pituitrin and Infections

The role of corticosteroid therapy in patients with cardiac arrest (CA) is uncertain. We aimed to evaluate the efficacy and safety of corticosteroid therapy in CA patients.. Randomised controlled trials were identified using PubMed, EMBASE, Cochrane Central Register of Controlled Trials, the Chinese National Knowledge Infrastructure and the Chinese Biomedical Literature Database. The primary outcome was overall survival. Secondary outcomes were positive neurological status and probability of sustained restoration of spontaneous circulation (ROSC). Complications were infection and bleeding. Given the significant heterogeneity across previous studies, combining the data using meta-analysis was deemed not appropriate.. Five studies (551 patients) met the criteria. Two studies of co-intervention therapy (corticosteroid, vasopressin and epinephrine protocol) found that this approach could benefit in-hospital CA patient survival rates at hospital discharge, improve neurological function at hospital discharge and yield sustained ROSC rate. However, further two studies failed to demonstrate that corticosteroid therapy alone could improve survival and neurological outcomes among CA patients. Additionally, corticosteroid therapy did not increase the risk of infection and bleeding.. Due to the inherent limitations of the studies in this review, we have not been able to reach definitive conclusions. Larger-scale and better-designed studies are therefore recommended, to further evaluate the potential and rational use of corticosteroid therapy in CA patients.

Topics: Cardiopulmonary Resuscitation; Drug Therapy, Combination; Epinephrine; Glucocorticoids; Heart Arrest; Hemorrhage; Hospital Mortality; Humans; Infections; Randomized Controlled Trials as Topic; Risk Assessment; Survival Rate; Treatment Outcome; Vasopressins

The syndrome of inappropriate antidiuresis (SIAD; formerly the syndrome of inappropriate secretion of antidiuretic hormone) is the most frequent cause of hyponatremia. A strong association exists between mortality and hyponatremia, which reflects the severity of the underlying disease. In SIAD, hyponatremia is associated with normovolaemia but the assessment of extracellular volume can be difficult. Clinical features are mainly neurological and can lead to death but mechanisms of adaptation can limit cerebral oedema. The notion of mild asymptomatic hyponatremia was questioned by the observation of subclinical neurocognitive impairment, a greater risk of falls and fractures. Aetiologies are classified into six groups: neurologic disorders, infections mainly cerebral, meningeal and pulmonary, drugs in particular antidepressants, tumors, genetic causes, and idiopathic. Symptomatic acute hyponatremia is a therapeutic emergency that is not specific of SIAD. When hyponatremia is asymptomatic, fluid restriction with salt intake is generally sufficient but urea can be an alternative. In chronic SIAD, there is currently no recommendation. Fluid restriction is not always feasible; urea has proved its efficacy, its good tolerance and its long-term harmlessness. Vaptans have demonstrated their good tolerance and their efficacy on the correction of hyponatremia from SIAD in studies subgroups, for moderate hyponatremia and asymptomatic patients. In the only study having compared vaptans and urea, efficacy and tolerance were similar. Because of the cost difference between vaptans and urea and while waiting for follow-up studies, urea appears at present as the first-line treatment of hyponatremia in SIAD.

Topics: Diagnosis, Differential; Genetic Predisposition to Disease; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infections; Neoplasms; Neurophysins; Protein Precursors; Vasopressins; Water-Electrolyte Balance

Topics: Dehydration; Fluid Therapy; Glucose; Humans; Hyponatremia; Infections; Meningitis; Pediatrics; Sodium Chloride; Vasopressins

A survey is given on the regulation of the formation of corticoliberin and of pro-opiomelanocortin and of ACTH, respectively, and on the significance of these compounds. The formation of pro-opiomelanocortin is furthered by corticoliberin, vasopressin, oxytocin and angiotensin II. Receptors for the binding of corticoliberin appear in numerous parts of the central nervous system. In various diseases the content of corticoliberin in the plasma and in certain tissues is changed. The inhibition of the ACTH secretion by glucocorticosteroids takes place via a decrease of the formation of corticoliberin and by a reduction of the equipment of the corticotrophic cells with receptors for its binding. The secretion of corticoliberin and of ACTH, respectively, is increased by loads, by hypoglycaemia, by blood losses, by hypoxia and by infections. In the glucocorticosteroid receptors there are 2 types with different affinity to cortisol and corticosterone.

Topics: Adrenocorticotropic Hormone; Angiotensin II; Corticotropin-Releasing Hormone; Hemorrhage; Humans; Hypoglycemia; Hypoxia; Infections; Oxytocin; Pro-Opiomelanocortin; Receptors, Cell Surface; Vasopressins

Topics: Adrenal Cortex Hormones; Adult; Analgesics; Antifibrinolytic Agents; Blood Transfusion; Cardiovascular Diseases; Child; Contraceptives, Oral; Estrogens; Factor IX; Factor VIII; Gastrointestinal Diseases; Hemarthrosis; Hemophilia A; Hemophilia B; Hemorrhage; Home Nursing; Humans; Infections; Inhalation; Nervous System Diseases; Social Adjustment; Thyroxine; Triiodothyronine; Urologic Diseases; Vasopressins

Topics: Angiotensins; Arginine Vasopressin; Blood Circulation; Bradykinin; Classification; Heparin; Histamine; Infections; Serotonin; Shock; Vasomotor System; Vasopressins

Topics: Aldosterone; Animals; Dextrans; Diuresis; Dogs; Infections; Polyuria; Vasopressins

Topics: Carcinoma, Bronchogenic; Endocrine System Diseases; Hormones, Ectopic; Humans; Hyponatremia; Infections; Lung Neoplasms; Male; Middle Aged; Myxedema; Pituitary Diseases; Porphyrias; Vasopressins