Summary
The effect of Caerulein, a decapeptide similar for action and structure to CCK, was studied in patients with hypokinetic gallbladder to a fatty meal, using a spot-photofluorogram technique.
Cut of 19 patients examined, in 4 cases there was a valid and prompt gallbladder contraction with a dose of Caerulein (1 hg/kg/min for 5 min) sufficient to induce a colecystokinesis similar to the one provoked by ingestion of the fatty meal. In 5 cases the gallbladder contraction was obtained only with a double load of Caerulein; in 5 patients only a treble load was effective in inducing a gallbladder contraction. In 3 patients it was necessary to inject higher doses and for longer lapses of time. Finally, in two cases, the examination had to be interrupted, due to intolerance phenomena.
So far, in all the patients, except the two above, a valid contraction was achieved, even if with different doses of Caerulein.
The hypothesis of an endogenous hormonal defect for the results obtained in the first group of patients may be suggested. On the contrary, for the other groups it is necessary to postulate some more hypothesis. The parallelism of the contraction curves, even if obtained with different loads of Caerulein, suggests the same that mechanism may be hindered by a reduced receptorial affinity or by the presence of a competitive antagonist.
Riassunto
Mediante metodica spotgotofluorografica è stato studiato il comportamento di colecisti ipocinetiche nei confronti della somministrazione e.v. lenta di Ceruleina, il decapeptide strutturalmente e funzionalmente simile alla CCK.
Sono state comprese in questo gruppo quelle colecisti la cui riduzione volumetrica al pasto grasso era uguale o inferiore al 20% dell’area iniziale, calcolata sui radiogrammi secondo la metodica di Boyden. Sono stati esaminati 19 pazienti (15 donne e 4 uomini); dal punto di vista chimico-laboratoristico era in genere presente una sindrome dispeptico-dolorosa, in alenni casi sfociante in caratteristiche coliche biliari. Frequente l’associazione con colon irritabile e cefalea vasomotoria. Non sono state riscontrate altre alterazioni. 4 dei pazienti hanno risposto con una valida e pronta contrazione colecistica ad una dose di 1 ng/kg/min. per 5 minuti (1x), dose atta ad indurre nei soggeti normali una colecistocinesi simile a quella provocata dall’ ingestione di pasto grasso. In 5 pazienti la contrazione colecistica è stata ottenuta solo a dosi doppie (2x), in 5 altri casi solo a dosi triple (3x); in 3 pazienti si è dovuto ricorrere a dosi nettamente superiori e per tempi prolungati; infine, in 2 casi la prova dovette essere interrotta per la comparsa di fenomeni di intolleranza.
In tutti i pazienti, quindi, tranne i 2 casi di cui sopra, è stata raggiunta una valida contrazione colecistica (uguale o superiore al 50% dell’area iniziale). Ma mentre, per il 1° gruppo (risposta ad 1x), si può avanzare l’ipotesi di un difetto ormonale endogeno, per gli altri gruppi è necessario prospettare altre cause. L’andamento parallelo delle curve di contrazione, se pure ottenuta a dosi diverse, suggerisce comunque un identico meccanismo d’azione, probabilmente ostacolato da una ridotta affinità del recettore o dalla presenza di un antogonista competitivo.
Résumé
Par la méthode spot-photofluorographique on a étudié le comportement des cholécystes-hypocinétiques après une lente administration intraveineuse de céruleine, le decapeptide qui rassemble par structure et fonction à la CCK. On a inclus dans le groupe les vésicules dont la réduction volumétrique après un repas gras était égale ou inférieure au 20% de la surface initiale, calculée sur les radiogrammes suivant la méthode de Boyden.
On a examiné 19 patients (15 femmes et 4 hommes); au point de vue clinique on a relevé en général un syndrome dyspeptique-douloureux avec, parfois, des crises de coliques vésiculaires. On a relevé aussi dans les mêmes sujets la présence de colon irritable et de céphalée vaso-motrice. Le bilan biologique était tout à fait normal.
Quatre sujets ont présenté une valide et prompte contraction vésiculaire à une dose de 1 ng/kg/min. pour 5’ (1 x); cette dose cause dans les sujets normaux une contraction égale à celle provoquée par l’ingestion d’un repas gras. Dans cinq cas on a obtenu la contraction vésiculaire seulement avec des doses doubles (2 x) ou, encertains cas, triples (3 x); pour trois patients on a utilisé des doses supérieures administrées en infusion prolongée.
Enfin, en deux cas, on a dû interrompre l’examen pour l’apparition de phénomènes d’intollerance. Dans tous les sujets, sauf les deux derniers cas, on a obtenu une contraction vésiculaire valide, égale ou supérieure au 50% de la surface initiale. Mais, si pour le premier groupe (réponse à 1 x) on peut avancer l’hypothèse d’un défaut hormonal endogène, pour les autres groupes il faut penser à d’autres causes.
Le comportement parallèle des courbes de contraction, quand même obtenue à des doses différentes, nous montre également un mécanisme d’action identique, probablement entravé par une affinité mineure du récepteur ou par la présence d’un antagoniste compétitif.
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Lanfranchi, G.A., Sciutti, R. & Turci, G. Caerulein cholecystography in the diagnosis of biliary dyskinesia. Acta Endosc 5, 161–169 (1975). https://doi.org/10.1007/BF02969001
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DOI: https://doi.org/10.1007/BF02969001