This study would give credence to the .. lack of blood flow /
hyperviscosity / erythrocytosis / polycythemia / increased red blood
cell production leading to / CAUSING .. colitis.

<<snip>>
The 30 that developed NEC were more likely  to have polycythemia
<<snip>>

J Perinatol. 2007 Mar 29; [Epub ahead of print]Necrotizing
enterocolitis in term neonates: data from a multihospital health-care
system.Lambert DK, Christensen RD, Henry E, Besner GE, Baer VL,
Wiedmeier SE, Stoddard RA, Miner CA, Burnett J.
[1] 1Intermountain Health Care, Ogden, UT, USA [2] 2Department of
Neonatology, McKay-Dee Hospital Center, Ogden, UT, USA.

Objectives:In the past 5(1/2) years, 30 term or near-term neonates in
the Intermountain Healthcare system developed necrotizing
enterocolitis (NEC) Bell's stage >/=II. We sought to identify
possible
explanations for why these patients developed NEC, by comparing them
with 5847 others that did not develop NEC, from the same hospitals
and
of the same gestational ages, cared for during the same 5(1/2)-year
period.Study design:Data were collected from neonates admitted to any
of the Intermountain Healthcare NICUs with a birth date from 1
January
2001 to 30 June 2006, and a gestational age >36 weeks. A variety of
patient features and feeding practices were compared between those
that did vs did not develop NEC.Results:Forty-one neonates >36 weeks
gestation were listed in the discharge records as having NEC of
Bell's
stage II or higher. However, on review of these 41 medical records,
11
were seen to have had NEC of Bell's stage I, whereas the remaining 30
had radiographs and clinical courses indicative of Bell's stage >/
=II.
Those 30 formed the basis of this study. Twenty-eight of the 30
developed NEC after having been admitted to an NICU for some other
reason; the other two developed NEC at home, within 2 days of being
discharged from an NICU. The 30 that developed NEC were more likely
than the 5847 that did not develop NEC, to have congenital heart
disease (P=0.000), polycythemia (P=0.002), early-onset bacterial
sepsis (P=0.004) or hypotension (P=0.017). All 30 received enteral
feedings before NEC developed; 29 were fed either artificial formula
or a mixture of formula and breast milk. The one that was exclusively
fed human milk was fed human milk with added fortifier (24 cal/oz).
The 30 that developed NEC were more likely to be fed formula
exclusively (P=0.000). Seven of the 30 had a laparotomy for NEC; two
of the seven had total bowel necrosis and support was withdrawn. The
other five had perforations and bowel resections. The mortality rate
was 13% (4/30).Conclusions:In our series, NEC among term or near-term
neonates was exclusively a complication developing among patients
already admitted to a NICU for some other reason. We speculate that
the combination of reduced mesenteric perfusion and feeding with
artificial formula were factors predisposing them to develop
NEC.Journal of Perinatology advance online publication, 29 March
2007;
doi:10.1038/sj.jp.7211738.

PMID: 17392837 [PubMed - as supplied by publisher]

Int J Colorectal Dis. 2002 Sep ;17 (5):287-97 12172921 [Cited: 1]
Crohn's disease: in defense of a microvascular aetiology.
[My paper] Michelle Thornton , Michael J Solomon
BACKGROUND AND AIMS: There appears little doubt that microvascular
ischaemia is involved in Crohn's disease. Studies have consistently
demonstrated that the number of blood vessels and the total volume of
blood feeding segments of bowel with Crohn's disease are reduced.
However, the aetiology of the microvascular ischaemia is yet to be
determined. Potential aetiological factors that appear to be disease
specific include increased mesenteric platelet aggregation and
increased platelet surface expression of P-selectin and GP53.
However,
there are several other factors known to be raised in active and
quiescent disease for which disease specificity is not yet known,
including increased submucosal endothelial endothelin-1 receptor
expression, increased m RNA expression for several interleukins and
cytokines including TNFalpha, increased PAF and thrombomodulin and
finally altered cellular adhesion molecule expression.CONCLUSION:
Proving cause and effect will always be a difficult task given the
self-perpetuating nature of the inflammatory and coagulation cascades
and our inability at present to identify persons who subsequently
develop Crohn's disease at a point prior to mucosal inflammation.
Results to date however, are supportive of each of these factors,
alone or in combination playing an integral part in the development
of
microvascular ischaemia, a pathological process which appears to
precede the classic changes which characterize Crohn's disease.
Mesh-terms: Blood Viscosity, physiology; Capillary Permeability,
physiology; Crohn Disease, etiology; Crohn Disease, physiopathology;
Digestive System, blood supply; Digestive System, physiopathology;
Endothelium, Vascular, physiopathology; Human; Ischemia,
complications; Ischemia, physiopathology; Regional Blood Flow,
physiology; Vascular Diseases, complications; Vascular Diseases,
physiopathology;

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High altitude brings .. *increased red blood cell production* ..

High-altitude gastrointestinal bleeding: An observation in Qinghai-
Tibetan railroad construction workers on Mountain Tanggula.
Wu TY, Ding SQ, Liu JL, Jia JH, Dai RC, Zhu DC, Liang BZ, Qi DT, Sun
YF
World J Gastroenterol. 2007 Feb 7; 13(5): 774-80

AIM: To investigate the gastrointestinal bleeding (GIB) in people
from
lowland to high altitude and in workers on Mountain Tanggula and its
causes as well as treatment and prophylaxis. METHODS: From 2001 to
October 2003, we studied GIB in 13502 workers constructing the
railroad on Mountain Tanggula which is 4905 m above the sea level.
The
incidence of GIB in workers at different altitudes was recorded.
Endoscopy was performed when the workers evacuated to Golmud (2808 m)
and Xining (2261 m). The available data on altitude GIB were
analyzed.
RESULTS: The overall incidence of GIB was 0.49% in 13502 workers. The
incidence increased with increasing altitude. The onset of symptoms
in
most patients was within three weeks after arrival at high altitude.
Bleeding manifested as hematemesis, melaena or hematochezia, and
might
be occult. Endoscopic examination showed that the causes of altitude
GIB included hemorrhage gastritis, gastric ulcer, duodenal ulcer, and
gastric erosion. Experimental studies suggested that acute gastric
mucosal lesion (AGML) could be induced by hypoxic and cold stress,
which might be the pathogenesis of altitude GIB. Those who consumed
large amount of alcohol, aspirin or dexamethasone were at a higher
risk of developing GIB. Persons who previously suffered from peptic
ulcer or high-altitude polycythemia were also at risk of developing
GIB. Early diagnosis, evacuation, and treatment led to early
recovery.
CONCLUSION: GIB is a potentially life threatening disease, if it is
not treated promptly and effectively. Early diagnosis, treatment and
evacuation lead to an early recovery. Death due to altitude GIB can
be
avoided if early symptoms and signs are recognized.

Who loves ya.
Tom

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