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E Monteiro

Publications and source records attributed to E Monteiro.

At least 73 records · Page 4Linked to original sources
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Histocompatibility antigens: markers of susceptibility to and protection from alcoholic liver disease in a Portuguese population.

The distribution of six HLA antigens in a population of 88 Portuguese chronic alcohol abusers with biopsy-proven liver disease was compared to that in 66 Portuguese normal controls. Among the group of 88 alcohol abusers, the presence of HLA antigens A1, A9, A28 and Bw35 marked a significant 2.5- to 3-fold increased estimated risk for the development of alcohol-induced cirrhosis, while the presence of HLA B5 was found to be associated with a significantly decreased risk of alcohol-induced cirrhosis. Further, compared to controls, the estimated risk of any stage of alcohol-induced liver disease was significantly increased in alcoholic individuals with HLA A28 and Bw35, and the protective effect of HLA B5 was again observed. The findings of this study suggest that at least in a relatively homogeneous population group such as the Portuguese, the presence of HLA B5 may confer protection against alcohol-induced liver disease, including cirrhosis. The presence of HLA Bw35 and A28 appear to mark susceptibility to all histologic manifestations of alcohol-induced liver disease, while in addition to Bw35 and A28, A1 and A9 may mark increased risk for cirrhosis in particular.

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[Hemichorea induced by diabetic ketoacidosis and striatal hyperdensity on computerized axial tomography].

INTRODUCTION: Hyperglycaemia, usually not ketotic, may cause hemichorea hemiballism. The mechanism of this physiopathological syndrome is still not clear. It usually occurs in elderly ladies and is associated with hyperdensity in the striate area contralateral to the affected side, on CT and MR potentiated in T1. CLINICAL CASE: Three days before hospital admission, and 86 year old woman presented with the acute onset of choreiform movements of her left limbs, particularly her left arm. She had not taken neuroleptic drugs and there was no family history of chorea. On neurological examination there were no other unusual findings. Laboratory tests showed hyperglycemia with metabolic acidosis and ketone bodies in the urine. On the CT scan there was a hyperdense lesion in the right striate area, but this did not act as a space occupying lesion. Treatment was started with intravenous insulin and the symptoms disappeared 48 hours later. CONCLUSIONS: We emphasize the rarity of the association of hemichorea and diabetic ketoacidosis. From the histological studies done in some of these patients, it seems that the hyperdensity of the striate area may be due to the proliferation of hypertrophic astrocytes secondary to small ischemic lesions. When the hyperglycaemia is treated, the chorea disappears within a few days and it is unusual for neuroleptic treatment to be required. In cases of hemichorea, hyperglycaemia should be ruled out, as should structural causes (tumors, infarcts, hematomas, traumatic lesions, etc.).

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