Background
Chronic intestinal pseudo‐obstruction (CIPO) represents the most severe form of gastrointestinal dysmotility with debilitating and potentially lethal consequences. Symptoms can be ...non‐specific, and result in this condition being diagnosed incorrectly or too late with consequences for morbidity and even mortality.
Purpose
The present article aims to provide pediatric and adult gastroenterologists with an up to date review about clinical features, diagnosis and therapeutic options for CIPO. Although pediatric and adult CIPO share many clinical aspects distinctive features can be identified. There is no single diagnostic test or pathognomonic finding of CIPO, thus a stepwise approach including radiology, endoscopy, laboratory, manometry, and histopathology should be considered in the diagnostic work‐up. Treatment of patients with CIPO is challenging and requires a multidisciplinary effort with participation of appropriately experienced gastroenterologists, pathologists, dieticians, surgeons, psychologists, and other subspecialists based on the presence of comorbidities. Current treatment options invariably involve surgery and specialized nutritional support, especially in children. Medical therapies are mainly aimed to avoid complications such as sepsis or intestinal bacterial overgrowth and, where possible, restore intestinal propulsion. More efficacious therapeutic options are eagerly awaited for such difficult patients.
Chronic intestinal pseudo‐obstruction (CIPO) represents the most severe form of gastrointestinal dysmotility with debilitating and potentially lethal consequences. Symptoms can be non‐specific, and result in an incorrect or too late diagnosis with consequences in terms of morbidity and even mortality. Thus, the present article aims to provide pediatric and adult gastroenterologists with an up to date review about clinical features, diagnosis, and therapeutic options for CIPO.
Chronic intestinal pseudo‐obstruction (CIPO) is a severe form of gastrointestinal dysmotility (often due to derangement of the innervation/smooth muscle/interstitial cells of Cajal) with recurrent ...episodes of intestinal subocclusion mimicking a mechanical obstruction. Because of its complexity and heterogeneity, CIPO is often misdiagnosed or remains unrecognized until advanced stages. Management is a critical aspect in CIPO patient care. So far, most prokinetic drugs have not proven efficacy in restoring intestinal propulsion, thus nutritional support, fluid/electrolyte replacement, and antibiotics are the mainstay of treatment. In this issue of the journal, Ohkubo et al showed promising data indicating that percutaneous endoscopic gastro‐jejunostomy (PEG‐J) can be proposed as a measure for intestinal decompression, thereby improving CIPO‐associated abdominal symptoms, including pain. In addition to a concise update of clinical and diagnostic features, the present minireview tackles management options, with a major emphasis on PEG‐J, for CIPO patients.
Abbreviated : Chronic intestinal pseudo‐obstruction (CIPO) is one of the most severe forms of gastrointestinal dysmotility with many debilitating and potentially life‐threatening symptoms / manifestations. Since most drugs failed to restore gastrointestinal coordinated motility, nutritional support, fluid / electrolyte replacement and antibiotics are still mandatory as life‐saving measures. Promising data indicate that percutaneous endoscopic gastro‐jejunostomy (PEG‐J) can be proposed as a measure for intestinal decompression in CIPO, thereby improving symptoms and preventing malnutrition.
Summary
Background Considerable information has been gathered on the functional organization of enteric neuronal circuitries regulating gastrointestinal motility. However, little is known about the ...neuropathophysiological mechanisms underlying gastrointestinal motor disorders.
Aim To analyse the most important pathological findings, clinical implications and therapeutic management of idiopathic enteric neuropathies.
Methods PubMed searches were used to retrieve the literature inherent to molecular determinants, pathophysiological bases and therapeutics of gastrointestinal dysmotility, such as achalasia, gastroparesis, chronic intestinal pseudo‐obstruction, Hirschsprung’s disease and slow transit constipation, to unravel advances on digestive disorders resulting from enteric neuropathies.
Results Current data on molecular and pathological features of enteric neuropathies indicate that degenerative and inflammatory abnormalities can compromise the morpho‐functional integrity of the enteric nervous system. These alterations lead to a massive impairment in gut transit and result in severe abdominal symptoms with associated high morbidity, poor quality of life for patients and established mortality. Many pathophysiological aspects of these severe conditions remain obscure, and therefore treatment options are quite limited and often unsatisfactory.
Conclusions This review of enteric nervous system abnormalities provides a framework to better understand the pathological processes underlying gut dysmotility, to translate this knowledge into clinical management and to foster the development of targeted therapeutic strategies.
A
bstract
We measure the branching fractions and
CP
asymmetries for the singly Cabibbo-suppressed decays
D
0
→
π
+
π
−
η
,
D
0
→
K
+
K
−
η
, and
D
0
→
ϕη
, using 980 fb
−
1
of data from the Belle ...experiment at the KEKB
e
+
e
−
collider. We obtain
B
D
0
→
π
+
π
−
η
=
1.22
±
0.02
stat
±
0.02
syst
±
0.03
B
ref
×
10
−
3
,
B
D
0
→
K
+
K
−
η
=
1.80
−
0.06
+
0.07
stat
±
0.04
syst
±
0.05
B
ref
×
10
−
4
,
B
D
0
→
ϕη
=
1.84
±
0.09
stat
±
0.06
syst
±
0.05
B
ref
×
10
−
4
,
where the third uncertainty (
B
ref
) is from the uncertainty in the branching fraction of the reference mode
D
0
→
K
−
π
+
η
. The color-suppressed decay
D
0
→
ϕη
is observed for the first time, with very high significance. The results for the
CP
asymmetries are
A
CP
D
0
π
+
π
−
η
=
0.9
±
1.2
stat
±
0.5
syst
%
,
A
CP
D
0
→
K
+
K
−
η
=
−
1.4
±
3.3
stat
±
1.1
syst
%
,
ACP
D
0
→
ϕη
=
−
1.9
±
4.4
stat
±
0.6
syst
%
.
The results for
D
0
→
π
+
π
−
η
are a significant improvement over previous results. The branching fraction and
A
CP
results for
D
0
→
K
+
K
−
η
, and the
ACP
result for
D
0
→
ϕη
, are the first such measurements. No evidence for
CP
violation is found in any of these decays.
We measure the branching fractions and CP asymmetries for the singly Cabibbo-suppressed decays $D^0 → π^+π^-η, D^0 → K^+K^-η$, and $D^0 → Φη$, using 980 fb-1 of data from the Belle experiment at the ...KEKB e+e- collider. We obtain $$\mathcal{B}(D^0 → π^+π^-η = \mathrm{1.22 ± 0.02 (stat) ± 0.02(syst) ± 0.03}(\mathcal{B}_{\mathrm{ref}}) \mathrm{x 10^{-3}}$$ $$\mathcal{B}(D^0 → K^+K^-η = \mathrm{1.80^{+0.07}_{-0.06}(stat) ± 0.04 (syst) ± 0.05}(\mathcal{B}_{\mathrm{ref}}) \mathrm{x 10^{-4}}$$ $$\mathcal{B}(D^0 → Φη = \mathrm{1.84 ± 0.09 (stat) ± 0.0 (syst) ± 0.05}(\mathcal{B}_{\mathrm{ref}}) \mathrm{x 10^{-4}}$$ where the third uncertainty ($\mathcal{B}_{\mathrm{ref}}$) is from the uncertainty in the branching fraction of the reference mode $D^0 → K^-π^+η$. The color-suppressed decay $D^0 → Φη$ is observed for the first time, with very high significance. The results for the CP asymmetries are $$A_{CP} (D^0 → π^+π^-η) = \mathrm{0.9 ± 1.2 (stat) ± 0.5 (syst)}\%$$ $$A_{CP} (D^0 → K^+K^-η) = \mathrm{-1.4 ± 3.3 (stat) ± 1.1 (syst)}\%$$ $$A_{CP} (D^0 → Φη) = \mathrm{-1.9 ± 4.4 (stat) ± 0.6 (syst)}\%$$ The results for $D^0 → π^+π^-η$ are a significant improvement over previous results. The branching fraction and ACP results for $D^0 → K^+K^-η$, and the ACP result for $D^0 → Φη$, are the first such measurements. No evidence for CP violation is found in any of these decays.
A
bstract
Using a data sample of 980 fb
−
1
collected with the Belle detector at the KEKB asymmetric-energy
e
+
e
−
collider, we study the processes of
Ξ
c
0
→
Λ
K
¯
∗
0
,
Ξ
c
0
→
Σ
0
K
¯
∗
0
, and
Ξ
...c
0
→
Σ
+
K
∗
−
for the first time. The relative branching ratios to the normalization mode of
Ξ
c
0
→
Ξ
−
π
+
are measured to be
B
Ξ
c
0
→
Λ
K
¯
∗
0
/
B
Ξ
c
0
→
Ξ
−
π
+
=
0.18
±
0.02
stat
.
±
0.01
syst
.
,
B
Ξ
c
0
→
Σ
0
K
¯
∗
0
/
B
Ξ
c
0
→
Ξ
−
π
+
=
0.69
±
0.03
stat
.
±
0.03
syst
.
,
B
Ξ
c
0
→
Σ
+
K
∗
−
/
B
Ξ
c
0
→
Ξ
−
π
+
=
0.34
±
0.06
stat
.
±
0.02
syst
.
,
where the uncertainties are statistical and systematic, respectively. We obtain
B
Ξ
c
0
→
Λ
K
¯
∗
0
=
3.3
±
0.3
stat
.
±
0.2
syst
.
±
1.0
ref
.
×
10
−
3
,
B
Ξ
c
0
→
Σ
0
K
¯
∗
0
=
12.4
±
0.5
stat
.
±
0.5
syst
.
±
3.6
ref
.
×
10
−
3
,
B
Ξ
c
0
→
Σ
+
K
∗
0
=
6.1
±
1.0
stat
.
±
0.4
syst
.
±
1.8
ref
.
×
10
−
3
,
where the uncertainties are statistical, systematic, and from
B
Ξ
c
0
→
Ξ
−
π
+
, respectively. The asymmetry parameters
α
Ξ
c
0
→
Λ
K
¯
∗
0
and
α
Ξ
c
0
→
Σ
+
K
∗
−
are 0
.
15 ± 0
.
22(stat
.
) ± 0
.
04(syst
.
) and
−
0
.
52 ± 0
.
30(stat
.
) ± 0
.
02(syst
.
), respectively, where the uncertainties are statistical followed by systematic.
A
bstract
We report the first measurement of the exclusive cross sections
e
+
e
−
→
B
B
¯
,
e
+
e
−
→
B
B
¯
∗
, and
e
+
e
−
→
B
∗
B
¯
∗
in the energy range from 10
.
63 GeV to 11
.
02 GeV. The
B
...mesons are fully reconstructed in a large number of hadronic final states and the three channels are identified using a beam-constrained-mass variable. The shapes of the exclusive cross sections show oscillatory behavior with several maxima and minima. The results are obtained using data collected by the Belle experiment at the KEKB asymmetric-energy
e
+
e
−
collider.
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