PubMed Health⌕ Search

Biomedical subjects

S Maccari

Publications and source records attributed to S Maccari.

72 records · Page 4Linked to original sources
PubMed1989

Contraceptive methods in the McCune-Albright syndrome.

We describe the case of a woman with McCune-Albright syndrome who had a pathological bone fracture while being treated with an oral contraceptive. In this syndrome the bone lesions contain estrogen and progesterone receptors. The possibility of progression of the bone lesions during pregnancy is well-known. We judge the use of oral contraceptives to be dangerous in this syndrome; the affected women must be orientated towards alternative contraceptive methods.

Adult↗
PubMed1985

[Value of some biological variables for the diagnosis of alcoholism in a hospital population].

279 male patients consecutively admitted to a medical ward were interviewed about their drinking habits using a CAGE-like questionnaire and were subdivided into teetotallers, normal-, borderline-, heavy-drinkers. The mean values of the following laboratory tests resulted significantly different in heavy drinkers compared with the others: mean cell volume, gamma-glutamyl-transpeptidase, serum urea (BUN), SGOT, SGPT, total bilirubin. No significant difference was found for triglycerides, uric acid, albumin and gamma-globulins. Sensitivity, specificity, predictive values of positive test and negative test, "goodness" were calculated for each of the 6 above-mentioned tests. Each of them had a linear correlation (inverse for BUN, direct for the others) between amount of alcohol intake and level of the test.

Alanine Transaminase↗
PubMed1985

Tangier disease. A case with sensorimotor distal polyneuropathy and lipid accumulation in striated muscle and vasa nervorum.

A 65-year-old man with Tangier disease (analphalipoproteinemia) had had a progressive sensorimotor distal neuropathy with sensory ataxia for 1 year. Muscle biopsy demonstrated excess lipid vacuoles on histochemical and electron-microscopic techniques. Sural nerve biopsy showed a marked loss of large fibers and an increase in small myelinated fibers, with presence of remyelinating fibers and clusters of regeneration; a few aspects of active demyelination and some onion-like formations were also present. Lipid accumulation chiefly affected the Schwann cells of unmyelinated fibers and, to a lesser degree, of myelinated fibers, endoneurial fibroblast, and vasa nervorum. Teased fibers showed prevalent aspects of de-/remyelination and, often in association, marked myelin wrinkling suggesting axonal atrophy. This Tangier patient differs from known cases for the presence of a distal symmetrical sensorimotor polyneuropathy (not previously reported in Tangier disease) and because of the morphological findings of de-/remyelination coexisting with aspects of axonal atrophy and previous degeneration, and of lipid accumulation within striated muscle and vasa nervorum. This latter finding contrasts with the assumption that in Tangier disease vessel walls are not a site of lipid storage: probably the vasa nervorum are different, in this respect, from other vessels, because of the intense lipid metabolism of the nervous tissue. Thus we suggest that involvement of vasa nervorum in Tangier disease may be more important than previously suspected, possibly playing a role in the causation of neuropathy.

Aged↗
PubMed1984

Bile lipid composition and haemostatic variables in a case of high density lipoprotein deficiency (Tangier disease).

A 62-year-old man with clinical and biochemical findings consistent with homozygous Tangier disease is presented. Widespread atherosclerosis was present. Bile lipid analysis showed a low molar percentage of cholesterol with a low saturation index. The data suggest that high density lipoprotein cholesterol may act as a preferential precursor of biliary cholesterol. Coagulation and platelet studies indicated that the patient's platelets were hyper-responsive to aggregating agents and produced an increased amount of thromboxane B2. A platelet storage pool deficiency was also found.

Aged↗
PubMedDate not supplied

Hippocampal type I and type II corticosteroid receptors are modulated by central noradrenergic systems.

The effects of corticosteroids on various brain functions, including the negative feedback control of hypothalamo-pituitary-adrenal (HPA) axis activity, are mediated by two types of receptors (type I, or mineralocorticoid, and type II, or glucocorticoid) in the central nervous system. Although receptor numbers are thought to be regulated by circulating levels of corticosterone, there may be a direct neural control of corticosteroid receptors. In the present experiments, we demonstrate that 6-OHDA lesioning of noradrenergic (NA) ascending pathways in the pedunculus cerebellaris superior (PCS) reduces corticosterone secretion in response to novelty and increases the number of hippocampal type I corticosteroid receptors in rats 24 hr after adrenalectomy. The same lesion in adrenalectomized animals in which corticosterone levels were maintained within normal limits by corticosterone replacement implants also led to an increase in the number of type I corticosterone receptors and a decrease in the apparent affinity (Kd) of type II receptors in the hippocampus. These results suggest that the NA system may regulate HPA axis activity via a direct control of the number of type I receptors and the apparent affinity of type II receptors in the hippocampus. The possibility that there is a neural control of corticosteroid receptors may throw light on mechanisms controlling HPA axis activity and may suggest other approaches to the treatment of dysregulation of the HPA axis observed during stress and in certain psychopathological conditions.

Adrenalectomy↗
PubMedDate not supplied

Prenatal stress and long-term consequences: implications of glucocorticoid hormones.

We have shown that prenatal restraint stress (PNRS) induces higher levels of anxiety, greater vulnerability to drugs, a phase advance in the circadian rhythm of locomotor activity and an increase in the paradoxical sleep in adult rats. These behavioral effects result from permanent modifications to the functioning of the brain, particularly in the feedback mechanisms of the hypothalamic-pituitary-adrenal (HPA) axis: the secretion of corticosterone is prolonged after stress and the number of the central glucocorticoid receptors is reduced. These abnormalities are associated with modifications in the synthesis and/or release of certain neurotransmitters. Dysfunction of the HPA axis is due, in part, to stress-induced maternal increase of glucocorticoids, which influences fetal brain development. Some biological abnormalities in depression can be related to those found in PNRS rats reinforcing the idea of the usefulness of PNRS rats as an appropriate animal model to study new pharmacological approaches.

Animals↗
PubMedDate not supplied

[Significance of "minor" genetic mutations in hereditary hemochromatosis: 2 case reports].

We describe a case of homozygosity due to the substitution of aspartic acid with histidine at position 63 of the protein encoded by the gene (known as HFE) associated with hereditary hemochromatosis. Liver biopsy did not disclose stainable iron accumulation; serum ferritin was elevated (639 ng/mL), while the transferrin saturation index was within the normal range (38.1%). As the patient was affected by chronic hepatitis C virus, the high serum ferritin could be attributed to this disease, a frequent occurrence. We also describe a case of heterozygosity for both the substitution of tyrosine with cysteine at position 282 and the substitution of histidine to aspartic acid at position 63 (so-called "compound heterozygosity"). The patient had the typical biochemical abnormalities of iron overload: transferrin saturation index of 53.1% and elevated serum ferritin (658 ng/mL). The removal of > 5 g of iron by phlebotomies did not precipitate iron deficiency. Although the patient refused to undergo liver biopsy, clinical evidence alone enabled a diagnosis of hemochromatosis. These two cases concord with the present scientific orientation, i.e.: 1) homozygosity for the major mutation is associated with the phenotypical (clinical) picture of hemochromatosis, but compound heterozygosity also determines significant iron metabolism abnormalities; 2) homozygosity for the minor mutation does not appear to determine important phenotypical abnormalities.

Adult↗
PubMedDate not supplied

[Pharmacologic profile of protirelin tartrate].

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

A model for later-life effects of perinatal drug exposure: maternal hormone mediation.

In the female rat chronic ethanol intake increased plasma levels of corticosterone; acute stress in the pregnant or lactating rat increased plasma levels of corticosterone in the fetuses or sucklings. In the lactating rat, corticosterone rapidly equilibrated between plasma and milk, so that variations in the mother's adrenocortical secretion could be promptly reflected in the suckling's body. The role of maternal adrenocortical hormone with regard to the development of pituitary-adrenocortical and behavioral activities was indicated by endocrine (plasma corticosterone), neurochemical (hippocampal corticosterone binding) and behavioral (avoidance performance) anomalies in the adult offspring of lactating rats with adrenocortical "hyperfunction" or "insufficiency." Further, the offspring of rats with adrenocortical "insufficiency" showed abnormalities in "in vitro" hypothalamus, pituitary and adrenocortex release of hormones. When searching for later effects in the offspring of drugs given to the mother in perinatal life one must be cognizant that, aside from their expected pharmacological action, drugs can produce variations in the mother pituitary-adrenocortical activity, sensed by the conceptus through the placenta or milk.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

[Collateral effects of disulfiram on the central nervous system in alcoholics that have become totally abstemious. Description of 8 cases].

Disulfiram is used in alcohol rehabilitation because it inhibits aldehyde dehydrogenase and consequently causes the disulfiram-ethanol reaction (vomiting, vertigo, anxiety, cardiovascular effects) after ingestion of alcoholic beverages. However, adverse effects on the central nervous system (for the most part psychotic reactions, acute organic brain syndrome, catatonia) may appear as a direct result of the drug itself. Disulfiram and its metabolite carbon disulfide inhibit dopamine beta-hydroxylase, increasing the levels of dopamine and reducing those of norepinephrine in the central nervous system. We observed direct disulfiram-induced toxicity on the central nervous system in 8 abstinent patients in whom a disulfiram-ethanol reaction had been excluded. Risk is increased when 1) excessive amounts of the drug are ingested; 2) the patient is already suffering from a major psychiatric illness; 3) the patient has anatomical brain lesions. In all cases observed, the toxic effects appeared in the first weeks and were reversed after suspension of the drug (except in one patient who died from severe bronchopulmonary infection). We thus suggest the following protocol: 1) physical examination and interview 3-4 weeks after initiation of treatment; 2) as a general rule, in abstinent patients, the lowest possible maintenance dosage should be administered. This strategy, despite the risk of underdosage, meets the goals inherent in an integrated medical and psychosocial approach to the treatment of alcoholism with which these patients seem better able to comply.

Adult↗