| 1. |
- Löfdahl, Elisabet, et al.
(författare)
-
Compromised quality of life in adult patients who have received a radiation dose towards the basal part of the brain. A case-control study in long-term survivors from cancer in the head and neck region.
- 2012
-
Ingår i: Radiation oncology (London, England). - 1748-717X. ; 7:1
-
Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: BACKGROUND: Adult patients with hypothalamic-pituitary disorders have compromised quality of life (QoL). Whether this is due to their endocrine consequences (hypopituitarism), their underlying hypothalamic-pituitary disorder or both is still under debate. The aim of this trial was to measure quality of life (QoL) in long-term cancer survivors who have received a radiation dose to the basal part of the brain and the pituitary. METHODS: Consecutive patients (n=101) treated for oropharyngeal or epipharyngeal cancer with radiotherapy followed free of cancer for a period of 4 to10 years were identified. Fifteen patients (median age 56 years) with no concomitant illness and no hypopituitarism after careful endocrine evaluation were included in a case-control study with matched healthy controls. Doses to the hypothalamic-pituitary region were calculated. QoL was assessed using the Symptom check list (SCL)-90, Nottingham Health Profile (NHP), and Psychological Well Being (PGWB) questionnaires. Level of physical activity was assessed using the Baecke questionnaire. RESULTS: The median accumulated dose was 1.9 Gy (1.5--2.2 Gy) to the hypothalamus and 2.4 Gy (1.8--3.3 Gy) to the pituitary gland in patients with oropharyngeal cancer and 6.0--9.3 Gy and 33.5--46.1 Gy, respectively in patients with epipharyngeal cancer (n=2). The patients showed significantly more anxiety and depressiveness, and lower vitality, than their matched controls. CONCLUSION: In a group of long time survivors of head and neck cancer who hade received a low radiation dose to the hypothalamic-pituitary region and who had no endocrine consequences of disease or its treatment QoL was compromised as compared with well matched healthy controls.
|
|
| 2. |
- Norjavaara, Ensio, et al.
(författare)
-
Glucokinase Activators AZD6370 and AZD1656 Do Not Affect the Central Counterregulatory Response to Hypoglycemia in Healthy Males
- 2012
-
Ingår i: Journal of Clinical Endocrinology and Metabolism. - : Endocrine Society. - 0021-972X .- 1945-7197. ; 97:9, s. 3319-3325
-
Tidskriftsartikel (refereegranskat)abstract
- Context: Glucokinase is expressed in the hypothalamus, but effects of glucokinase activators (GKAs) on counterregulatory responses to hypoglycemia are unknown. less thanbrgreater than less thanbrgreater thanObjective: Two separate studies assessed the counterregulatory hormone responses to hypoglycemia induced by the GKAs, AZD6370 and AZD1656, compared with insulin infusion. less thanbrgreater than less thanbrgreater thanDesign and Setting: Both studies were randomized, open, two-way crossover studies, conducted in separate clinical research centers. less thanbrgreater than less thanbrgreater thanParticipants: Both studies involved 12 healthy adult male volunteers. less thanbrgreater than less thanbrgreater thanInterventions: Each subject received two treatments in randomized order, separated by a washout. In the AZD6370 study, overnight-fasted subjects received either a single oral AZD6370 dose (300 mg) or insulin infusion (0.8 mU/kg . min). In the AZD1656 study, overnight-fasted subjects received either a single oral dose of AZD1656 (80 mg) plus supporting insulin (1 mU/kg . min) or insulin alone (1 mU/kg . min). Insulin was added to support AZD1656 because AZD1656 alone did not produce the desired hypoglycemia. Plasma glucose was lowered during a stepwise hypoglycemic clamp with a glycemic nadir of 2.7 mmol/liter for 30 min. less thanbrgreater than less thanbrgreater thanMain Outcome Measures: Epinephrine, norepinephrine, GH, cortisol, and glucagon plasma levels were assessed. Results: No safety issues were raised. AZD6370 and AZD1656 had no effect on counterregulatory responses for norepinephrine, GH, or cortisol, but epinephrine increased slightly with AZD1656. Glucagon responses were reduced by approximately 30% with both GKAs vs. insulin. less thanbrgreater than less thanbrgreater thanConclusions: These data suggest the central nervous system-mediated counterregulatory response during GKA-induced hypoglycemia was preserved, whereas the glucagon response was attenuated; the latter was possibly mediated by a local pancreatic effect (intraislet hyperinsulinemia) rather than by impairment of the central nervous system-mediated response.
|
|
