[Oncological intensive care: 2013 and 2014 years'review]. / Soins Intensifs Oncologiques: Revue des années 2013 et 2014.

The objective of this paper is to review the literature published in 2013 and 2014 in the field of intensive care and emergency related to oncology. Are discussed because of new original publications: prognosis, life-supporting techniques, septic shock and infectious complications, anticancer treatment in intensive care, tumoral lysis syndrome, respiratory, thromboembolic and vascular, digestive and hepatic, and neurologic complications, oncologic emergencies, therapeutic limitations.

L'objectif de l'article est de revoir la littérature publiée en 2013 et 2014 dans le domaine des soins intensifs et des urgences en rapport avec l'oncologie. Sont envisagés en raison de nouvelles publications originales le pronostic, les techniques de support vital, le choc septique et les complications infectieuses, le traitement anticancéreux en soins intensifs, le syndrome de lyse tumorale, les complications pulmonaires, thromboemboliques et vasculaires, digestives et hépatiques, neurologiques, les urgences oncologiques, les limitations thérapeutiques.

Medical anticancer treatment of lung cancer associated with comorbidities: a review.

Comorbidities are frequent in patients with lung cancer, who are often treated with systemic anticancer therapy. The purpose of the present review is to report the adaptations recommended for the various drugs used in lung cancer treatment, in the context of a specific comorbidity. The literature was reviewed for neurologic, endocrine, hepatic, renal, digestive, cardiovascular, pulmonary, blood and systemic diseases. The comorbidities impact on the systemic anticancer treatment is poorly assessed. There are no good data with a high level of evidence and literature is often limited to experts' opinion and to case reports. We need to improve our knowledge about those patients by adequate multicentric and prospective studies and registries in order to offer them better care in term of evidence-based medicine.

[Metabolic risks of salbutamol in diabetic patients. A study using somatostatin (author's transl)]. / Risques métaboliques induits par le salbutamol. Etude à l'aide de la somatostatine.

Salbutamol-induced diabetic ketoacidosis having recently been reported, the authors have studied the metabolic changes produced by the drug in 6 nondiabetic patients. All patients received a 3-hour infusion of salbutamol (S) 20 z g/minm. On the following day, three of these were given somatostatin (SRIF) 100 mg/hour mixed with S infused at the same rate, whilst the remaining 3 patients received SRIF alone. On the 3rd day, patients of the first sub-group received the same infection of S and SRIF as before plus exogenous glucagon 90 ng/kg/hour. Somatostatin is know to inhibit insulin and glucagon secretion. Exogenous glucagon was given in order to reproduce the metabolic conditions of insulin-deficient diabetes mellitus. Salbutamol alone induced a small rise in blood glucose and insulin, free fatty acids, glycerol and ketonic bodies, but no changes in endogenous glucagon. SRIF alone produced no significant metabolic variations. In the presence of SRIF, all salbutamol-induced metabolic changes were increased. Adding glucagon mainly resulted in high levels of ketonic bodies. All variations correlated with each other. Thus, whilst the hyperglycaemic, lipolytic and ketogenic effects of S in non-diabetic patients are partly masked by insulin hypersecretion, they are enhanced in the absence of insulin and, to an even greater extent, by an excess of glucagon. Diabetic patients treated with salbutamol should therefore be under close surveillance and have their insulin dosage increased.

Influence of nutritional factors on the renotrophic action of ACTH in the uninephrectomized rat.

In the rat, renal compensatory hypertrophy (RCH) was apparent 48 h after uninephrectomy; it was significantly enhanced by long-acting beta1-24-corticotrophin (ACTH) when the animals had free access to food and a NaCl solution (9 g/l). In rats starved after uninephrectomy but drinking the NaCl solution freely, RCH was suppressed: the weights of the body, heart, liver, and solitary kidney were reduced. In similarly starved rats treated with ACTH, the weights of the heart and the solitary kidney were normal. RCH was also impaired in rats fed only a glucose solution (30 g/dl) after uninephrectomy, but it is restored by ACTH, which significantly increases the weight of the remaining kidney. This renotrophic action of ACTH may be related to hyperglycemia and, perhaps, elevated urinary K excretion, which occur in hyper-adrenocorticism and increase the work load of the nephron.

[Effects of fasting and of ACTH on renal compensatory hypertrophy in the 48 hour uninephrectomized rat]. / Effets du jeûne et de l'ACTH sur l'hypertrophie rénale compensatrice chez le rat uninéphrectomisé depuis 48 heures.

Renal compensatory hypertrophy (R.C.H.) is determined 48 h. after uninephrectomy in fed and fasting rats having free access to a NaCl solution. ACTH (18 gamma/100 g BW/d/2d) enhances R.C.H. in the fed animals. R.C.H. is severely impaired by food deprivation and the remaining kidney looses weight; a normal kidney weight can be maintained if the fasted, uninephrectomized rat is treated with ACTH. These experiments suggest that the stimulation of the adrenal cortex by ACTH has a renotrophic effect. This action may be related to the elevation of blood glucose or/and to the fall of the concentration of plasma K+.

[Enhancement of compensatory renal hypertrophy by beta-1-24 corticotropin in the rat]. / Stimulation de l'hypertrophie rénale compensatrice par la beta1-24 corticotrophine chez le rat.

In the rat, the administration of beta1-24-corticotrophin during 7 days following an uninephrectomy enhances significantly the compensatory hypertrophy of the remaining kidney. There is no increase in renal compensatory hypertrophy when ACTH is injected to previously adrenalectomized rats. This action of ACTH could be related to the diabetes mellitus induced by this hormone or to an increase in sodium reabsorption by the tubular epithelial cells.