Purpose: In recent times, growing uncertainty has emerged regarding the effectiveness of standard pressure ulcer (PU) risk assessment tools, which are suspected to be no better than clinical judgment, especially in the frail and comorbid elderly population. This study aimed to identify the primary clinical predictive variables for PU development and severity in hospitalized older adults, utilizing a multidimensional frailty assessment, and compare them with the Braden scale.
Patients And Methods: The population consisted of 316 patients, admitted to the Geriatric Unit and Transitional Care of San Bartolomeo Hospital in Sarzana (Italy) during the period 21/02/22-01/07/22.
Objective: Several alterations of magnesium metabolism have been associated with type 2 diabetes pathophysiology, a condition particularly frequent in older persons. We aimed to evaluate serum total (Mg-tot) and serum ionized magnesium (Mg-ion) in older persons with type 2 diabetes in order to explore clinically applicable methods for the detection of magnesium deficit.
Material/methods: Mg-tot and Mg-ion were measured in 105 fasting subjects with type 2 diabetes (mean age: 71.
Aim: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level.
Methods: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present.
Iron overload diseases are due to a progressive increase in total body iron stores that leads to deposition of iron in parenchymal organs and to subsequent damage to these organs. The commonest inherited form of iron overload is hereditary hemochromatosis (HH), an autosomal recessive disorder affecting the white population. Although in the western world and in northern Europe the majority of cases of HH are associated with an HFE gene mutation (C282Y and H63D), there are families with a familial iron overload disorder in whom neither the C282Y nor the H63D mutations were found.
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