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Biomedical subjects

A P van Seters

Publications and source records attributed to A P van Seters.

At least 19 recordsLinked to original sources
PubMed1992

The distribution of o,p'-DDD (mitotane) among serum lipoproteins in normo- and hypertriglyceridemia.

We found that the distribution of the lipophilic chemotherapeutic agent o,p'-DDD (mitotane) among serum (lipo)proteins was altered in hypertriglyceridemia, with relatively more o,p'-DDD accumulating in the chylomicron and very-low-density lipoprotein (VLDL) fraction. Intralipid, an artificial chylomicron emulsion, or isolated VLDL could extract o,p'-DDD from the other serum (lipo)proteins. There was an inverse relationship between the relative amount of o,p'-DDD found in the fraction exhibiting a density of less than 1.006 g/ml (chylomicrons plus VLDL) and the relative amount observed in the LDL or HDL fractions of serum. Our results indicate that hypertriglyceridemia may impede the entry of o,p'-DDD into the brain or the adrenals. For therapeutic monitoring of o,p'-DDD levels in severe hypertriglyceridemia, we recommend that the chylomicron and VLDL fraction first be removed from the serum by ultracentrifugation.

Adrenal Cortex Neoplasms↗
PubMed1992

Adult adrenoleukodystrophy: the clinical spectrum in a large Dutch family.

A large family with adrenoleukodystrophy is described and the case histories of two clinically symptomatic and related male patients are presented. Clinical, biochemical and genetic screening of their family demonstrated two clinically affected males, one biochemically affected male and five carrier females. Two women were symptomatic; one suffered an acute exacerbation. One female was diagnosed as a carrier, based on genetic analysis and the family history only. Endocrinological screening was performed in the five affected males, demonstrating an elevated adrenocorticotrophic hormone level and a normal cortisol level in two, as evidence of compensated adrenocortical failure.

Adrenocorticotropic Hormone↗
PubMed1992

A case of recurrent adrenocortical carcinoma, with observations on long-term o,p'-DDD therapy and complications.

This report describes a patient with a recurring, one stemline-aneuploid, adrenocortical carcinoma. The condition showed a number of unusual characteristics over a period of 22 yr. It changed from a biochemically functioning, low-grade malignant tumour into a non-functioning malignancy with pronounced mitotic activity, accompanied by an ovarian carcinosarcoma 1 yr before death. Quality of life was reasonable for many years despite chemotherapy, consisting of a total of almost 10 kg of o,p'-DDD administered over a period of 8 yr, and the subsequent side effects (e.g. low T4; increased bleeding time). A reduced mineralocorticoid activity, induced by o,p'-DDD, was reversed after discontinuation of o,p'-DDD treatment. During o,p'-DDD administration the substitution requirements for both hydrocortisone and fludrocortisone acetate increased, leading to periods of hypoadrenocorticism with prerenal uraemia.

Adrenal Gland Neoplasms↗
PubMed1991

Prolonged bleeding time due to mitotane therapy.

After finding prolonged bleeding times in 2 patients treated with mitotane, we prospectively studied 7 patients with adrenocortical cancer on mitotane therapy. Before and 1 and 2 or more weeks after starting mitotane we determined the platelet counts, bleeding times and global coagulation parameters. All patients had a normal bleeding time before treatment. In 6 cases the bleeding time became prolonged (245-555 s). 4 patients exhibited platelet aggregation responses compatible with an aspirin-like defect. It is concluded that mitotane may cause a clinically relevant defect of platelet function.

Adolescent↗
PubMed1991

Mitotane increases the blood levels of hormone-binding proteins.

In 3 patients with adrenocortical carcinoma the effects of long-term mitotane therapy on the serum levels of three hormone-binding globulins and vitamin D-binding protein were studied. Within the first month of treatment cortisol-binding globulin increased two to three times, in close correlation with sex hormone-binding globulin. The rises in thyroxine-binding globulin and vitamin D-binding protein were considerably less. Elevated cortisol-binding protein appeared to be associated with increased binding of cortisol, whereas the binding of thyroxine and vitamin D remained below normal. Binding proteins returned to normal in 2 patients within a year after mitotane discontinuation. This phenomenon of hormone-binding protein enhancement invalidates the use of total serum hormone levels to monitor the effects of mitotane on endocrine function and could provide an explanation for the increased cortisol substitution requirement during mitotane therapy.

Adrenal Cortex Neoplasms↗
PubMed1989

Bromocriptine therapy for non-functioning pituitary adenoma.

Over a 6-year period, 25 patients with non-functioning pituitary adenomas were treated with bromocriptine, while 18 other patients with this condition underwent surgery as the first therapeutic modality. The medically treated group, consisting of those patients without alarming eye symptoms, was analysed in retrospect. Eight of these patients had previously undergone surgery and radiotherapy. Bromocriptine was used in a dose of 5 to 22.5 mg per day; the mean duration of treatment was 18 months. For 11 patients, radiological findings obtained during the year before treatment with bromocriptine revealed progression in five cases and stable tumour size in the others. Three of the five patients with progression showed tumour size reduction during bromocriptine therapy while no further growth occurred in the other two. When medication was stopped in one responding patient, the tumour grew again. One other patient, without pretreatment radiological investigation, exhibited tumour size reduction during bromocriptine therapy, and one patient exhibited radiological progression during the study period. In one case visual fields improved and in one other deteriorated without parallel changes in tumour size on computerized tomography. The favourable reactions were equally divided between the groups with and without previous radiotherapy. We conclude that bromocriptine is rarely capable of reducing the size of non-functioning pituitary adenomas (16% in this series). However, pituitary adenomas exhibiting recent growth may be sensitive to this drug, leading to size reduction or growth arrest.

Adenoma↗
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↗