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Biomedical subjects

J Lindholm

Publications and source records attributed to J Lindholm.

At least 73 records · Page 4Linked to original sources
PubMed1988

Tumor markers carcinoembryonic antigen, CA 50, and CA 19-9 and squamous cell carcinoma of the esophagus. Pretreatment screening.

Pretreatment serum levels of the tumor markers carcinoembryonic antigen (CEA), CA 50, and CA 19-9 in 95 patients with squamous cell carcinoma of the esophagus and 32 age-matched controls were compared. Thirty-nine percent of the cancer patients showed elevated (greater than or equal to 5 micrograms/l) serum CEA levels, 41% had elevated (greater than or equal to 17 U/ml) CA 50 levels, and 13% showed elevated (greater than or equal to 37 U/ml) CA 19-9 levels. The tumor markers showed a considerable degree of complementarity, and combined tumor marker analysis increased the sensitivity to 59%. Raised CEA levels were found significantly more frequently in intrathoracically localized tumors than in cervical cancers. Patients surviving less than 6 months showed a higher rate of elevated CEA assays than those who survived 6 to 18 months. No certain correlation was established between tumor marker elevation and tumor stage or tumor differentiation.

Antigens, Neoplasm↗
PubMed1988

Acute monocular disturbances mimicking optic neuritis in pituitary apoplexy.

Three patients with acute monocular central scotoma and headache had the initial diagnosis of optic neuritis. Computed tomography showed large pituitary adenomas with necrosis and cyst formation consistent with the clinical symptoms of a previous pituitary apoplexy. After transsphenoidal adenomectomy the visual disturbances disappeared.

Adenoma↗
PubMed1987

Pituitary tumors containing cholecystokinin.

We found small amounts of cholecystokinin in the normal human adenohypophysis and therefore examined pituitary tumors from 87 patients with acromegaly, Cushing's disease, Nelson's syndrome, prolactinoma, or inactive pituitary adenomas. Five adenomas associated with Nelson's syndrome contained increased amounts of cholecystokinin, the concentrations being extremely high in two: 8281 and 13,453 pmol per gram as compared with less than 30 pmol per gram in normal pituitary glands. The cholecystokinin concentrations were moderately increased in adenomas from another 12 patients, of whom 5 had Cushing's disease and 7 acromegaly with adenomas containing ACTH. The cholecystokinin peptides from the tumors were smaller and less sulfated than cholecystokinin from normal pituitary glands. We conclude that ACTH-producing pituitary cells may also produce an altered form of cholecystokinin.

Acromegaly↗
PubMed1987

Plasma sex hormones and ischemic heart disease.

The reason why men have a higher incidence of ischemic heart disease than women, and women rarely develop ischemic heart disease before the menopause, is not known. However, elevated plasma estradiol and estrone concentrations have been found in men surviving myocardial infarction. Hence, hyperestrogenemia has been suggested as a coronary risk factor. To assess this theory we review the literature on sex steroid production, the relationship between established coronary risk factors and plasma sex hormones, as well as results from clinical trials in which estrogens have been administered to men and women. Other possible explanations why plasma estradiol levels are elevated in male survivors of myocardial infarction are discussed. Based on earlier and recent evidence, it is hypothesized that the elevated plasma estradiol concentration found in men surviving myocardial infarction is due to either the myocardial infarction itself or established risk factors such as smoking or hypertension.

Androstenedione↗
PubMed1987

Investigation of the criteria for assessing the outcome of treatment in acromegaly.

The outcome of treatment in acromegaly is usually assessed by measuring plasma concentrations of growth hormone (GH)--either basal spontaneous levels or during hyperglycaemia. There is no consensus on how cure should be defined. Many studies have considered basal plasma growth hormone concentrations below 20 mU/l (10 ng/ml) as proof of cure, although some recent studies have applied lower values. At present a limit of 10 mU/l (5 ng/ml) seems to be accepted as evidence of cure. We have studied 28 acromegalic patients after transsphenoidal adenomectomy. Plasma GH concentrations (basal and during hyperglycaemia) as well as plasma somatomedin C (SMC) concentrations were measured and compared to the clinical symptoms. There was a close correlation between plasma GH and SMC concentrations (except when plasma GH levels were low) and between the clinical assessment and SMC concentrations. Very low plasma GH levels (less than 1 mU/l or 0.5 ng/ml) were associated with normal SMC values and clinical cure, high GH levels (greater than 10 mU/l or 5 ng/ml) with elevated SMC levels and persisting acromegaly. Moderately elevated plasma GH concentrations (1.9-9.6 mU/l) did not allow any conclusions on the outcome of treatment as assessed from SMC determinations and clinical evaluation. It is concluded that the usual criteria for cure in acromegaly may not be sufficiently strict.

Acromegaly↗
PubMed1987

Re-evaluation of the clinical value of the 30 min ACTH test in assessing the hypothalamic-pituitary-adrenocortical function.

The insulin hypoglycaemia test has been widely used for assessing the hypothalamic-pituitary-adrenocortical function. The outcome of this test has been compared to that of the 30 min ACTH test in 200 consecutive patients with proven or suspected hypothalamic-pituitary disorder. A significant correlation (R = 0.83, P less than 0.001) between the results of the two tests was found. In patients in whom blood glucose levels fell to 2.2 mmol/l (40 mg/dl) or below, the ratio between the peak plasma cortisol concentration during hypoglycaemia and plasma cortisol concentration 30 min after ACTH was 1.002. In patients in whom blood glucose concentration declined to 2.3-3.0 mmol/l (41-54 mg/dl) the ratio was significantly lower (0.828). In eight patients discordant results between the two tests were found. In two patients the ACTH test was normal despite impaired response to insulin. They were studied shortly after acute symptoms of a pituitary adenoma necrosis. Two patients had subnormal responses to insulin despite the fact that pituitary-adrenal function appeared to be intact. In both cases relative insufficiency of the hypoglycaemic stimulus was the likely cause of the discrepancy. In the remaining four patients results of one test was marginally below, and that of the other test marginally above the lower limit of normal. It is concluded that the 30 min ACTH test is reliable for assessing integrated hypothalamic-pituitary-adrenal function (except shortly after acute ACTH deprivation).

Adrenocorticotropic Hormone↗
PubMed1987

Gastrin in pituitary tumours.

Twelve of 87 pituitary adenomas from patients with acromegaly, Cushing's syndrome. Nelson's syndrome, hyperprolactinaemia and without symptoms of hormone hypersecretion contained gastrin in concentrations from 0.5 to 166 pmol/g. Only ACTH-producing tumours contained gastrin, which occurred in forms smaller than those present in the normal adenohypophysis. The results indicate that corticotropic tumours may synthesize gastrin in moderate amounts.

Adenoma↗
PubMed1986

Pituitary apoplexy with sterile meningitis.

In 255 patients with evidence of a pituitary tumor, 7 patients presented with typical symptoms of meningitis, which all proved to be sterile. In these patients a pituitary adenoma was surgically verified in 4. In one patient the presence of acromegaly indicated a pituitary adenoma. In 2 patients an enlarged, empty sella was found, taken to reflect spontaneous disappearance of an adenoma. It is thought that the cause of the sterile meningeal reaction in the 7 patients was a spontaneous necrosis of the adenoma with expulsion of necrotic material into the suprasellar subarachnoid space. Although this sequence has been described before it has been considered to occur very rarely. Pituitary apoplexy as the underlying cause of meningitis should be suspected in patients with evidence of pituitary endocrine disturbances or lesion of structures adjacent to the fossa. The diagnosis may be established by computer tomography. Therapeutically, it may be of importance that the nature of the meningeal reaction is promptly recognized. Swift neurosurgical decompression of the sella and adequate hormonal substitution therapy may be essential.

Adenoma↗
PubMed1986

The spontaneous course of pituitary adenomas and occurrence of an empty sella in untreated acromegaly.

Twenty-three untreated patients with acromegaly for 6-46 yr who were followed for 2-13 yr were studied. High resolution computed tomographic scans in 11 patients revealed herniation of the subarachnoidal space into the pituitary fossa (empty sella) and an intrasellar cyst in 2. Suprasellar tumor extension developed during the follow-up period in only 1 patient. Eleven patients previously (in 10 patients more than 4 yr earlier) had been treated with bromocriptine; 6 of these patients at follow-up had a solid intrasellar adenoma. Six of the patients with an empty sella or intrasellar cyst had had symptoms suggesting pituitary apoplexy. The sellar volume did not increase during follow-up in any patient with an empty sella. Plasma GH levels (basal and mean concentrations during an oral glucose load) increased (greater than 50 ng/ml) in 3 and decreased in 3 patients during follow-up. Normalization of plasma GH levels was rare, and physical well-being with complete absence of acromegalic symptoms was reported by only 4 patients. These results demonstrate that GH-secreting pituitary tumors may remain stationary for extended periods of time and that complete or partial disappearance occurs frequently, probably as a result of pituitary adenoma infarction.

Acromegaly↗
PubMed1986

Subarachnoid hemorrhage with normal cerebral angiography: a prospective study on sellar abnormalities and pituitary function.

Ten consecutive patients with subarachnoid hemorrhage (SAH) of unknown cause were examined for sellar abnormalities and pituitary dysfunction. The diagnosis of SAH rested on a typical history and the demonstration of blood in the cerebrospinal fluid (computed tomography (CT), lumbar puncture). Initial CT and four-vessel angiography were performed in all patients, and five had repeat angiography. Endocrinological assessment was done after the initial angiography, and abnormal findings from this first study were reassessed 3 months later. The follow-up study included a high resolution CT scan of the sellar region. One patient had panhypopituitarism. Insufficient growth hormone secretion alone or combined with a low plasma concentration of estradiol or testosterone was found in another seven patients. The sella was ballooned or enlarged in three patients, and four patients had at follow-up a partly empty sella. A spontaneous development of a partly empty sella from an adenoma with suprasellar extension was observed in the patient with panhypopituitarism. This patient had experienced pituitary apoplexy with resulting SAH. Based on sellar enlargement, an empty sella, and pituitary dysfunction, this pathogenesis was suggested in another three patients. Our findings suggest that hemorrhagic necrosis in a pituitary adenoma may be an important cause of SAH with normal angiography.

Adenoma↗
PubMed1985

Pituitary apoplexy, the Houssay phenomenon, and accelerated proliferative retinopathy.

A 42-year-old man with diabetes mellitus and probably acromegaly had a pituitary apoplexy with left-sided oculomotor palsy. There was an immediate fall in blood glucose concentration. Pituitary insufficiency promptly developed. Blood glucose levels remained normal for the next two years. During the first year after the pituitary apoplexy, severe proliferative retinopathy developed in the left eye, which became almost blind. Only mild retinopathy was present on the right side. Plasma concentrations of growth hormone remained low after the apoplexy, and the acromegalic features subsided. The explanation of these findings may be that the proliferative retinal angiopathy was caused by compression of the cavernous sinus at the time of the apoplexy. This would lead to impaired venous drainage, thus resembling occlusion of the central retinal vein, which may cause retinopathy similar to that seen in diabetes mellitus.

Acromegaly↗
PubMed1984

Plasma vasopressin, cortisol, and growth hormone concentrations in relation to surgery in the suprasellar region.

Posterior and anterior pituitary functions were assessed in 8 patients before, during, and after surgery for tumors in the suprasellar region. Preoperatively, all patients but one responded adequately to an osmotic stimulus with a rise in plasma vasopressin (AVP) and all but one showed adequate cortisol response to adrenocorticotropic hormone (ACTH) and hypoglycemia. During surgery a transient rise was seen in plasma levels of AVP (5 out of 8 patients), cortisol (7 out of 8 patients) and growth hormone (4 out of 8 patients). This response could be predicted from the preoperative stimulation tests. Postoperatively the AVP response to osmotic stimuli was impaired in 4 out of 5 patients, although urine volume had returned to normal after a transient polyuric phase. The response of plasma cortisol to ACTH was still adequate but lower than preoperatively.

Adenoma↗
PubMed1984

Value of the 30 min ACTH-test in assessing hypothalamic-pituitary-adrenocortical function after pituitary surgery in Cushing's disease.

Adrenocortical responses to a 30 min ACTH-test were measured before pituitary surgery and 8-12 d, 2-3 months and 6 months after, in 13 patients with Cushing's disease. The decrease in adrenocortical response to the short ACTH-test performed 8-12 d postoperatively correlated with the outcome as assessed 6 months after surgery. Adrenocortical response to ACTH became subnormal or borderline 8-12 d after surgery in patients demonstrating postoperative HPA insufficiency. These results add further support to the value of the short ACTH-test in assessing integrated HPA function in various clinical situations.

Adrenal Cortex↗
PubMed1984

Adult hydrocephalus and the empty sella.

A 51-year-old man presented with a pituitary apoplexy with symptoms and signs predominantly of meningitis. Later on, hydrocephalus and an empty sella were disclosed. It is likely that the empty sella and the hydrocephalus were both caused by the adenoma necrosis. Based on this case and cases reported in the literature, it is suggested that concomitant presence of an empty sella and hydrocephalus results from necrosis in a pre-existing pituitary adenoma.

Adenoma↗
PubMed1983

Pituitary abscess.

All cases of pituitary abscesses (19 patients) reported in the literature since 1970 are reviewed. Based on the data available, it is suggested that a pituitary abscess is not a bacterial infection as commonly assumed. Probably, it represents a normal tissue reaction to an infarction of a pituitary adenoma. The frequent association with negative cultures from the abscesses, previous sterile meningitis and endocrine disturbances, and concurrent rhinorrhoea are well explained in this way.

Abscess↗