This large series suggests that the patients with classical pituitary apoplexy, who are without neuro-ophthalmic signs or exhibit mild and non-progressive signs, can be managed conservatively in the acute stage.
Transsphenoidal pituitary surgery is a safe method of treatment in patients with Cushing's disease. Operative findings, radiological and histological findings, together with early postoperative serum cortisol and urine free cortisol estimates may identify failures in treatment. Alternative treatment might then be required for these patients. Because of the risk of late relapse, patients require life-long follow-up.
As stated in our paper, the principal difficulty with the method is reflex movement in response to pain. Provided the anaesthetic technique requires muscle paralysis and ventilation, the site of the surgery is immaterial and anaesthesia is always satisfactory. The great difficulty at present is preventing all reflex movement in non-paralysed patients breathing spontaneously. We are confident, however, that techniques will be developed perhaps using additional drugs that will overcome this problem.
Cell culture methods were used to assess whether human pituitary adenomas secreting GH and associated with clinical acromegaly also secreted the structurally unrelated glycoprotein hormone alpha-subunit. Thirty-two tumours, together with peri-adenomatous tissue from two of them and three normal pituitaries were studied. Anterior pituitary hormones were measured by radioimmunoassay and included PRL, TSH, LH, FSH, and ACTH, as well as GH and alpha-subunit. Normal pituitary tissues secreted all hormones assayed. All 32 tumours secreted GH ranging from 241 to 5556 ng/2 X 10(5) cells/24 h and 12 (37.5%) secreted alpha-subunit in amounts which could not be accounted for by cross-reaction of other hormones or contamination by normal pituitary tissue, and which ranged from 10.3 to 73.5 ng/2 X 10(5) cells/24 h. Ten other tumours also secreted alpha-subunit but in very small amounts, not exceeding 1.8 ng/2 X 10(5) cells/24 h. PRL was secreted from 21 tumours (66%), and small amounts of other hormones, chiefly LH and TSH, were occasionally secreted from tumours. These cell culture studies would suggest that pituitary adenomas causing acromegaly are hormonally heterogeneous and that PRL and glycoprotein alpha-subunit are commonly detected in addition to GH.
The effect of GH-releasing factor(1-44)(GRF) alone, or together with somatostatin (SRIF), dopamine (DA), vasoactive intestinal peptide (VIP) or cycloheximide was studied in a total of ten human somatotrophinomas using a static cell culture system. Growth hormone-releasing factor (2.0 X 10(-8) mol/l) significantly (P less than 0.05) stimulated GH release from nine out of ten tumours over 4-h incubations, and a dose-related effect (2.0 X 10(-10) -2.0 X 10(-8) mol/l) was observed in five tumours thus studied. Repeated GRF (2.0 X 10(-8) mol/l)-mediated GH release was seen during 96% (n = 25) of experiments performed on six tumours over 4 h and up to 27 days in culture. Growth hormone-releasing factor (2.0 X 10(-8) mol/l) also stimulated GH release from five out of seven somatotrophinomas during 60-min incubations. Somatostatin (6.1 X 10(-9) mol/l) completely inhibited GRF-induced GH secretion from four tumours studied over 4 h, but in each case there was significant (P less than 0.05) 'rebound' of GH release from cultures exposed to both GRF and SRIF during a subsequent recovery period. Dopamine suppressed basal GH release from two out of four tumours, but in each case had a greater inhibitory effect on GRF-mediated GH release. Vasoactive intestinal peptide directly stimulated GH release from two out of three tumours, and the effects were additive to maximal stimulatory doses of GRF. Cycloheximide significantly (P less than 0.01) enhanced GRF-stimulated release of GH during a 60-min incubation, but inhibited both basal and GRF-stimulated release over 4 and 8 h.(ABSTRACT TRUNCATED AT 250 WORDS)
Serum concentrations of LH and FSH and their response to the separate administration of GnRH (100 micrograms i.v.) and TRH (200 micrograms i.v.) have been studied preoperatively in 12 patients with a clinically functionless pituitary adenoma, of whom nine (3F: 6M) were found to secrete gonadotrophins in vitro. In three patients with a gonadotrophin-secreting adenoma (GSA) the pulsatile release of LH and FSH was also assessed preoperatively. An elevated serum FSH was recorded in six of nine patients with a GSA, and was subnormal in one, whilst an elevated LH was recorded in only two and was subnormal in six. A doubling of LH occurred in only four of the nine patients after GnRH and in three of six after TRH. None of the three patients with a non-GSA was shown to have an aberrant response to GnRH or TRH. In patients with a GSA, pulsatile release of LH and FSH was usually asynchronous and neither hormone demonstrated any regular harmonic pattern. These data show that in patients with a GSA the serum FSH level is usually elevated but this is not invariable, and the LH may well be low. Pathological responses of LH are frequently found following the administration of either GnRH or TRH and these stimulation tests should be performed separately in patients presenting with a clinically 'non-functioning' pituitary tumour to assist in the preoperative diagnosis. The absence of normal LH and FSH pulsing also appears to be a feature of GS adenomas, and suggests that tumorous gonadotrophin secretion is not under physiological control by hypothalamic GnRH.
A case of nasal septal perforation secondary to cryoglobulinaemia is reported. In this instance the cryoglobulinaemia was due to Waldenstrom's macroglobulinaemia (lymphoplasmocytic lymphoma with IgM paraprotein) in which the paraprotein was a potent cryoglobulin.
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