57 patients with multiple organ failure. Immunohistochemical studies showed no loss of capillaries and no luminal thrombosis, while neutrophil leucocytes were more prevalent in the patients' biopsies than in controls. Deposition of the complement membrane attack complex (C5-9MAC) in capillaries was observed in 41% of cases. Endothelial activation was suggested by an increased intensity of expression of ICAM-1, and by an increased proportion of capillaries expressing P selectin and E selectin, although this was not directly associated with neutrophil accumulation. Endothelial swelling was present in many biopsies with 38% of the biopsies having larger capillary profiles on immunohistochemical labelling for von Willebrand factor (vWF), thrombomodulin and CD34, and on Ulex europaeus agglutinin 1 binding. Endothelial swelling was confirmed by image analysis and morphometric evaluation of capillary ultrastructure, however, the capillary luminal area was not reduced as the capillaries were dilated. Increased vWF labelling was associated with C5-9MAC deposition and with fibre necrosis, but the vascular changes were not related to fibre atrophy nor to clinical indices of the severity of the patients' illness. The results suggest that microvascular damage and ischaemia may not be major factors in the pathogenesis of muscle fibre damage in multiple organ failure, but that endothelial activation is a common occurrence. The variability in the patterns of markers of endothelial activation, and the small proportion of capillaries affected, may reflect the complexity of the endothelial response to circulating or locally produced cytokines.

Adult↗
PubMed1998

Muscle fibre atrophy in critically ill patients is associated with the loss of myosin filaments and the presence of lysosomal enzymes and ubiquitin.

Muscle wasting and weakness are common features of patients with critical illnesses, and may impair their recovery. This study examines whether cytoskeletal and contractile proteins are damaged, and which proteolytic mechanisms might be involved, in the muscle fibre atrophy or necrosis associated with the acute myopathy of critically ill patients. Ninety-eight muscle biopsies were obtained by the conchotome method from 57 critically ill patients and examined morphometrically and by immunohistochemical labelling. Sequential biopsies showed a mean reduction in fibre cross-sectional areas of 3-4% per day. More intense immunolabelling for desmin was seen in the smaller fibres of 52% of the biopsies, while immunolabelling for dystrophin, actin and myosin heavy chains was maintained. Myosin ATPase activity was weak in the smaller fibres in some biopsies, and electron microscopy showed the loss of myosin filaments in atrophic fibres. These changes suggest that loss of the filamentous structure of myosin, without degradation of the immunolabelled epitopes, leads to the collapse of the intermyofibrillar desmin network. Fibres with abnormal desmin labelling showed increased cathepsin B, lysozyme and ubiquitin immunolabelling. Nine cases showed increased immunolabelling for heat shock protein 72. The changes in desmin immunolabelling were more prevalent in patients with higher APACHE II scores on admission, but were not related to other clinical features. The results indicate that fibre atrophy is associated with myosin filament depolymerization and the presence of several proteolytic enzymes. In our study, these changes occurred in patients who were critically ill but who did not receive large doses of steroids or neuromuscular blocking agents.

Adult↗
PubMed1997

Six-month outcome of critically ill patients given glutamine-supplemented parenteral nutrition.

An abundant amino acid in the human body, glutamine (Gln) has many important metabolic roles that may protect or promote tissue integrity and enhance the immune system. Low plasma and tissue levels of Gln in the critically ill suggest that demand may exceed endogenous supply. A relative deficiency of Gln in such patients could compromise recovery and result in prolonged illness and an increase in late mortality. This study examines this hypothesis. Using a prospective, block-randomized, double-blind treatment study design, we tested whether a Gln-containing parenteral nutrition (PN) compared with an isonitrogenous, isoenergetic control feed would influence outcome, with the endpoints of morbidity, mortality, and cost at 6 mo postintervention. In one general intensive care unit (ICU), to ensure consistency of management policies, 84 critically ill adult patients, with Acute Physiological and Chronic Health Evaluation II score > 10, requiring nutritional support received PN only if enteral nutrition was contraindicated or unsuccessful. Survival at 6 mo was significantly improved in those receiving Gln PN (24/42 versus 14/42; P = 0.049). Significantly more deaths occurred in patients requiring control PN for > 10 d (P = 0.03). The excess control deaths occurred later and those patients had had a significantly longer postintervention stay (P = 0.012) and use of ICU. In the Gln recipients, the total ICU and hospital cost per survivor was reduced by 50%. In critically ill ICU patients unable to receive enteral nutrition, a Gln-containing PN solution improves survival at 6 mo and reduces the hospital costs per survivor.

Adult↗
PubMed1996

Effect of parenteral L-glutamine on muscle in the very severely ill.

Glutamine (Gln)-supplemented perioperative total parenteral nutrition (TPN) has been reported to reduce the loss of intramuscular glutamine following routine surgery. This study investigates whether glutamine-supplemented TPN can alter muscle biochemistry acutely in the very severely ill patient. Thirty-eight patients (age 19-77 yr; mean 55 yr), critically ill (APACHE II range 8-31; median 17) admitted to the intensive care unit (ICU) were recruited to receive either conventional TPN (CTPN) or an isonitrogenous, isoenergetic feed supplemented with 25 g crystalline L-glutamine per 24 h (GTPN) in a prospective, double blind, block-randomized study. In a representative sample of these patients, relatives consented to a paired muscle biopsy taken before feeding (10 GTPN/9 CTPN patients; ICU Day 2-4) and repeated 5 days later (16 patients; ICU Day 7-9). Muscle biopsies and matching plasma samples were analyzed using a coupled glutaminase-glutamate dehydrogenase enzymatic assay. A correction was made using sodium to account for the massive changes in extracellular fluid volume. The average muscle Gln content before feeding was very low. Between biopsies no consistent pattern of change was seen with or without exogenous Gln. It also proved difficult in these very sick patients to correct a low plasma Gln with L-Gln-TPN during the initial phase of the severe illness. TPN supplementation with 25 g/24 h, L-glutamine appears inadequate in the acute period to counteract the muscle and plasma biochemical changes seen in these patients. It is unknown whether any larger dose could alter this state.

Adult↗
PubMed1994

Providing psychological support for patients after critical illness.

The majority of patients have little or no memory of their stay in ICU or remember only pain, suctioning or lack of sleep. Dreams and nightmares while in the intensive care unit (ICU) and after discharge home have also been reported. The few studies investigating the longer-term psychological problems of critical illness point to a picture of social isolation with patients avoiding company and showing less affection to their partners. Our own experience, running a special outpatient clinic and following up patients by post, showed a picture of depression, anxiety, irritability and social isolation. This led to the setting up of an ICU staff-led support group for patients recovering from critical illness. This article outlines the possible problems and pitfalls of setting up and running a support group for patients recovering from critical illness. The type of patients suitable to attend such a group is examined. Two case histories give an illustration of the type of problems ICU patients experience during their recovery and how an informal support group can help. In addition to possible benefits to the patients, support groups can also give ICU staff a chance to understand the process of recovery from critical illness and to examine the effects on patients of their own practice. However, they must also have enough insight to know when a patient needs professional help; for example, a patient displaying symptoms of post-traumatic stress disorder should be referred, with their agreement, to a clinical psychologist.

Anxiety↗
PubMed1994

The incidence of gestational diabetes mellitus in the Illawarra area of New South Wales.

The incidence of gestational diabetes in the Illawarra area is 7.2% (95% CI: 6.0-8.4). This was determined by data collected by 2 prenatal clinics and 3 private practitioners during 1993. The incidence rate varied between 5.1% at one hospital to 11.3% with a private practitioner. This variation was mainly due to differences in age and ethnic background. The highest incidence rate of 11.9% was found in women of Asian background.

Adult↗
PubMed1993

Diabetes in the workplace. Employment experiences of young people with diabetes mellitus.

OBJECTIVE: To assess some of the employment experiences of people with diabetes mellitus and to compare their experiences with those of a non-diabetic sibling control group. DESIGN: A questionnaire about employment experiences was administered to diabetic subjects aged 16-39 years, and an abbreviated questionnaire was administered to their eligible siblings. SETTING: The Illawarra area of New South Wales. PARTICIPANTS: The names of diabetic subjects were obtained from the Illawarra diabetes register. RESULTS: Interviews were conducted with 184 of 226 (81.4%) eligible diabetic subjects and with 70 eligible siblings. There were no significant differences between the diabetic subjects and their siblings with respect to educational achievements and rates of employment. Siblings reported a mean of 2.6 days sickness absenteeism in the year prior to the survey. Diabetics were absent from work for a mean of 4.5 days for reasons not related to their diabetes and for a mean of 2.6 days for diabetic causes. Within the diabetic group, 50% felt that having diabetes would make it more difficult to find another job, 33.7% felt that diabetes would influence their search for alternative employment and 19.6% felt that at some stage they had been refused employment because of their diabetes. Fifteen per cent of diabetics were aware of an example of discrimination and 24.2% of diabetics in employment had at some stage tried to hide their diagnosis from their employer. CONCLUSIONS: Diabetics do not appear disadvantaged compared with their siblings with respect to employment participation but are more likely to be absent from work due to sickness. However, many diabetic subjects had experienced a job refusal, had tried to hide their diagnosis from employers, were aware of examples of discrimination and were very negative about future employment prospects.

Absenteeism↗