PubMed Health⌕ Search

Biomedical subjects

A P van Seters

Publications and source records attributed to A P van Seters.

At least 37 records · Page 2Linked to original sources
PubMed1989

Plasma growth hormone profiles and sleep: a study of 13 treated acromegalics.

The plasma growth hormone profiles and sleep patterns of 13 treated male acromegalic patients, aged 29-67 years, were studied. All patients had undergone selective pituitary transsphenoidal surgery 4-9 years previously; five patients had also undergone supplemental pituitary irradiation. Blood samples were taken at 20-min intervals; the sleep patterns were obtained by EEG. GH reserve was assessed after insulin-induced hypoglycaemia and GHRH (1-44) with and without pyridostigmine. The profiles were analysed with the aid of the Pulsar program. Seven out of eight non-irradiated patients had 1-3 nocturnal GH peaks; in the irradiated group only one patient had a normal profile. The GH reserve after insulin-induced hypoglycaemia was normal in seven out of eight non-irradiated patients, and subnormal in all five irradiated patients. In the latter group the GH reserve was diminished when tested with GHRH. One patient from each group had a severe apnoea syndrome; in both cases there was no nocturnal GH increase. The percentage sleep stage 1 was lower for irradiated patients when compared with non-irradiated patients, but the 14 other sleep parameters did not differ. From this study we conclude that the physiological regulation of GH secretion is restored in surgically treated patients. Radiation therapy may lead to pituitary and hypothalamic damage, which could affect spontaneous GH secretion.

Acromegaly↗
PubMed1989

Large pituitary adenomas with extension into the nasopharynx. Report of three cases with a review of the literature.

Three cases of pituitary adenoma with extension into the nasopharynx and nasal cavity are reported. The occurrence of this rare tumor underscores the need to consider a pituitary tumor whenever a patient presents with rhinologic complaints and destruction of the sellar floor. Epistaxis, although exceptional, may be the first manifestation of a pituitary tumor. Immunohistochemical analysis combined with staining for the pituitary hormones proved to be essential for reaching a definite diagnosis. Magnetic resonance imaging seems to be the modality of choice for differentiation between tumorous and nontumorous sinus obstruction.

Adenoma↗
PubMed1988

Mutually gratifying heterosexual relationship with micropenis of husband.

Three adult patients with micropenis are described: two genetic females, reared as boys, with congenital adrenocortical hyperplasia (CAH), and one male with anorchia. The patients had a male gender identity/role. All three had established a satisfying heterosexual relationship. For only one of the patients intravaginal intercourse was possible. In one patient (with CAH), penile reconstructive surgery was attempted but failed. Nevertheless, he developed a satisfactory sexual relationship with a woman friend. This report illustrates that for patients with micropenis, penile reconstructive surgery is not obligatory for the establishment of a satisfying sexual relationship.

Adrenal Hyperplasia, Congenital↗
PubMed1988

Bromocriptine-induced trigeminal neuralgia attacks in a patient with a pituitary tumor.

We describe a patient who suffered from ophthalmic trigeminal neuralgia as an isolated symptom of a noninvasive pituitary tumor. Bromocriptine appeared to provoke the attacks within hours. This provocation could be prevented by domperidone. After adenomectomy, both spontaneous and induced attacks disappeared. Acute transient cell swelling may be the mechanism by which bromocriptine induced the neuralgic attacks.

Adenoma↗
PubMed1987

Magnetic resonance imaging of the adrenal glands.

Although CT should be used as the initial procedure, MRI potentially can identify most adrenal masses without the hazard of ionizing radiation or the injection of iodinated contrast material.

Adenoma↗
PubMed1986

'Dementia with contractures' as presenting signs of secondary adrenocortical insufficiency.

Report of a 61-year-old man with progressive mental deterioration and flexion contractures of abdominal muscles and legs as initial signs of hypopituitarism. Five years after onset of symptoms, an endocrinologically non-functioning pituitary adenoma was demonstrated. Thyroid replacement therapy had no effect, but administration of hydrocortisone was followed by rapid recovery. The opportunity to treat such cases of curable dementia is easily missed.

Adenoma, Chromophobe↗
PubMed1986

Computed tomography in untreated adults with virilizing congenital adrenal cortical hyperplasia.

Thirteen adult patients with biochemically proven congenital adrenal hyperplasia (CAH) were examined by computed tomography (CT). Six patients had never received glucocorticoid therapy. In three of those six patients, CT revealed a tumorous transformation in one of the hyperplastic adrenal glands. In the seven patients with CAH who were treated since childhood, no mass could be demonstrated on CT. The development of an adrenocortical tumour due to chronic adrenal cortical stimulation by excessive adreno-cortico-trophic hormone (ACTH) production in adult patients with untreated CAH may not be a rare occurrence, as is demonstrated in this series. It is important not to confuse this entity with a primary virilizing adrenal tumour which requires a different form of treatment. In case of tumorous transformation in untreated adults with CAH, suppressive therapy with CT control should be favoured over surgery, as long as the tumour is ACTH-dependent. Moreover, these observations illustrate the desirability of lifelong glucocorticoid therapy in patients with CAH, including adult males who biochemically may not require suppression of steroid androgen excess.

Adrenal Hyperplasia, Congenital↗
PubMed1985

Detection of 3 beta-hydroxysteroid-dehydrogenase deficiency by urinary steroid profiling: solvolysis of urinary samples should be a necessary prerequisite.

A urinary steroid profile from a patient with suspected 3 beta-HSD deficiency was prepared using capillary gas chromatography, employing only enzymatic deconjugation with Helix pomatia juice. In the chromatogram only very small peaks of dehydroepiandrosterone and 5-pregnenetriol were visible apart from other, for the diagnosis non-significant, peaks. However, after repeating the analysis including an additional solvolysis step, highly significant peaks of DHEA and 5-pregnenetriol became apparent, which suggests the necessity for a solvolysis step for a positive proof of 3 beta-HSD deficiency by urinary steroid profiling.

3-Hydroxysteroid Dehydrogenases↗
PubMed1985

Metastasis of an occult gastric carcinoma suggesting growth of a prolactinoma during bromocriptine therapy: a case report with a review of the literature.

The treatment of a slowly growing invasive prolactinoma with bromocriptine for 8 months resulted in a substantial decrease in plasma prolactin levels despite rapid suprasellar tumor expansion. On exploration, this uncommon observation could be attributed to hematogenous metastasis from an occult gastric adenocarcinoma to the pituitary tumor. Apart from infiltration of neighboring parts of the hypothalamus, autopsy revealed no other hematogenous metastases. This extraordinary type of neoplasm-to-neoplasm metastasis was not shown by computed tomography. This possibility should be considered whenever progressive growth of a pituitary mass is accompanied by a decrease in hormonal overproduction.

Adenocarcinoma, Mucinous↗
PubMed1984

Female pseudo-hermaphroditism due to an adrenal tumour in the mother.

This is a report of a case of almost complete external virilisation of a girl due to an adrenocortical adenoma of the mother. The tumour, though present for many years, caused only mild symptoms in the mother; therefore detection followed only after birth of the virilised girl.

Adenoma↗
PubMed1984

The treatment of adrenocortical carcinoma with o,p'-DDD: prognostic implications of serum level monitoring.

Thirty-four patients with adrenocortical carcinoma were treated with o,p'-DDD. Twenty-eight patients presented with metastases at entry, and spillage of tumour cells occurred at surgery in 6 other patients. Eight patients had objective tumour regression, of whom 7 had serum levels over 14 micrograms/ml. The 3 patients with a lasting remission had levels of greater than 15, greater than 25, greater than 25 micrograms/ml respectively during prolonged periods. Increased survival times were found in the group of 14 patients with o,p'-DDD serum levels higher than 14 micrograms/ml when compared with patients not treated after discovery of metastases. In the patients with levels less than or equal to 10 micrograms/ml no therapeutic effect was seen. Levels of over 20 micrograms/ml are associated with symptoms of reversible neuromuscular toxicity. Monitoring of serum levels during treatment is mandatory. It is suggested that serum levels of about 25 micrograms/ml during longer periods may be curative.

Adrenal Cortex Neoplasms↗
PubMed1982

O,p'-DDD (mitotane) levels in plasma and tissues during chemotherapy and at autopsy.

The distribution of o,p'-DDD in various body compartments of patients being treated for metastatic adrenocortical carcinoma was studied. A highly significant semilogarithmic relationship was found between plasma and adipose tissue concentrations during therapy and between plasma and brain at autopsy. A linear relationship was found at autopsy between concentrations in adipose tissue and those in various other tissues, such as tumour and brain. The semilogarithmic relationship can be explained by the assumption of two plasma pools for o,p'-DDD, one with low affinity and high capacity and one with high affinity and low capacity. Plasma concentrations must be carefully monitored to obtain an impression of the tumour concentration and to detect impending central nervous system intoxication.

Adipose Tissue↗
PubMed1981

Blood levels of o,p'-DDD following administration in various vehicles after a single dose and during long-term treatment.

Plasma levels of o,p'-DDD were measured after ingestion of a single oral dose. At the onset of therapy o,p'-DDD was administered as commercially available tablets and granules and in milk, chocolate, and an oil emulsion to 9, 12, 14, 10, and 6 patients, respectively. Following administration in chocolate, emulsion, and milk significantly higher mean plasma levels were recorded in the first 5- and 10-h periods than after tablets. Granules gave significantly lower plasma levels than all other forms. Plasma levels were also measured during maintenance therapy, when a total of 200 g o,p'-DDD was administered to 22 patients with adrenocortical carcinoma. The plasma disappearance rate after termination of long-term therapy was found to be between 18 and 159 days. The recovery of o,p'-DDD from faeces was about five times higher after ingestion of tablets than after administration in oil emulsion and milk. As far as the rapid increase in plasma levels and patient compliance are concerned, the best results were obtained with the milk powder mixture.

Administration, Oral↗
PubMed1981

Adrenocortical tumour in untreated congenital adrenocortical hyperplasia associated with inadequate ACTH suppressibility.

Data are presented concerning a 60-year-old woman with untreated congenital adrenocortical hyperplasia due to 21-hydroxylase deficiency, who presented with a tumour of the left adrenal gland. Steroid excretion was partly suppressed with dexamethasone. After removal of the tumour, the excretion of several steroid fractions decreased substantially, but suppression by dexamethasone remained inadequate. Preoperatively, plasma ACTh was elevated in the afternoon and decreased only slightly after dexamethasone administration. After surgery, cortisol secretion decreased markedly, whereas ACTH dysregulation became more prominent. Negative feedback failure precluded the use of normal suppressive therapy with low doses of glucocorticosteroids and led to the therapeutic removal of the right adrenal gland, which showed histological signs of nodular hyperplasia.

Adenoma↗