Contradictory results have been reported on the use of goats' milk in cows' milk allergy. In this study the hypothesis was tested, using a guinea pig model of cows' milk allergy, that these discrepancies could be due to the high genetic polymorphism of goats' milk proteins. Forty guinea pigs were fed over a 20 d period with pelleted diets containing one of the following: soyabean proteins (group S), cows' milk proteins (group CM), goats' milk proteins with high (group GM1) or low (group GM2) αs1-casein content. Parenteral sensitization to GM1 and GM2 proteins was also assessed. The sensitization was measured (1) by systemic IgG1 antibodies directed against bovine or caprine β-lactoglobulin (β-lg), α-lactalbumin (α-la) and whole caseins, and (2) by intestinal anaphylaxis measured in vitro in Ussing chambers, by the rise in short-circuit current (ΔIsc) in response to milk proteins. Guinea pigs fed on CM and GM1 developed high titres (> 1500) of anti-β-lg IgG1, with an important cross reactivity between goat and cow β-lg. However, in guinea pigs fed on GM2, anti-goat β-lg IgG1 antibodies were significantly decreased compared with GM1 guinea pigs (mean IgG1 titres were 546 and 2046 respectively), and the intestinal anaphylaxis was significantly decreased (3·5±4·5 μA/cm2) compared with that observed in GM1 guinea pigs (8·3±7·6 μA/cm2). Animals receiving GM1 or GM2 proteins via the parenteral route developed a marked sensitization. These results suggest that the discrepancies observed in the use of goats' milk in cows' milk allergy could be due, at least in part, to the high genetic polymorphism of goats' milk proteins.

In a general hospital-based population in France, peptic ulcer disease appears idiopathic in a fifth of cases.

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An 80-year-old hypertensive woman developed right hemiplegia and died 24 hours after admission. Neuropathologic examination revealed multiple cerebral infarcts of various ages and diffuse subcortical arteriosclerotic encephalopathy. Clusters of asymptomatic "expanding" lacunes, due to dilatation of the perivascular spaces, were found in both dentate nuclei. These cavities, which presented as space-occupying lesions, were surrounded by a single layer of flattened cells and contained 1 or more sections of normal-looking arterioles. Such a topographic grouping of lacunes in the dentate nucleus has not been described previously. The mechanism of widening of the perivascular compartment remains unclear; its occurrence in a hypertensive patient and its association with typical Binswanger's subcortical arteriosclerotic encephalopathy and severe atherosclerosis with multiple infarcts suggest a common pathophysiologic mechanism possibly including an alteration of the blood-brain barrier.(Stroke 1987;18:1087-1092) C erebral lacunes are usually considered to be old, small, deep cerebral infarcts 12 due to occlusive arterial lesions. 34 However, old hemorrhages can be a cause of lacunes and have been recently reviewed.5 Dilatations of perivascular spaces, well known since the historic paper of Marie 6 and the thesis of Ferrand, 7 have been reemphasized recently as a possible mechanism of genesis of cerebral lacunes. 89To avoid the semantic confusion that surrounds the term cerebral lacune, 10 a new neuropathologic classification has been proposed." 12 Lacunes due to dilatation of the perivascular space are usually asymptomatic. 8 A new type of space-occupying lacune due to dilatation of the perivascular space was described as an "expanding cerebral lacune" by Poirier et al. 9 In this initial report, the thalamo-mesencephalic "expanding lacunes" were responsible for clinical symptoms.In this article, we report a new case of expanding lacune involving the cerebellum with three major points of interest: 1) the lesion was asymptomatic, presenting as an incidental autopsy finding, 2) the topographic grouping of lacunes in the dentate nuclei had never been described, and 3) the lacunes were associated with Binswanger's subcortical arteriosclerotic encephalopathy (SAE) and multiple cerebral infarcts. Such an association in a hypertensive patient suggests com- Received March 5, 1987; accepted June 22, 1987. mon pathogenetic mechanisms as the origin of these various lesions. Report of a CaseAn 80-year-old woman known to be hypertensive for many years had received various antihypertensive treatments. She suffered from left ventricular failure and coronary insufficiency. She was admitted to the hospital on March 8, 1983, because of dyspnea. Blood pressure was 170/100 mm Hg. She became somnolent, then comatose, and developed right hemiparesis 24 hours after admission and died within a few hours. Computed tomography (CT) scan was not obtained.Postmortem examination revealed diffuse and severe atherosclerotic lesions in the thoracic ...

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