Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of its wide distribution in the organism, natural somatostatin (SRIF) demonstrates an ample spectrum of actions, involving mainly the central neuroendocrine system and the enteropancreatic area. In the former, this peptide may find its field of application in conditions characterized by excessive GH, TSH or ACTH secretion, depending on the central or peripheral cause of the inappropriate hormone control. The inhibitory effect of SRIF on gastrointestinal and pancreatic hormones may be useful in the management of tumors originating in this system and also in the treatment of inflammatory processes such as pancreatitis, in malignant diarrhea, and in gastrointestinal bleeding. A complex action of SRIF and its derivative on insulin release and glucose homeostasis may offer some advantages in the control of unstable diabetes. Dampening of organic functions in the upper digestive tract may also render SRIF and its analogues useful in the exploration of the gallbladder, gastric and pancreatic functions. The effect of such peptides on tissue growth and on the regulation of blood pressure are the subject of present investigations. Cytoprotection, an interesting aspect of SRIF application, is discussed elsewhere in this compendium. Finally, some comments on the possible use of SRIF as an additive to the conventional treatment of burns and sepsis close this review.
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PMID:Clinical applications of somatostatin. 290 Feb 4

Adrenal hemorrhage is uncommon and usually associated with severe stress, sepsis, or anticoagulant therapy. The association of adrenal hemorrhage and acute ulcerative colitis is rare, and is probably related to exogenous therapy with ACTH. The case of a 29-year-old woman who was hospitalized with severe ulcerative colitis, treated with ACTH, and who developed bilateral adrenal hemorrhage is presented. The difficulties of diagnosis and management are discussed. A review of the relevant literature concerning the pathophysiology of adrenal hemorrhage is presented also.
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PMID:Bilateral adrenal hemorrhage during ACTH treatment of ulcerative colitis. Report of a case and review of the literature. 300 34

The effect of naloxone (4.4-5.9 mg i.v.) was evaluated in 10 patients with circulatory shock (sepsis, n = 7; intoxication, n = 1; cardiogenic shock, n = 2) not responding to full conventional therapy. In addition, we measured plasma ACTH and immunoreactive beta-endorphin before and 60 min after administration of naloxone and compared the results with hormone concentrations in 10 intensive care patients without shock. Only in two patient with septic shock a transient increase (duration 15 min and 60 min, respectively) of systolic blood pressure was observed, while naloxone was ineffective in the remaining eight patients. No adverse effects of naloxone were found. Plasma ACTH and immunoreactive beta-endorphin concentrations in patients with shock were not different from those in controls (ACTH, 79 +/- 28 vs 120 +/- 60 pg/ml; immunoreactive beta-endorphin, 952 +/- 262 vs 1,070 +/- 378 pg/ml). Our findings suggest that naloxone in a single dose of 4.4-5.9 mg i.v. does not improve the management of circulatory shock unresponsive to conventional treatment. beta-endorphin seems to play no major role in the hypotension of shock.
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PMID:Naloxone in treatment of circulatory shock resistant to conventional therapy. 303 94

The regulatory mechanisms of the hypothalamo-pituitary-adrenal system were studied in critically ill, intensive care unit patients. Serial measurements of immunoreactive ACTH-(1-39) (ACTHi), cortisol, endothelin-1 (ETi), and atrial natriuretic hormone (ANHi) were performed in blood samples of 18 patients with clinically defined sepsis, 12 critically ill patients after multiple trauma, and 15 hospitalized matched control subjects without acute illness for 8 consecutive days after admission. On admission, plasma levels of cortisol and ACTHi were significantly elevated in patients with sepsis (1.32 +/- 0.21 mumol/L and 130.0 +/- 38.2 pmol/L, mean +/- SD) and with multiple trauma (1.23 +/- 0.28 mumol/L and 123.7 +/- 41.3 pmol/L) compared to those in the control subjects (0.37 +/- 0.08 mumol/L and 15.6 +/- 5.8 pmol/L, respectively). The plasma cortisol levels of critically ill patients remained high (> 0.8 mumol/L) during the whole observation period. In contrast, plasma ACTHi levels decreased between days 3-5, reaching significantly lower levels on day 5 compared to those in the control group and remained below 5.0 pmol/L during the rest of the observation period. Plasma levels of ETi and ANHi were significantly elevated during the whole period in both patient groups (ETi, > 10 ng/L; ANHi, > 250 ng/L) compared to those in control subjects (< 5 and < 50 ng/L, respectively). The high plasma concentration of ETi observed in our patients may stimulate the steroid secretion of the adrenal cortex directly or potentiate the adrenal effect of ACTH. On the other hand, the increased concentration of ANHi found in critically ill patients together with the increased plasma cortisol level may explain the inhibition of ACTH secretion. Accordingly, we speculate that the high ET level exerts a positive drive on the adrenocortical level, that the high ANH level has an inhibitory effect on the hypothalamo-pituitary level, and that both mechanisms play a role in regulation of the hypothalamo-pituitary-adrenal axis during critical illness.
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PMID:Dissociation of plasma adrenocorticotropin and cortisol levels in critically ill patients: possible role of endothelin and atrial natriuretic hormone. 1048 19

However, side-effects such as severe infections, hypertension and electrolyte imbalance have been found, assumed to be related to hypercortisolism induced by chronic ACTH treatment. The authors treated 18 patients with infantile spasms with non-depot ACTH(1-24). The therapeutic effect of non-depot ACTH was comparable to that of depot ACTH, with no severe bacterial infection or sepsis. The incidence of hypertension was significantly lower in the non-depot ACTH group, and persistent hypercortisolaemia was not found. Non-depot ACTH(1-24) appears to be as effective as ACTH(1-24) depot therapy in the treatment of infantile spasms, and its side-effects are mild. It would appear that the effect of non-depot ACTH is not mediated by hypercortisolism, but by a direct neurotropic effect on the brain.
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PMID:The effect of non-depot ACTH(1-24) on infantile spasms. 825 87

Cortisol concentrations are usually elevated in sepsis, during major surgery and in burns. Adrenocortical response to stress seems to be essential for survival. To investigate the endogenous adrenocortical response to multiple organ failure, rapid ACTH stimulation tests were used in 15 patients. Patients were divided to nonsurvival group and survival group. Patients in both groups appeared to have increased adrenocortical activity, because basal cortisol concentrations were above normal (non-survival group: 33.8 +/- 13.7 micrograms.dl-1, survival group: 19.1 +/- 3.8). There are no significant differences between the two groups. We could not find absolutely adrenal insufficient patient. Plasma cortisol concentrations increased significantly in patients of both groups following ACTH stimulation. We found poor response to ACTH in two patients in non-survival group with very high basal cortisol concentrations. But there is no significant difference of cortisol response between the two groups. We could not determine whether the high mortality is associated with poor response to ACTH or not.
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PMID:[Cortisol responses to rapid ACTH test in patients with multiple organ failure]. 839 Oct 88

Adrenalin insufficiency associated with adrenal hemorrhage, is a rare complication after cardiac surgery in neonates. A boy suffering from transposition of the great arteries, who had an arterial switch-operation on day three of his life, acquired a bilateral adrenal hemorrhage. Clinically the situation resembled a septic shock. Despite large doses of catecholamines, he continued to have severe arterial hypotension, anuria, and kyperkalemia. The clinical condition did not change, although sepsis specific therapy was initiated. Consequently adrenal insufficiency, as a possible postoperative complication, was considered and prednisolon, initially in a dose of 15 mg/kg/d, was administered. The clinical condition improved dramatically. The diagnosis could be confirmed by ultrasound examination and determination of cortisol and ACTH plasma levels. Adrenal insufficiency was only transitory, adrenal sonography on day 135 returned to normal. The surgical procedure on heart-lung bypass, the obligatory anticoagulation and the perioperative stress have to be considered as pathogenetic factors.
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PMID:[Therapy refractory arterial hypotension after heart operation]. 912 Oct 76

The basal cortisol level and cortisol response to ACTH stimulation test were assessed in patients with sepsis, the results being compared to a control group of 30 healthy persons. The study group included 49 patients with sepsis and 30 healthy subjects as a control group. The mean age in the study group was 42.6 +/- 18.7 years and 41.4 +/- 12.1 years in the control group. Fifteen of the 49 (30.6%) patients had hospital-acquired and 34 (69.4%) patients community-acquired sepsis. Etiological agent was isolated in 35 (71.4%) patients (57.1% gram negative bacteria and 34.3% gram positive bacteria, plus 8.6% polymicrobial). Fourteen of 49 (28.6%) patients died. Mean basal cortisol level was 597.1 +/- 304.6 nmol/l (range 217.8-1667.9) in the study group and 460.2 +/- 180.8 nmol/l (range 253.6-988.9) in the control group. Mean basal cortisol level in the study group was significantly higher than that of the control group (p < 0.05). Mean basal cortisol level was found to be 725.5 +/- 448.9 nmol/l in the patients who died and 545.8 +/- 210.9 nmol/l in the patients who recovered. The difference between the two groups was found to be significant (p < 0.05). ACTH stimulation test was performed in 43 of the patients and 30 healthy subjects. Cortisol response was significantly lower (mean 277.7 +/- 216.9 nmol/l) in the patients than that detected in the control group (mean 519.6 +/- 279.2) (p < 0.001). Mean cortisol response in the patients who died was 227.2 +/- 224.5 nmol/l and 302.1 +/- 212.7 nmol/l in the patients who recovered (p > 0.05). Adrenocortical insufficiency was detected in 16.3% of the patients and 42.9% of these patients died. In conclusion, sepsis is characterized by high basal cortisol level which may show a poor prognosis and a blunted cortisol response to ACTH stimulation. A small percentage of patients with sepsis may develop adrenocortical insufficiency.
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PMID:Adrenal functions in patients with sepsis. 922 16

Recent animal and human studies have suggested that leptin secretion is closely linked to the functions of the hypothalamic-pituitary-adrenal (HPA) axis and the immune system, both of which are crucial in influencing the course and outcome of critical illness. Therefore, we measured basal plasma leptin levels and examined the circadian secretion of leptin, in parallel with the hormones of the HPA axis and a key cytokine, interleukin-6, in critically ill patients with acute sepsis. Sixteen critically ill patients from the University of Leipzig Intensive Care Unit were recruited for this study. All of these patients fulfilled the standard diagnostic criteria for sepsis. Plasma leptin levels were measured in all patients and controls at 09:00. In addition, in a subgroup of eight critically ill patients and all of the nine controls plasma leptin, cortisol, ACTH and interleukin-6 concentrations were measured every 4 hours for 24 hours. Mean plasma leptin levels were three-fold higher (18.9 +/- 4.5 ng/ml) in critically ill patients than controls (3.8 +/- 1.0 ng/ml, p < 0.05). Similarly, ACTH levels were lower (7.8 +/- 3.4 pmol/l) in patients than in controls (17.1 +/- 1.5 pmol/l, p < .001), while plasma cortisol levels were increased (947.6 +/- 144 nmol/l) in patients compared to controls (361.1 +/- 29, p < 0.001). Morning plasma interleukin-6 levels were markedly elevated in all patients with sepsis (1238.0 +/- 543.1 pg/ml) versus controls (6.4 +/- 1.7, p < 0.001). The controls exhibited a nyctohemeral fluctuation in plasma leptin levels with peak levels at 23:00; in contrast, septic patients, had no nocturnal rise of leptin. In healthy controls, plasma leptin and cortisol had reciprocal circadian rhythms with high nocturnal leptin levels and low nocturnal cortisol concentrations; in critically ill patients, this relation was abolished. Mean leptin levels were three-fold higher in patients who survived the septic episode (25.5 +/- 6.2, n = 10) than in non-survivors (8.0 +/- 3.7, n = 6, p < 0.01). We conclude that in addition to its function as an anti-obesity factor, leptin may play a role in a severe stress state such as acute sepsis.
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PMID:Plasma leptin levels are increased in survivors of acute sepsis: associated loss of diurnal rhythm, in cortisol and leptin secretion. 943 56

Immune neuroendocrine interactions are vital for the individual's survival in certain physiopathological conditions, such as sepsis and tissular injury. It is known that several animal venoms, such as those from different snakes, are potent neurotoxic compounds and that their main component is a specific phospholipase A type 2 (PLA2). It has been described recently that the venom from Crotalus durissus terrificus [snake venom (SV), in the present study] possesses some cytotoxic effect in different in vitro and in vivo animal models. In the present study, we investigated whether SV and its main component, PLA2 (obtained from the same source), are able to stimulate both immune and neuroendocrine functions in mice, thus characterizing this type of neurotoxic shock. For this purpose, several in vivo and in vitro designs were used to further determine the sites of action of SV-PLA2 on the hypothalamo-pituitary-adrenal (HPA) axis function and on the release of the pathognomonic cytokine, tumor necrosis factor alpha (TNF alpha), of different types of inflammatory stress. Our results indicate that SV (25 microg/animal) and PLA2 (5 microg/animal), from the same origin, stimulate the HPA and immune axes when administered (i.p.) to adult mice; both preparations were able to enhance plasma glucose, ACTH, corticosterone (B), and TNF alpha plasma levels in a time-related fashion. SV was found to activate CRH- and arginine vasopressin-ergic functions in vivo and, in vitro, SV and PLA2 induced a concentration-related (0.05-10 microg/ml) effect on the release of both neuropeptides. SV also was effective in changing anterior pituitary ACTH and adrenal B contents, also in a time-dependent fashion. Direct effects of SV and PLA2 on anterior pituitary ACTH secretion also were found to function in a concentration-related fashion (0.001-1 microg/ml), and the direct corticotropin-releasing activity of PLA2 was additive to those of CRH and arginine vasopressin; the corticotropin-releasing activity of both SV and PLA2 were partially reversed by the specific PLA2 inhibitor, manoalide. On the other hand, neither preparation was able to directly modify spontaneous and ACTH-stimulated adrenal B output. The stimulatory effect of SV and PLA2 on in vivo TNF alpha release was confirmed by in vitro experiments on peripheral mononuclear cells; in fact, both PLA2 (0.001-1 microg/ml) and SV (0.1-10 microg/ml), as well as concavalin A (1-100 microg/ml), were able to stimulate TNF alpha output in the incubation medium. Our results clearly indicate that PLA2-dependent mechanisms are responsible for several symptoms of inflammatory stress induced during neurotoxemia. In fact, we found that this particular PLA2-related SV is able to stimulate both HPA axis and immune functions during the acute phase response of the inflammatory processes.
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PMID:A phospholipase A2-related snake venom (from Crotalus durissus terrificus) stimulates neuroendocrine and immune functions: determination of different sites of action. 944 33


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