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Trace elements and rat pouchitis

100%
EN
The procedure of restorative proctocolectomy is associated with a complete removal of the colon and slight reduction of ileum length, which together can lead to systemic shortages of trace elements. Inflammatory changes in the pouch mucosa may also have some impact. However, there is no data on trace elements in pouchitis. Therefore, in the present study we aimed to assess the effect of acute pouchitis on the status of selected trace elements in rats. Restorative proctocolectomy with the construction of intestinal J-pouch was performed in twenty-four Wistar rats. Three weeks after the surgery, pouchitis was induced. Eight untreated rats created the control group. Liver concentrations of selected micronutrients (Zn, Cu, Co, Mn, Se) were measured in both groups six weeks later, using inductively coupled plasma mass spectrometry. Liver concentrations of trace elements did not differ between the study and the control groups. However, copper, cobalt and selenium concentrations [μg/g] were statistically lower (p<0.02, p<0.05 and p<0.04, respectively) in rats with severe pouchitis (n=9) as compared with rats with mild pouchitis (n=7) [median (range): Cu - 7.05 (3.02-14.57) vs 10.47 (5.16-14.97); Co - 0.55 (0.37-0.96) vs 0.61 (0.52-0.86); Se - 1.17 (0.69-1.54) vs 1.18 (0.29-1.91)]. In conclusion, it seems that acute pouchitis can lead to a significant deficiency of trace elements.
EN
Background: Steatorrhea, which is a consequence of pancreatic insufficiency, occurs in 85% of patients with cystic fibrosis. In clinical practice, fecal fat concentration is used to diagnose and monitor fecal fat losses. Because compliance with this method is insufficient, new tests are needed. One of the alternatives may be the acid steatocrit. Aim: This study aimed to investigate the value of acid steatocrit in the assessment of fecal fat excretion in pancreatic-insufficient infants with cystic fibrosis: before and after the initiation of pancreatic enzyme supplementation. Patients and methods: The study included 10 infants with cystic fibrosis diagnosed through the newborn screening program and 16 healthy control infants. In all the children, fecal elastase-1, fecal fat concentration (%) and acid steatocrit were measured. Results: Fecal fat concentration in cystic fibrosis infants (range: 14.5%–32,1%) was significantly higher (p<0.0001) compared with control subjects (1.7%–15.1%). Acid steatocrit in cystic fibrosis (19.8%–68.7%) was also greater (p<0.0001) than in the control group (10.7%–22.7%). The area under the receiver operating characteristic curve (ROC) for the 95th percentile of normal values was 0.981 (95% confidence interval: 0.941–1.0) indicating high diagnostic accuracy of acid steatocrit. When acid steatocrit and fecal fat concentration cut-offs were set at 90th and 95th percentile for healthy infants, the specificity of acid steatocrit in detecting elevated fecal fat concentration was 100%, and the sensitivity 80% and 100%, respectively. Conclusions: Compared with the assessment of fecal fat concentration, sensitivity/specificity of acid steatocrit in steatorrhea detection in infants are potentially lower, but still satisfactory. The measurement of acid steatocrit may constitute a useful method of fecal fat concentration assessment in infants identified by the newborn screening program in whom the replacement enzyme therapy has not yet been commenced.
PL
Przedmiot badań: U 85% pacjentów z mukowiscydozą (ang.: cystic fibrosis, CF) stwierdza się niewydolności zewnątrzwydzielniczej trzustki (nzt). Złotym standardem rozpoznawania biegunki tłuszczowej jest ocena stężenia tłuszczu w stolcu. Ze względu na małą akceptowalność tej metody szuka się nowych procedur. Alternatywę może stanowić pomiar wskaźnika kwaśnego steatokrytu (KS). Cel badań: Celem badania była ocena przydatności oznaczania KS w ocenie wydalania tłuszczu w stolcu u niemowląt z CF z nzt, przed włączeniem suplementacji enzymatycznej. Materiał i metody: Do badania włączono 10 niemowląt z CF wykrytą w przesiewie noworodkowym oraz 16 zdrowych niemowląt. U wszystkich dzieci wykonano oznaczenie stężenia elastazy-1 w kale, stężenia tłuszczu (%) w kale w oparciu o metodę Van de Kamera oraz wartości wskaźnika KS. Wyniki: Stężenie tłuszczu w stolcu dzieci z CF wynosiło od 14,5% do 32,1% i było statystycznie większe (p<0,0001) niż w grupie zdrowych niemowląt, w której wynosiło od 1,7% do 15,1%. Wartość wskaźnika KS w grupie badanej mieściła się w zakresie od 19,8% do 68,7% i również była większa niż w grupie kontrolnej (p<0,0001), w której wynosiła od 10,7% do 22,7%. Nie wykazano korelacji między wskaźnikiem KS a stężeniem tłuszczu w stolcu. Pole pod krzywą ROC dla wartości 95 percentyla wartości prawidłowych wynosiło 0,981 (95% przedział ufności: 0,941-1,0) odzwierciedlając dużą wartość diagnostyczną metody oznaczania KS. Wnioski: Pomiar wskaźnika KS dobrze różnicuje grupy niemowląt zdrowych oraz niemowląt chorych na CF z nzt. W porównaniu do metody Van de Kamera, czułość/swoistość oznaczania KS w wykrywaniu biegunki tłuszczowej u niemowląt, jest potencjalnie mniejsza, ale wciąż bardzo zadowalająca. Należy podkreślić prostotę oznaczania KS i możliwość uzyskania wyniku danego dnia. To sprawia, że oznaczenie KS może być przydatną metodą oceny stężenia tłuszczu w stolcu u niemowląt ze skryningu noworodkowego, u których nie włączono jeszcze suplementacji enzymatycznej.
EN
The etiology of altered blood fatty acid (FA) profile in phenylketonuria (PKU) is understood only partially. We aimed to determine whether FAs deficiency is dependent on the diet or metabolic disturbances. The study comprised 40 PKU patients (20 female, 20 male; aged 11 to 35 years; 12 children and 28 adults) and 40 healthy subjects (HS; 20 female, 20 male, aged 18 to 33 years). We assessed the profile of FAs (gas chromatography/mass spectrometry) and analyzed the 72-hour dietary recalls. The amount of C14:0, C16:0 and C16:1n-7, C18:1n-9 did not differ between the analyzed groups. The percentage of C18:0 was higher, while C20:3n-9, C18:2n-6, C20:2n-6, C20:4n-6, C22:4n-6, C22:5n-6 and C22:6n-3 was lower in PKU than in HS. However, C18:3n-6, C18:3n-3 and n-6/n-3 ratio were higher in PKU patients. The C20:4n-6/C20:3n-6 ratio (reaction catalyzed by Δ5-desaturase), the C22:5n-6/C22:4n-6 and the C22:6n-3/C22:5n-3 ratio (both reactions catalyzed by Δ6 desaturase) were significantly lower in PKU patients. Therefore, the deficiency of long-chain polyunsaturated fatty acids in PKU patients may result not only from inadequate supply but also from metabolic disturbances.
4
84%
EN
Background: The available data on the incidence of lactose malabsorption are contradictory. Potential bias in random selection is a major drawback of studies performed to-date. Moreover, molecular analysis of polymorphism -13910 C>T upstream of the lactase (LCT) gene (NM_005915.4:c.1917+326C>T; rs4988235) has not been reported in those studies. Therefore, in this study we aimed to assess genetic predisposition and clinical manifestation of adult-type hypolactasia (ATH). Patients and methods: In two-hundred randomly chosen healthy subjects (HS) aged from 18 to 20 years, the presence of -13910 C>T polymorphic variants upstream of the LCT gene was assessed. In a subgroup of subjects with genotype predisposing to ATH, hydrogen-methane breath test (BT) with lactose loading was conducted to determine the current state of lactase activity. In addition, clinical symptoms typical for lactose malabsorption were assessed using the questionnaire method. Results: Sixty-three out of 200 (31.5 %) HS had -13910 C/C genotype. Thus, genetically determined lactase persistence is expected in the remaining 137 (68.5 %) subjects. Thirteen out of 53 (24.5 %) HS having -13910 C/C genotype were proved to be lactose intolerant. Recalculating the data for the entire studied population it implies the incidence of lactose malabsorption in 7.7 % of subjects. Only three out of 13 (23.1 %) subjects with abnormal BT results, reported clinical symptoms related to lactose consumption. Conclusions: Significantly lower than previously reported incidence of clinically detectable lactose malabsorption in young healthy adults in Poland has been documented. The -13910 C/C genotype upstream of the LCT gene indicates a predisposition to ATH, but definitely does not define the current ability to tolerate lactose.
5
Content available remote

Inulin supplementation in rat model of pouchitis

84%
EN
Available data indicates potential effectiveness of prebiotic therapy in alleviating inflammation and prolonging the remission in inflammatory bowel disease. Documented successes of such therapies were the basis for this study. So far, there is no data related to the effectiveness of inulin application in symptomatic or severe pouchitis in humans or in animal model. The aim of the study was to determine the effect of inulin supplementation on the expression of intestinal inflammation and feeding efficiency in rats with induced pouchitis. Twenty-four Wistar rats were operated. After induction of pouchitis animals were randomly divided into control and supplementation groups receiving, respectively, semi-synthetic diet with or without inulin (in a lower (LD) or higher (HD) dose: 2.5 % or 5 % of total dietary content of mass) for a period of 6 weeks. Selected nutritional parameters were assessed throughout the study. Histopathological and immunohistochemical analysis of pouch mucosa specimens was also performed. The energy intake, weight gain, feeding efficiency, quality of stools were comparable in all studied groups. The intensity of inflammation (Moskovitz scale) and adaptive changes (Laumonier scale) did not differ between compared groups. The tissue expression of pro- and anti-inflammatory interleukins (IL-1α, IL-6, IL-10 and IL-12) was not different either. Inulin supplementation does not improve the quality of stools or the expression of intestinal inflammation in rats with induced pouchitis. It has no impact on the intensity of pouch adaptation or on feeding efficiency.
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