Combined patterns of social support and coping style and correlations with adjustment to cancer were investigated in early-stage melanoma patients. The authors studied 358 consecutive patients attending regular follow-up who answered standardized instruments that assess social support, coping behavior, and tumor-related distress. Regression analyses identified high active and low depressive coping behavior as stronger predictors for perceived support than sociodemographic and clinical variables. Cluster analyses yielded four coping-support patterns. High social support, combined either with active coping or with stoicism, was associated with good adjustment, whereas low perceived support in the subjects living alone or in the patients exhibiting depressive coping behavior was associated with poor adjustment.

Adaptation, Psychological↗

PubMedDate not supplied

A comparison of magnetization transfer ratio, magnetization transfer rate, and the native relaxation time of water protons related to relapsing-remitting multiple sclerosis.

BACKGROUND AND PURPOSE: Magnetization transfer (MT) imaging and measurements of the magnetization transfer ratio (MTR) have extended our capability to depict and characterize pathologic changes associated with multiple sclerosis (MS). We wanted to investigate whether the analysis of other MT parameters, such as magnetization transfer rate (k(for)) and relative measure of water content (T1(free)), adds insight into MS-related tissue changes. METHODS: Quantitative MT imaging by use of phase acquisition of composite echoes was performed in nine patients with clinically definite relapsing-remitting MS and eight healthy control subjects on a 1.5-T MR system. We analyzed a total of 360 regions of interest and compared control white matter with various types of lesions and normal-appearing white matter in MS. RESULTS: We found a strong correlation between the MTR and k(for), but this relation was non-linear. A slight but significant reduction of the MTR in normal-appearing white matter of patients with MS was attributable to a reduced transfer rate only, whereas a lower MTR was associated with both a reduction of k(for) and an increase of T1(free) in regions of dirty white matter. Moreover, areas such as edema and T1-isointense lesions had a similar MTR but could be differentiated on the basis of Tl(free). CONCLUSION: Estimates of k(for) and T1(free) appear to complement MTR measurements for the understanding of MT changes that occur with different types of MS abnormalities in the brain.

Adult↗

PubMedDate not supplied

[Buccodental apparatus and endocrine glands].

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Acromegaly↗

PubMedDate not supplied

[Considerations of the advent and evolution of climacteric during Cushing's disease and secondary hypercorticism].

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Adrenocortical Hyperfunction↗

PubMedDate not supplied

The role of the renin-angiotensin system in arterial hypertension in hypercorticism.

The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.

17-Ketosteroids↗

PubMedDate not supplied

Plasma renin activity (PRA) and plasma aldosterone in the adrenal cortex hyperactivity. Studies on 50 hypertensive patients.

The authors have studied on 50 patients hospitalized in the Adrenal Pathology unit of the Institute of Endocrinology, the etiopathogeny of arterial hypertension (AH) in hypercorticism and the therapeutic implications, arriving at the conclusion that in 20% of the cases AH was probably due to an increased activity of renin-angiotensin and in 47% to elevated levels of aldosterone. The authors hypothesize that AH in the remaining 30% of the hypercorticism cases in this study is due to other mineralocorticoids in excess and suggest that the treatment should be pathogenic and strictly individualized.

Adrenocortical Hyperfunction↗