Biomedical subjects
G Delmore
Publications and source records attributed to G Delmore.
Should cancer patients with incurable disease receive parenteral or enteral nutritional support?
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Assessment of nutritional status in cancer patients: widely neglected?
Frank cachexia is usually evident in the clinical evaluation, but important metabolic alterations in tumour-bearing patients with slight weight changes are frequently overlooked. Since several factors are involved in cancer-induced malnutrition (marasmus type descriptive of general inadequate food intake, kwashiorkor type descriptive of inadequate protein intake/increased turnover), medical/dietary history and physical examination (dynamic weight loss, vitamin/mineral deficiency) should be complemented by simple additional laboratory tests. Minimal baseline testing may include: weight loss (> 5%/month = severe) and serum albumin (< 24 g/l = severe). Anthropometric measurements (triceps skin fold, midarm muscle circumference) for the assessment of fat deposits and lean body mass are rarely used in a routine clinical setting owing to great variations among individuals and interobserver measurement variability. The Prognostic Nutritional Index (PNI), including serum parameters, immune competence testing and anthropometrics (but no further dietary parameters, i.e. dynamic weight loss), has proved to be quite a reliable method of predicting postoperative morbidity/mortality and of selecting cancer patients for aggressive preoperative nutritional interventions. For clinical studies including the evaluation of nutritional status (stratification, prognostic impact) and/or outcome (nutritional interventions), a simple standardized and validated assessment protocol including dietary history, specific physical examination and widely available laboratory testing should be implemented to document significant nutritional alterations. Body weight alone will often fail to demonstrate important disease- or therapy-related changes in caloric intake or metabolic rate.
Nutrition in cancer patients: frustrating neglect and permanent challenge.
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Fighting cancer cachexia--what about today's armory?
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Healing and relapse of reflux esophagitis during treatment with ranitidine.
In 108 patients the healing and relapse of reflux esophagitis, defined endoscopically by the presence of epithelial defects (erosions and ulcerations) of the esophageal mucosa, were studied. In the first study, with open treatment of ranitidine, the healing rate after 6 wk was 50%. The most important factor that negatively influenced healing was the extent of esophageal erosions. Patients with isolated erosions had a 6-wk healing rate of 78%; the healing rate was 38% in patients with longitudinally confluent lesions and 23% in those with circumferential erosions of the distal esophagus. Smoking also had an unfavorable effect. Age, sex, duration of history, body weight, and alcohol consumption were not related to outcome. Symptoms improved during treatment with ranitidine, but the correlation between symptoms and endoscopic findings at 6 wk was weak. In the second study, relapse was investigated in 61 patients with healed esophagitis in a randomized, double-blind trial comparing placebo and ranitidine (150 mg at bedtime for 6 mo). In both groups, relapse occurred in more than one-third of the patients, with no significant difference between ranitidine and placebo treatment. Patients with worse daytime symptoms at the time of previous healing had a higher relapse rate. The initial severity of esophagitis and smoking did not influence recurrence. Thus, the initial endoscopic findings are of prognostic value in reflux esophagitis. Smoking retards healing. Low-dose maintenance treatment with ranitidine does not prevent relapse.
[Sonography of the biliary tract].
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[Treatment of reflux esophagitis with ranitidine. A multicentric prospective study].
Thirty-eight patients with erosive-ulcerative reflux esophagitis were treated in an open trial with the histamine-H2-receptor antagonist ranitidine (150 mg twice daily). At endoscopy after 6 weeks there was evidence of complete healing of all epithelial defects in 20 of 38 patients (53%). Continuation of treatment for another 6 weeks in 13 patients was followed by healing in 6 additional patients as judged by endoscopy. Although the symptoms of the group as a whole improved significantly during treatment, there was no correlation between the degree of symptomatic improvement and healing of esophagitis. Also, the healing rate did not depend on age, sex, smoking and drinking habits or on the severity of esophagitis. It is concluded that medical treatment of reflux esophagitis with ranitidine is promising, even in severe cases previously considered candidates for surgery.
[Liver fascioliasis with unusual abscess formation. Case report].
The case is reported of a 34-year-old Swiss who presented with signs of liver abscess after returning from South America. The symptoms regressed under trial treatment with a tissue amoebicide. The initial blood hypereosinophilia could be explained only 8 months later by the presence of eggs of Fasciola hepatica in the patient's faeces. Serological investigations were negative for amoebiasis an hydatid disease but positive for fascioliasis. The possibility of abscess formation by infestation with F. hepatica is discussed.
The role of augmented breaths (sighs) in bronchial asthma attacks.
The study is based on plethysmographic, neurophysiological and respiratory mass-spectrographic records established during anaphylactic or histamine-induced bronchial asthma attacks in guinea-pigs. The frequency of occurrence of the augmented breaths (sighs) is correlated with the intensity of the lung deflation reflex (tachypnoea) which arises during the attack. In the acute phase of the asthma attack, the sighs increase in number and reinforce the uneven ventilation which underlies stimulation of the pulmonary deflation receptors. The sigh becomes an essential component of the vicious circle of uneven ventilation and vagal lung deflation reflex induced. This circle is broken in the recovery phase of the asthma attack, during which the sighs decrease in number, as the conditions underlying their occurrence subside; they now lessen the uneven ventilation and by reopening closed lung units promote a return to normal conditions in lung mechanics. It is concluded that augmented breaths, like the asthmatic tachypnoea, are caused by uneven ventilation resulting in pulmonary self-compression and in turn stimulation of the pulmonary deflation (irritant) endings. Some factors which possibly contribute to the elicitation of augmented breaths are discussed.