Showing papers by "Niki Karavitaki published in 2006"

Do the limits of serum prolactin in disconnection hyperprolactinaemia need re-definition? A study of 226 patients with histologically verified non-functioning pituitary macroadenoma.

Abstract: BACKGROUND: The differentiation of a pituitary non-functioning macroadenoma from a macroprolactinoma is important for planning appropriate therapy. Serum PRL levels have been suggested as a useful diagnostic indicator. However, values between 2500 and 8000 mU/l are a grey area and are currently associated with diagnostic uncertainty. OBJECTIVE: We wished therefore, to investigate the serum PRL values in a large series of patients presenting with apparently non-functioning pituitary macroadenomas. PATIENTS AND METHODS: All patients presenting to the Department of Endocrinology in Oxford with clinically non-functioning pituitary macroadenomas (later histologically verified) between 1990 and 2005 were studied. Information documented in the notes on the medications and on the presence of conditions capable of affecting the serum PRL levels at the time of blood sampling was also collected. RESULTS: Two hundred and twenty-six patients were identified (median age at diagnosis 55 years, range 18-88 years; 146 males/80 females; 143 gonadotroph, 46 null cell, 25 plurihormonal and 12 silent ACTH adenomas). All tumours had suprasellar extension. At the time of blood sampling 41 subjects were taking medications capable of increasing serum PRL. Hyperprolactinaemia was found in 38.5% (87/226) of the patients. The median serum PRL values in the total group were 386 mU/l (range 16-3257) (males: median 299 mU/l, range 16-1560; females: median 572 mU/l, range 20-3257) and in those not taking drugs capable of increasing serum PRL 363 mU/l (range 16-2565) (males: median 299 mU/l, range 16-1560; females: median 572 mU/l, range 20-2565). Serum PRL 2000 mU/l, two were taking oestrogen preparations. CONCLUSIONS: Based on a large series of histologically confirmed cases, serum PRL > 2000 mU/l is almost never encountered in nonfunctioning pituitary macroadenomas. Values above this limit in the presence of a macroadenoma should not be surrounded by diagnostic uncertainty (after acromegaly or Cushing's disease have been excluded); a prolactinoma is the most likely diagnosis and a dopamine agonist should be considered as the treatment of choice.

GH replacement does not increase the risk of recurrence in patients with craniopharyngioma.

Abstract: Summary Background A significant number of patients with craniopharyngioma are GH deficient. The safety of GH replacement in these subjects has not been established. Objective To assess the effect of GH replacement upon recurrence in patients with craniopharyngioma. Patients and methods All the patients with craniopharyngioma followed-up at the Departments of Endocrinology or Paediatrics in Oxford and treated or not with GH were studied retrospectively. These were recruited from the databases of the departments consisting of subjects diagnosed between January 1964 and July 2005. The impact of GH replacement upon recurrence was evaluated after adjusting for possible confounding factors. Results Forty-one subjects received GH replacement. Nine of them did not have follow-up imaging during GH therapy and were not included in the statistical analyses. The remaining 32 (22 males/10 females) received GH for a mean period of 6·3 ± 4·6 years (median 5·1, range 0·8–22); 21 started during childhood (13 of them continued after the achievement of final height with an adult dose) and 11 during adult life. The mean duration of their follow-up (from surgery until last assessment) was 10·8 ± 9·2 years (range 1·9–40). Fifty-three subjects had not received GH therapy (30 men/23 women). The mean duration of their follow-up (from surgery until last assessment) was 8·3 ± 8·8 years (range 0·5–36). During the observation period, 4 patients treated with GH and 22 non-GH treated ones developed tumour recurrence. After adjusting for sex, age at tumour diagnosis and type of tumour therapy (gross total removal, partial removal, surgery + irradiation), GH treatment was not a significant independent predictor of recurrence (P = 0·06; hazard ratio = 0·309). Similar results were obtained when the impact of GH replacement was assessed according to its duration (P = 0·18; hazard ratio = 0·991/month of treatment). None of the nine patients with insufficient imaging data for inclusion in the statistical analyses [5 men/4 women, 3 treated with GH during childhood/6 during adult life, mean duration of GH therapy 2·9 ± 2·4 years (median 1·8, range 0·4–7)] showed clinical features suggestive of recurrence during the period of GH replacement. Conclusion Based on the data of the craniopharyngiomas database in Oxford, there is no evidence that GH replacement is associated with an increased risk of tumour recurrence.

A case of post-traumatic isolated ACTH deficiency with spontaneous recovery 9 months after the event.

Abstract: Survivors of traumatic brain injury (TBI) often suffer from significant adverse physical, neuropsychological, and social sequelae. TBI may pose significant risks to pituitary function;1–5 untreated hypopituitarism may aggravate these adverse consequences. Studies on the natural history of post-TBI hypopituitarism are lacking, and the reversibility of hormone deficits remains uncertain. We describe a case of a man who suffered a transient period of secondary hypoadrenalism after a serious TBI. This is the first reported case of reversible isolated adrenocorticotrophic hormone (ACTH) deficiency following head trauma. An 18 year old man was assaulted on 14 September 2003 and immediately admitted to the local accident and emergency unit with a Glasgow Coma Scale (GCS) score of 3/15 and constricted pupils. Brain computed tomography (CT) revealed multiple small bleeds involving the basal ganglia, left cerebellum, and midbrain, and a left maxilla linear fracture. No other serious injuries were found. He was ventilated on admission, supported in the intensive care unit, and 4 days later transferred to a trauma ward with an unaltered brain CT. Over the next 7 weeks, his GCS remained reduced (6–11/15) with a marked improvement after this time. During his acute recovery phase, no hypotensive insults were recorded, but he had episodes of …