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Biomedical subjects

P Fossati

Publications and source records attributed to P Fossati.

At least 217 records · Page 12Linked to original sources
PubMedDate not supplied

Is it still worthwhile to treat bone metastases from differentiated thyroid carcinoma with radioactive iodine?

From 1964 to 1989, bone metastases were found in 28 of 600 patients operated on for differentiated thyroid carcinoma. Bone metastasis was the presenting symptom in 15 (54%) patients, was detected from the initial symptom in 4 (14.5%) patients, and occurred subsequently in 9 (32%) patients, with an average lag time of 4.5 years after surgical treatment. Pathological pattern of the thyroid cancer was follicular in 26 (93%) patients and papillary in 2 (7%) patients. Bone metastatic involvement was multiple in 21 (75%) patients and associated with other synchronous or metachronous distant metastases in 13 (46%) patients, especially in the lung (10 patients) or the brain (3 patients). The primary treatment of thyroid carcinoma was total thyroidectomy in all 28 patients, with additional modified neck dissection in 8 patients. All 15 patients presenting with symptoms had bone metastases demonstrated by x-ray studies. Six of the bone metastases only took up radioactive iodine 6 weeks after total thyroidectomy, as did 2 of 4 bone metastases detected at initial observation and 4 of 9 metachronous bone metastases. All 12 patients with functioning bone metastases were given radioactive iodine therapy; 4 of the metastases were surgically resected. Only 2 patients with bone metastases showed a complete response after an ablative dose of I-131; none of the metastases had been demonstrated by x-ray studies. Radioactive iodine therapy cures no more than 17% of patients with bone metastases taking up radioactive iodine and 7% of all patients with bone metastases. All patients cured of bone metastases were given radioactive iodine, either alone, or combined with other treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMedDate not supplied

Executive functions and updating of the contents of working memory in unipolar depression.

BACKGROUND: Depression is characterized by cognitive impairments, including executive dysfunctions. These executive deficits could reflect impairments of more basic executive processes, such as updating, set shifting and inhibition. While shifting and inhibition impairments are often reported, studies on depression have been somewhat obscure about specific deficits of the updating process. The main goal of that study was to assess the updating process in young in-patients with depression. METHODS: We used a verbal n-back task to assess updating process. Load and mental manipulation within working memory (WM) were incremented by using three different levels of complexity (1,2,3-back). Neuropsychological tests and an attentional task (0-back) were also administered to subjects. Twenty-two individuals meeting DSM-IV criteria for Major Unipolar Depression and 22 healthy control subjects, matched on age, verbal IQ and education, were included in the study. RESULTS: Subjects with depression showed significant deficits at the n-back task compared to control subjects. They were normal in tasks assessing the short-term maintenance in WM and attention. This suggests that depressed patients exhibit impairment in the updating process. Depressed patients also showed set shifting and inhibition deficits. Only the n-back task was correlated with the number of hospitalizations and the longitudinal course of the illness. CONCLUSIONS: Our results suggest that young depressed in-patients have widespread executive dysfunctions, including updating, shifting and inhibition processes. We also found a correlation between a longitudinal measure of depression severity and an updating task performance. We suggest that using multiple executive tasks gives the opportunity to distinguish the specific influence of various executive processes on clinical dimensions in depression.

Adult↗
PubMedDate not supplied

[Valpromide, Valproic acid and removal of small intestine in the treatment of a chronic depression: a case report].

Valpromide (VPD) is an antiepileptic drug, derivative of Valproic acid (VPA), used as a mood-stabilizer in bipolar disorder for 25 years in several European countries. VPD is also used as an augmentation strategy in refractory depression. Despite chemical similarity between VPA and VPD, the pharmacokinetics of the 2 drugs in humans are quite distinct. We report a case of a patient, suffering from a bipolar treatment resistant depression, who dramatically improved after substituting VPD to VPA in association with fluoxetine. Mme X, 68 years old, has been hospitalized in March 2001 for the treatment of a resistant depression (TRD). She was suffering from removal of small intestine with chronic diarrhoea after a suicidal attempt two years ago. She had a bipolar disorder treated with VPD (1,200 mg/d) since 1 year. She presented a major depressive episode according to DSM IV with various symptoms like depressed mood, hypersomnia and difficulty initiating sleep, diminished ability to concentrate and to think, markedly diminished pleasure in all activities and major anxiety. Mme X fulfilled TRD diagnosis after resistance to two adequate antidepressants trials from different classes (clomipramine 175 mg/day and venlafaxine 300 mg/day). The antidepressant treatment (venlafaxine) was interrupted and she has been receiving a SSRI (fluoxetine 20 mg/day) for 4 weeks. After four weeks, she had a partial remission with persistent sleep problems, mood lability and anxiety. The VPA blood concentration was very low: 27 mg/L (normal range: 50 to 100 mg/L) in spite of a high dosage: 1,200 mg/day. Pharmacokinetic analysis of VPD shown that VPD transformation to VPA usually done in the intestine, was reduced because of the removal of hail intestine. We substituted VPD by VPA. Valproate blood concentration returned to normal range, induced dramatic improvement of depression within three days. VPD is an amide derivative of valproic acid (valproate), biotransformed by hydrolysis to its corresponding valproic acid. VPD is a prodrug of VPA. VPD is absorbed after transformation in gastro-intestinal mucous membrane. The adequate dosage of VPD (Depamide, 300 mg) is 4 to 6 tablets in acute manic phases, 2 to 4 tablets in long term treatment, 1 to 3 tablets in depressive episode. The biodisponibility of VPD is around 100% 75 and 90% of VPD is linked with protein albumin. The daily dosage determined the blood concentration of the active form (VPA), but this relation isn't linear. The optimal blood concentration of VPA (Depakine) ranges between 50 and 100 mg/L. the free form of VPA is influenced by protein disorders such as of hypoalbuminemia and by presence of fat acids in food. This case report demonstrates at a clinical level that VPD and VPA are not equivalent for treating bipolar depression. This case also suggests that a deep investigation of the pharmacokinetic of psychotropic drugs can help clinicians to resolve clinical problems of treatment of depression.

Aged↗
PubMedDate not supplied

Prolactin regulation in 14 cases of galactorrhea and hypogonadism with minimal modifications of the sella turcica (author's transl).

In this study we report 13 cases of amenorrhea-galactorrhea and one of a male patient complaining of gynecomastia, galactorrhea, sexual impotence and sterility with oligoasthénospermy. In these cases, the size of the sella turcica was normal but we found a localized depression of the bottom of the sella turcica; these modifications were situated at the antero-inferior part of the sella in 12 cases and posteriorly in the 2 others. Basal prolactin level was higher than normal values in 13 cases (12 female and 1 male patients): individual values varied between 45 and 367 ng/ml. Nycthermeral rhythm disappeared in the 9 cases studied. Administration of L-Dopa (500 mg orally) significantly suppressed the prolactin values in the 11 cases studied. Oral water loading (20 ml/kg) left prolactin values unchanged (10 cases). After oral glucose tolerance test (1 g/kg) no significant systematic variation occurred. The increase of prolactin values after stimulation by 200 microg. TRH IV as a bolus (4 cases) was not significant. We have found similar prolactin variations in cases of hyperprolactinemia with either normal pituitary fossa (7 cases) or macro-adenoma (6 cases).

Adenoma↗
PubMedDate not supplied

[Proceedings: Plasma renin activity in management of Addison's disease (author's transl)].

13 patients with Addison's disease, 7 men and 6 women, 19 to 61 years old, were investigated. Plasma Renin Activity (P.R.A.) is measured by radioimmunoassay of Angiotensin I (ng/ml/h) in the supine (S) and the upright (U) position. These patients are studied before treatment and under normal sodium diet in 11 cases: the P.R.A. value is constantly increased [5 men: MS = 10,09 (range: 6,2-12,5) and MU = 23,22 (range : 17,1-31,09), 6 women : MS = 24,48 (range : 3,46-45,04) and MU = 42,23 (range : 42,23 (range 17,37-69,34), to be compared with our normal values (M +/- S.D.) : MS = 1,02 +/- 0,39 and MU = 2,56 +/- 0,99 for men - MS = 0,82 +/- 0,14 and MU = 2,32 +/- 0,93 for women in follicular phase - MS = 1,45 +/- 0,56 and MU = 4,59 +/- 1,63 for women in luteinic phase. After dietary sodium restriction (10 mEq/24 h) in 2 cases, the P.R.A. is significantly increased with respect to the basal value]. Under Hydrocortisone alone (25 to 30 mg/24 h) and normal sodium diet, 4 patients kept significantly increased P.R.A. values. Under Hydrocortisone (20 to 40 mg/24 h) and 9-alpha-fluorohydrocortisone (50 to 100 microgrammes/24 h) for 6 days to 14 months, the P.R.A. value decrease into the normal range [men : MS = 1,02 (range : 0,54-1,92) and MU = 1,68 (RNAGE : 0,81-2,57) - 2 Menopausal women : MS = 1,55 and MU - 1,16. The P.R.A. measurement seems useful in the adaptation of Addision's disease treatment.

Addison Disease↗
PubMedDate not supplied

[Executive functioning in unipolar depression: a review].

While several neuropsychological studies have demonstrated that cognitive deficits are seen across a broad range of cognitive domains, executive deficits associated with frontal lobe dysfunction may be prominent in depression. Executive function refers to cognitive processes that control and integrate other cognitive activities such as episodic memory. These executive functions involve a set of cognitive behaviors which include: dealing with novelty, selecting strategies, inhibiting incorrect responses, monitoring performance and using feedback to adjust future responding. The measurement of executive function relies mainly on the use of neuropsychological tests known to be sensitive to frontal lobe damage such as the Wisconsin and California Card Sorting Tests, verbal fluency tests, Stroop-test, Tower of London Task and Trail Making Test. The present review focuses on studies investigating executive functions in primary unipolar depression with these neuropsychological tasks. Unipolar depressed patients mainly exhibit cognitive inhibition deficits, problem-solving impairments and planning deficits. Cognitive inhibition deficits in depressed patients have been related to a reduction of cognitive resources and psychomotor retardation. Inhibition disturbance could lead depressed patients to process irrelevant information and consequently reduce their capacity to control transient mood changes. Several studies have found evidence of problem solving impairments in depressed patients. Depressed subjects show with card sorting tests difficulties in hypothesis testing with a loss of spontaneous and reactive cognitive flexibility. The cognitive rigidity and hypothesis-testing associated with dorsolateral prefrontal dysfunction in depression may prevent patients to cope with life events and lead to a perpetuation of depressed mood by a continuation of stress exposure. Planning tasks, such as the Tower of London Test, also demonstrate that depressed patients fail to use negative feedback as a motivational boost to improve their performance. Both trait and state factors influence the executive level of depressed patients. Executive deficits have been reported in more severely depressed subjects with melancholic or psychotic features. Executive functioning also might predict a poorer outcome in depression. Thus initiation and perseveration scores - a measure of cognitive flexibility - is associated with relapse and recurrence of depression and residual depressive symptoms. Brain imaging studies show that reduced blood flow, particularly in medial prefrontal cortex and dorsal anterior cingulate cortex subserve executive impairments in depression. However neuroimaging studies underscore the importance of mood-cognitive interactions in depression. A recent working model of depression (Mayberg et al., 1999) implicates failure of the coordinated interactions of distributed cortical-limbic pathways in the neuropsychopathology of depression. According to this model, neocortical (prefrontal and parietal regions) and superior limbic elements (dorsal anterior cingulate) are postulated to mediate impaired attention and executive function, whereas ventral limbic regions (ventral anterior cingulate, subcortical structures) are postulated to mediate circadian and vegetative aspects of depression. Further studies are needed to validate this model at the neuropsychological level as well as the brain level and to elucidate the complex interactions between mood, cognitive resources and executive function in depression.

Cognition Disorders↗
PubMedDate not supplied

[Dissociation of results obtained with an immunofluorescence technique by using anti-ACTH antibodies in three cases of pituitary "chromophobe" adenoma without hypercorticism; ultrastructural study (author's transl)].

Morphological studies of 3 pituitary "chromophobe" adenoma in patients without hypercorticism show positive immunofluorescenct cells with anti alpha, 17-39 ACTH antibody which are not revealed with anti beta, 1-24 ACTH antibody. These cells observed at the ultrastructural level contain secretory granules of 1,000 to 1,500 A in diameter. The existence in these cells of a substance having an immunological relationship with ACTH without biological activity is discussed.

Adenoma, Chromophobe↗
PubMedDate not supplied

[Therapeutical effects of bromocriptine (CB 154) in 10 acromegalic subjects. Study of somatotrophic function and clinical survey (author's transl)].

Plasma GH levels were studied following acute administration of 2.5 mg of bromocriptine (CB 154) in 12 acromegalic patients. In 9 responders, reduction of GH levels was obvious 2 to 4 hours after bromocriptine administration and the lowest values were achieved between 5 and 8 hours following drug absorption. This pattern suggested the use of bromocriptine at a dose of 2.5 mg six-hourly in chronic treatment of acromegaly. Chronic administration of CB-154 in 10 acromegalic patients was followed by a stable reduction of plasma GH levels in seven subjects. No appreciable variation in GH levels were observed in one patient who was unresponsive to acute administration of CB-154 and in two other subjects treated with 2.5 mg 12-hourly. In three patients who had high plasma GH levels inspite of an anterior treatment by hypophyseal surgery and/or physiotherapy, plasma GH values were normalised under bromocriptine therapy. (9 to 24 months). In the four other subjects, high basal plasma GH levels were reduced with at least 50% reduction rate from baseline. Nevertheless, in two subjects from the latter group bromocriptine daily dose was increased to 20 mg divided in four fractions, because of an escape phenomenon to initial dose regimen. Normalisation or reduction of plasma GH levels was associated with considerable clinical improvement. Tolerance of the drug was excellent in all patients but four who experienced nausea and vomiting; these side effects disappeared when treatment was reduced and then increased gradually.

Acromegaly↗