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Biomedical subjects

L Deftos

Publications and source records attributed to L Deftos.

16 recordsLinked to original sources
PubMed2000

The pattern of serum markers in patients with androgen-independent adenocarcinoma of the prostate.

In this exploratory study, our objectives were to correlate the serum and bone marrow concentrations of putative markers of prostate cancer progression in patients with advanced androgen-independent prostate cancer (AIPC), to assess the frequency and quantity of relative expression of these markers, and to correlate the expression of the markers with extent of disease (EOD) and overall survival. In a cohort of 50 patients with AIPC with bone metastases, we obtained serum and bone marrow samples and measured prostate specific antigen (PSA), serum interleukin-6 (sIL-6), bone marrow interleukin-6, serum chromogranin A (sCgA), bone marrow chromogranin A, and prostate specific membrane antigen (PSMA) by immunoassays. EOD was determined by quantifying identifiable bone lesions on radionuclide bone scans. Each variable was categorized into two groups (low and high) based on the median found in this cohort or on the cutoff based on normal limits when available. Analyses were performed in two subsets of patients with EOD either <20 or >/=20. Results showed that: (1) PSA is associated with EOD but not with outcome; (2) sIL-6 and sCgA may be intermediate markers of early progression in AIPC, because they are predictive of outcome only in patients with EOD <20; (3) elevated PSMA is associated with elevated sIL-6 but not with PSA, suggesting that PSMA may be a useful marker in AIPC; and (4) the ratio of PSA to putative markers of progression may reflect the complex clonal progression of prostate cancer. We conclude that patients with advanced AIPC exhibit one of two patterns of serologic marker expression: in some patients the disease status is reflected by PSA, and in others it is reflected by other markers. If these data are prospectively confirmed, this would help group patients with advanced AIPC into clinically relevant categories.

Journal Article↗
PubMed1988

Multiple markers for lung cancer diagnosis: validation of models for localized lung cancer.

Sera from 71 patients with localized lung cancer, from 70 normal controls, and from 73 patients with benign lung diseases were analyzed for 10 substances to detect lung cancer: ferritin, lipid-bound sialic acid, total sialic acid, beta 2-microglobulin, lipotropin, the alpha and beta subunits of human chorionic gonadotropin, calcitonin (two assays), parathyroid hormone, and carcinoembryonic antigen (CEA). Individual markers were studied, and optimal combinations of markers were sought for discriminating patients with localized lung cancer from normal controls and from patients with benign lung disease. Both logistic regression and recursive partitioning methods for discrimination were tried. The best rules involved only CEA and ferritin for discriminating patients with lung cancer from normal controls, and CEA and age for discriminating patients with lung cancer from those with benign lung diseases. The performance of these rules was validated on an independent serum panel containing sera from 56 patients with localized lung cancer, 75 normal controls, and 75 patients with benign lung diseases. Three rules designed to achieve 95% specificity against normal controls attained 14%-36% sensitivity for localized lung cancer in the validation panels, whereas three rules designed to achieve 95% specificity against benign lung diseases attained 30%-39% sensitivity. Some aspects of potential clinical applications are discussed.

Age Factors↗
PubMed1986

Multiple markers for lung cancer diagnosis: validation of models for advanced lung cancer.

Sera from 171 patients with advanced lung cancer, from 110 normals, and from 123 subjects with benign respiratory diseases were analyzed for 10 substances to detect lung cancer: ferritin, lipid-bound sialic acid, total sialic acid, beta 2-microglobulin, lipotropin, the alpha and beta subunits of human chorionic gonadotropin, calcitonin (two assays), parathyroid hormone, and carcinoembryonic antigen. Individual markers were studied, and optimal combinations of markers were sought for discriminating lung cancer patients from normals and from patients with benign lung disease. Numerous methods for combining the markers were examined, but the methods of logistic regression and recursive partitioning were finally adopted. The best discrimination rules we could find used only carcinoembryonic antigen (CEA) and total sialic acid (TSA). The performance of these rules was validated on an independent serum panel containing sera from 68 patients with advanced lung cancer, from 40 normals, and from 52 patients with benign respiratory disease. The combination rules based on TSA and CEA performed better than a rule based on CEA alone. Logistic discrimination rules with TSA and CEA that were designed to have 95% specificity achieved 54% sensitivity for discriminating advanced lung cancer from normal controls and 52% sensitivity for discriminating advanced lung cancer from controls with benign disease. Some aspects of clinical applicability are discussed, including planned studies for localized lung cancer and the requirement for further testing in specific clinical settings.

Aged↗
PubMed1985

Uncoupling of bone formation and resorption by combined oestrogen and progestagen therapy in postmenopausal osteoporosis.

10 healthy early postmenopausal women were treated with oestrogen and progestagen for two cycles of 28 days. Serum alkaline phosphatase and bone Gla protein increased during progestagen administration, whereas urinary excretion of calcium and hydroxyproline fell significantly during treatment, independently of progestagen intake. Thus, bone formation increases when progestagen is added to oestrogen treatment, whereas bone resorption may be kept constantly low during oestrogen plus progestagen treatment, leading to a positive calcium balance. This makes possible effective treatment of postmenopausal osteoporosis--treatment of elderly postmenopausal women with substantial bone loss before their bones have fractured or when they have just started to fracture. This study design can be used for easy and rapid screening of potential drugs for the prevention and treatment of postmenopausal bone loss.

Bone Development↗
PubMed1984

Primary hyperparathyroidism, pregnancy, and neonatal hypocalcemia.

Primary hyperparathyroidism in the mother during pregnancy is known to result in a high rate of fetal complications; spontaneous abortions, still births, and neonatal tetany occur in excessive incidence. To understand the pathophysiology of neonatal hypocalcemia that accompanies this disorder, transplacental calcium dynamics were studied in female sheep during the last trimester of pregnancy and in their fetal lambs after hysterotomy. Calcium ion was shown to move rapidly across the placenta. However, this organ blocked the passage of both parathyroid hormone and calcitonin from the maternal and to the fetal circulations. Our studies support the hypothesis that in primary hyperparathyroidism maternal hypercalcemia results in fetal hypercalcemia, which leads to suppression of fetal parathyroid gland function. In such a situation, neonatal hypocalcemia would occur after birth when maternal calcium flow is interrupted. Parathyroidectomy performed in the mother, especially during the second trimester of pregnancy when operation is safest, would break this cycle and permit normal serum calcium homeostasis in the fetus.

Animals↗
PubMed1982

The interaction of lithium and time-of-day on calcium, magnesium, parathyroid hormone, and calcitonin in rats.

Effects of lithium on the concentrations and temporal patterns of serum and cerebellar calcium and magnesium, parathyroid hormone, and calcitonin were studied in 186 rats sacrificed around 24 hours of clock time. Serum calcium, serum and cerebellar magnesium, and parathyroid hormone were increased and calcitonin decreased in lithium-fed animals. Lithium-fed rats also showed different temporal patterns in serum calcium, parathyroid hormone, cerebellar magnesium, and calcitonin. Data support the hypothesis that lithium competes for calcium receptor sites, causing a compensatory increase in parathyroid hormone and decrease in calcitonin until a new, higher set-point for calcium is established. Lithium strongly affected biological rhythms, an effect which may account in part for the diverse literature on lithium's influence on calcium and magnesium regulation.

Animals↗
PubMed1982

Lithium delays biochemical circadian rhythms in rats.

Recent evidence has indicated that a fast circadian oscillator or pacemaker might contribute to affective illnesses, particularly manic depressive disease. In order to test the hypothesis that lithium exerts its therapeutic effect by slowing or delaying overly fast circadian rhythms, 95 rats were fed a lithium-containing diet for a period of 3-4 weeks, and 91 rats were fed a control diet. The animals were sacrificed at times around the clock. Eight of the eleven substances measured (plasma prolactin, PTH, corticosterone, and aldosterone, serum calcium and magnesium, and cerebellar calcium and magnesium) showed large delays in their circadian rhythms in the lithium-fed rats. This supports the hypothesis that lithium's therapeutic action is to delay overly fast circadian rhythms.

Animals↗
PubMedDate not supplied

Effects of high calcium intake on blood pressure and calcium metabolism in young SHR.

Increased dietary calcium intake in the adult spontaneously hypertensive rat (SHR) has been reported to correct low serum ionized calcium concentration ([Ca++]) and to result in a significant amelioration of the prevailing hypertension. In the present study we examined several parameters of calcium metabolism in young (6-week-old) SHR and compared them with those observed in normotensive Wistar-Kyoto (WKY) rats fed equal amounts of a diet containing normal quantities of calcium (0.4%, wt/wt) for 4 weeks. A separate group of SHR was placed on an equal amount of a high calcium (2.8%, wt/wt) but otherwise identical diet. In SHR and WKY eating a normal calcium diet, serum total calcium concentration was not different, but [Ca++] was lower in SHR (1.58 +/- 0.06 vs 1.91 +/- 0.07 mmol/liter, p less than 0.01). Serum immunoreactive parathyroid hormone (PTH) was increased in some, but not all, SHR. No difference was noted between the two groups in the following parameters: calcium intake, serum 1,25 dihydroxycholecalciferol (1,25(OH)2D3), urinary calcium excretion, fractional stool calcium content ([stool calcium/calcium intake] X 100), and in vitro 45Ca uptake by everted gut sacs constructed from segments of duodenum, mid-jejunum, ileum, and proximal colon. A high calcium diet corrected the abnormal serum [Ca++] and PTH but did not alter the progression or severity of the hypertension in SHR. A lower net weight gain was observed in SHR on a high calcium diet when compared to SHR eating normal calcium diet (9.1 +/- 1.8 vs 27.0 +/- 2.0 g).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗