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Relapsing clostridium difficile enterocolitis cured
by rectal infusion
Schwan A.; Sjolin S.; Trottestam U.; Aronsson B.
Institute of Clinical Bacteriology, S-75122 Uppsala
Sweden
Scand. J. Infect. Dis. (Sweden), 1984, 16/2
(211-215
Repeated recurrence of Clostridium difficile-associated
enterocolitis is uncommon but troublesome for the afflicted
patient. The patient described here received vancomycin
treatment several times but always had a relapse of C.
difficile enterocolitis 2-3 weeks after discontinuation of
treatment. She did not form serum antibodies to C. difficile
cytotoxin (toxin B). Rectal infusion of enemas prepared from
fresh faeces resulted in final cure.
Antibiotics and intestinal flora
Reichlin B.; Gyr K.
Abt. Gastroenterol., Dept. Inn. Med., Univ. Basel
Switzerland
Ther. Umsch. (Switzerland), 1980, 37/3 (194-197)
There are many interactions between antibiotics and the
intestinal microflora. The purpose of this review is to focus
above all on four such interactions with some clinical
importance: General side-effects of antibiotics on the
gastrointestinal tract are described briefly, problems of
antibiotic resistance in intestinal bacteria and the new
understanding of pseudomembranous colitis are explained in
more detail. Finally some aspects of colonisation of the
gastrointestinal tract with Lactobacillus acidus are
discussed.
Altered bone metabolism in inflammatory bowel
disease
Bischoff S.C.; Herrmann A.; Goke M.; Manns M.P.; Von Zur
Muhlen A.; Brabant G.
Dr. S.C. Bischoff, Dept. of Gastroenterology/Hepatology,
Medical School of Hannover, D-30623 Hannover Germany
American Journal of Gastroenterology (USA), 1997, 92/7
(1157-1163)
A reduced bone mineral density has been reported in
inflammatory bowel disease (IBD).
Objective: To assess the mechanisms of bone disease in
IBD.
Methods: We studied in 90 patients (61 with Crohn's
disease, 22 with ulcerative colitis, 7 with indeterminate
colitis) biochemical markers of bone metabolism in serum and
bone mineral density by peripheral quantitative computed
tomography at the forearm.
Results: Forty-five percent of the patients had a reduced
bone density (Z score < -1). Serum calcium was normal in
most patients, vitamin D deficiency was documented in 17%.
Osteocalcin, a serum marker of bone formation, was decreased
in 26% (1.2 plus or minus 0.1 ng/ml), whereas the
carboxyterminal cross-linked telopeptide of type I collagen
(ICTP), a recently described serum parameter of bone
breakdown, was stimulated in 38% (10.4 plus or minus 2.3
microg/L). Of 33 patients with increased ICTP levels, 19
showed a decreased bone density (Z score < -1), and 2 of
them never received steroids. An active status of the
underlying disease in most patients with increased ICTP levels
suggests a direct effect of the underlying IBD. In the whole
series of patients with a history of active disease (n = 34),
47% had signs of an increased bone degradation (ICTP > 5
microg/L; mean, 12.9 plus or minus 4.7 microg/L). Data derived
from a retrospective survey of 245 patients with IBD suggest
that the prevalence of bone fractures in IBD is unexpectedly
high, particularly in patients with a long duration of
disease, frequent active phases, and high cumulative doses of
corticosteroid intake.
Conclusions: Several mechanisms may be involved in
IBD-associated bone disease: (1) a high inflammatory activity
directly induces bone degradation via yet unknown pathways,
(2) treatment with corticosteroids may exert catabolic effects
on the bone, or (3) malabsorption and vitamin D deficiency may
activate bone turnover.
The major complications of coeliac disease
Wright D.H.
University Department of Pathology, Southampton General
Hospital, Tremona Road, Southampton SO16 6YD United
Kingdom
Bailliere's Clinical Gastroenterology (United Kingdom), 1995,
9/2 (351-369)
Neoplasms constitute the major complication of coeliac
disease, and high-grade T-cell lymphoma of the small intestine
(enteropathy-associated T-cell lymphoma) is the most common
neoplasm in this category. HLA genotyping indicates that in
patients with enteropathy-associated T-cell lymphoma have the
coeliac disease associated DQA1*0501, DQB1*0201 phenotype,
although additional HLA-DR/DQ alleles may represent risk
factors for lymphoma development. Molecular biological and
immunohistochemical studies have shown that the intestinal
mucosa distant from the tumour contains clonal populations of
small T cells, often of tile same clone as the high-grade
T-cell lymphoma. These findings suggest that
enteropathy-associated T-cell lymphoma arises in the setting
of coeliac disease and evolves from reactive intraepithelial
lymphocytes through a low-grade lymphocytic neoplasm to a
high-grade tumour, which is usually the cause of the
presenting symptoms. Most cases of chronic ulcerative
enteropathy (ulcerative jejunitis) are probably part of the
same disease process. If the ulceration occurs at a time when
the neoplastic T-cells are of a low grade, morphological
recognition of tumour cells in the ulcers may be impossible.
Carcinoma of the pharynx and oesophagus, and adenocarcinoma of
the small intestine, are increased in frequency in patients
with coeliac disease. The increased risk of carcinoma of the
oesophagus may be related to vitamin A deficiency. A number of
reports have indicated an increased prevalence of various
types of chronic hepatitis in patients with coeliac disease,
but no coherent view of the cause of this association has
emerged. Similarly, patients with coeliac disease have been
reported to have various forms of fibrosing lung disease of
uncertain causation. In recent years, there have been several
reports, mainly from Italy, of a syndrome of epilepsy and
bilateral brain calcification occurring in coeliac patients.
The pathogenesis of this condition is not known and its
prevalence in other communities is uncertain. Splenic atrophy
occurs frequently in patients with coeliac disease and is
related to the severity of the disease and degree of dietary
control. Splenic atrophy predisposes to infection with
capsulated bacteria, although mortality studies indicate that
infection with these organisms is not a major cause of death
in patients with coeliac disease.
Osteoporosis, corticosteroids and inflammatory
bowel disease
Compston J.E.
Department of Medicine, Addenbrooke's Hospital, Cambridge CB2
2QQ United Kingdom
Alimentary Pharmacology and Therapeutics (United Kingdom),
1995, 9/3 (237-250)
Osteoporosis is a serious complication of inflammatory
bowel disease which has not received adequate recognition
despite its high prevalence and potentially devastating
clinical effects. Its pathogenesis remains poorly defined
although corticosteroid therapy and sex hormone deficiency are
likely to play a major role. Recent advances in the diagnosis
and management of osteoporosis have facilitated early
detection of bone loss and identified means by which this may
be prevented. Bone density measurements to predict fracture
risk and define thresholds for prevention and treatment should
be performed routinely in patients with inflammatory disease.
Hormone replacement therapy is effective in prevention of bone
loss in peri- and post-menopausal patients, but the treatment
of younger women and men of all ages requires further
study.
Bone mineral density and calcium regulating
hormones in patients with inflammatory bowel disease (Crohn's
disease and ulcerative colitis)
Scharla S.H.; Minne H.W.; Lempert U.G.; Leidig G.; Hauber M.;
Raedsch R.; Ziegler R.
Innere Medizin I, Universitatsklinik Heidelberg, Bergheimer
Strasse 58, D-69115 Heidelberg Germany
Exp. Clin. Endocrinol. (Germany), 1994, 102/1
(44-49)
Inflammatory bowel disease (Crohn's disease and ulcerative
colitis) is associated with decreased bone mineral density and
increased risk of osteoporosis. However, the pathogenesis of
this bone loss is not yet fully understood. In the present
study we measured lumbar bone mineral density (by dual photon
absorptiometry), serum levels of parathyroid hormone (PTH) and
vitamin D metabolites, and serum markers of bone turnover
(alkaline phosphatase and osteocalcin) in 15 patients with
Crohn's disease and in 4 patients with ulcerative colitis. The
median duration of the disease was 4 years and the median
lifetime steroid dose was 10g of prednisone. We compared our
results to a control group of 19 normal persons, who were
matched for age and sex to the patients. We found that lumbar
bone density was reduced by 11% in patients compared with
control persons (Z-score -0.6 plus or minus 0.6 versus -0.1
plus or minus 0.8: p < 0.05). In patients, the serum levels
of PTH, 25-hydroxyvitamin D3, and calcitriol (1.25(OH)2D3)
were significantly reduced compared with control persons.
Serum alkaline phosphatase activity (AP) was significantly
higher in the patients and was inversely related to lumbar
bone density. Osteocalcin values were not different between
patients and control persons. There was also no difference in
serum levels of calcium between the two groups, whereas
phosphorus levels were higher in patients. We conclude that
malabsorption of calcium was not a primary cause of bone loss
in our patients, because we did not find secondary
hyperparathyroidism. Accordingly, we did not find a severe
vitamin D deficiency, since 25-hydroxyvitamin D3 levels were
within the normal range. Therefore, our results favor the
hypothesis that glucocorticoid therapy and/or the inflammatory
process itself caused changes in bone metabolism leading to a
negative bone balance with secondary reduction of PTH and
calcitriol levels.
Gastrointestinal infections in children
Gracey M.
Aboriginal Health Unit, Health Dept of Western Australia, 189
Royal Street, East Perth, WA 6004 Australia
Curr. Opin. Gastroenterol. (United Kingdom), 1994, 10/1
(88-97)
Gastrointestinal infections are common and important in
infants and young children, particularly where poor hygiene
and living conditions allow the spread of infectious agents.
With increasing information about microorganisms that cause
these infections and improved methods to detect them, many
episodes that were once undiagnosed can now be attributed to
previously unrecognized viruses, bacteria, and other
pathogens. These advances facilitate better management and
will permit more effective control and preventive strategies.
This review highlights some recent reports about
enterovirulent classes of Escherichia coli, including E. coli
O157:H7, which causes the hemolytic-uremic syndrome and
hemorrhagic colitis; Campylobacter species and a new
Campylobacter-like organism (Arcobacterbutzlerlli Helicobacter
pylori; Aeromonas species; and rotavirus. Important new
information about intestinal parasites, including Giardia and
Cryptosporidium, has emerged that should prove of practical
use in diagnosis and management in places where these
parasites are prevalent in children, particularly in parts of
the world where HIV infection has become established. A newly
described organism, so far called coccidian-like or
cyanobacterium-like body, has been found in patients with
prolonged diarrhea (including travelers and expatriate
residents) in several countries; the name Cyclospora
cayetanensis has been proposed for this organism. This year's
review concludes with a short commentary on some recent
reports about risk factors that predispose children to
gastrointestinal infections, eg, nutritional status, domestic
hygiene, maternal hygiene behavior, and young children
gathered in communal facilities like day care centers. Immune
function status is also important, and deficiencies of single
nutrients such as vitamin A, pyridoxine, folic acid, iron, and
zinc may also play a role.
Medical management of severe inflammatory disease
of the rectum: Nutritional aspects
Silk D.B.A.
United Kingdom
Bailliere's Clin. Gastroenterol. (United Kingdom), 1992, 6/1
(27-41)
It is clear that the nutritional state of patients with
inflammatory bowel disease is often impaired and can be
improved by the provision of nutritional support. Improvement
in nutritional status can be achieved as effectively with
enteral as with parenteral nutrition. Nutritional support
appears to have no primary therapeutic effect in patients with
ulcerative colitis. With regard to nutritional support in
Crohn's disease, parenteral nutrition should be restricted to
use as supportive rather than primary therapy. Available
information now seems to suggest that most of the benefits of
parenteral nutrition in Crohn's disease are related to an
improvement in nutritional state rather than as primary
therapy, and its use should be restricted to the treatment of
specific complications of Crohn's disease, such as intestinal
obstruction related to stricture formation or short bowel
syndrome following repeated resection. Although some doubt
exists over the efficacy of oligopeptide-containing elemental
and polymeric enteral diets, the present evidence indicates
that chemically defined free amino acid-containing elemental
diets have primary therapeutic efficacy in the management of
acute exacerbations of Crohn's disease. As such, these diets
are worthy of therapeutic trial in patients with severe
Crohn's disease involving the distal colon and rectum,
particularly in those patients who are malnourished and who
prove to be resistant to treatment with a combination of
topical corticosteroids and S-aminosalicylic acid-containing
compounds. Clinicians should be aware, though, that the
beneficial effects are likely to be restricted to the short
term, with high relapse rates by 1 year, this being
particularly so in patients with distal Crohn's proctocolitis
(Teahon et al, 1988). Volatile fatty acid enemas clearly have
potential in the management of patients with severe
steroid-resistant proctitis. Finally, one of the most
important observations made in recent years is the one
concerning the large losses of nitrogen that will occur in
patients with inflammatory bowel disease treated with
corticosteroids in the absence of adequate protein intake
(O'Keefe et al, 1989). Hopefully the days of treating patients
with severe inflammatory bowel disease with high dose
corticosteroids and a peripheral dextrose or dextrose-saline
drip have passed into history.
Metabolism of vitamin A in inflammatory bowel
disease
Janczewska I.; Bartnik W.; Butruk E.; Tomecki R.; Kazik E.;
Ostrowski J.
Department of Gastroenterology, Goszczynskiego 1, P-02-616
Warsaw Poland
Hepato-Gastroenterology (Germany), 1991, 38/5
(391-395)
The aim of this study was to determine serum retinol levels
in patients with inflammatory bowel disease and to attempt to
elucidate the mechanism of changes in vitamin A metabolism in
these disorders. It was found that in 15 patients with active
ulcerative colitis, 14 patients with active Crohn's disease
and in 3 operated patients with recurrent Crohn's disease
serum retinol levels and retinol-binding protein were
significantly lower than in controls. Concentrations of
vitamin A did not depend on the localization of inflammatory
bowel disease, previous ileal resections, duration of the
disease or age and sex of the patients. During successful
treatment of active ulcerative colitis normalization of serum
retinol levels without substitution of vitamin A was observed.
Repeated determinations in patients with Crohn's disease who
had low serum retinol levels in an active phase of disease
revealed normal vitamin A levels in an inactive phase. The
absorption of vitamins A and E in patients with inflammatory
bowel disease was normal. The normal serum retinol
concentrations in patients with diarrhea due to irritable
bowel syndrome, and in those with anorexia nervosa exclude the
influence of diarrhea and body weight itself on vitamin A
levels. The results of this study indicate that serum retinol
levels in patients with active inflammatory bowel disease are
secondary to the decreased serum retinol-binding protein
concentrations, and probably depend on the increased protein
catabolism in these disorders.
Neurologic manifestations of gastrointestinal
disease
Albers J.W.; Nostrant T.T.; Riggs J.E.
Neuromuscular Section, Department of Neurology, University of
Michigan Medical Center, Ann Arbor, MI 48109-0032 USA
Neurol. Clin. (USA), 1989, 7/3 (525-548)
The neurologic manifestations of gastrointestinal disease
are generally thought to be uncommon, although an increasing
number of previously unidentified associations are being
established. These neurologic disorders may result from
nutritional or non-nutritional causes. In the absence of clear
malnutrition, it is likely that many of these disorders are
underdiagnosed. As an example, Wernicke's encephalopathy is
found at autopsy in as many as 2 per cent of brains, a very
high percentage, given the rare recognition during life. The
likely underdiagnosis of nutritional neurologic disorders is
unfortunate because many are treatable and, more importantly,
are preventable if malabsorption is suspected and appropriate
supplementation initiated. For the neurologist, familiarity
with the occasional association between neurologic
abnormalities and specific gastrointestinal disorders is
important, as is familiarity with the neurologic
characteristics of disorders, such as Whipple's disease, that
may present as isolated neurologic syndromes without
gastrointestinal symptoms or signs. Renewed interest in
selective deficiency states has resulted in identification of
causative factors in several neurologic syndromes of
previously presumed degenerative etiology. Recognition of the
potential neurologic consequences of prolonged deficiency
states also is important for the internist, because many of
the syndromes are poorly reversible once symptomatic. The
benefits of prevention invariably exceed those of
treatment.
Vitamin status in patients with inflammatory bowel
disease
Fernandez-Banares F.; Abad-Lacruz A.; Xiol X.; Gine J.J.;
Dolz C.; Cabre E.; Esteve M.; Gonzalez-Huix F.; Gassull
M.A.
Department of Gastroenterology, Hospital de Bellvitge
'Princeps d'Espanya', Barcelona Spain
Am. J. Gastroenterol. (USA), 1989, 84/7
(744-748)
The status of water- and fat-soluble vitamins was
prospectively evaluated in 23 patients (13 men, 10 women, mean
age 33 plus or minus 3 yr) admitted to the hospital with acute
or subacute attacks of inflammatory bowel disease.
Protein-energy status was also assessed by means of
simultaneous measurement of triceps skin-fold thickness,
mid-arm muscle circumference, and serum albumin. Fifteen
patients (group A) had extensive acute colitis (ulcerative or
Crohn's colitis), and eight cases (group B) had small bowel or
ileocecal Crohn's disease. Eighty-nine healthy subjects (36
men, 53 women, mean age 34 plus or minus 2 yr) acted as
controls. In both groups of patients, the levels of biotin,
folate, beta-carotene, and vitamins A, C, and B1 were
significantly lower than in controls (p < 0.05). Plasma
levels of vitamin B12 were decreased only in group B (p <
0.01), whereas riboflavin was lower in group A (p < 0.01).
The percentage of patients at risk of developing
hypovitaminosis was 40% or higher for vitamin A,
beta-carotene, folate, biotin, vitamin C, and thiamin in both
groups of patients. Although some subjects had extremely low
vitamin values, in no case were clinical symptoms of vitamin
deficiency observed. Only a weak correlation was found between
protein-energy nutritional parameters and vitamin values,
probably due to the small size of the sample studied. The
pathophysiological and clinical implications of the suboptimal
vitamin status observed in acute inflammatory bowel disease
are unknown. Further studies on long-term vitamin status and
clinical outcome in these patients are necessary.
Wernicke's encehalopathy during total parenteral
nutrition: Observation in one case
Mattioli S.; Miglioli M.; Montagna P.; Lerro M.F.; Pilotti
V.; Gozzetti G.
Istituto di Clinica Chirurgica II, Universita di Bologna,
40138 Bologna Italy
J. Parenter. Enter. Nutr. (USA), 1988, 12/6
(626-627)
A patient operated for toxic megacolon secondary to
ulcerative colitis developed a Wernicke syndrome (thiamine
deficiency) during the postoperative period despite the
administration of the usually recommended doses of vitamin B1
during total parenteral nutrition (TPN) treatment. Vitamin B1
deficiency should be checked in order to evaluate the
patients' nutritional condition before starting TPN,
especially those suffering from severe chronic malnutrition.
Routine administration of vitamin B1 in repletion doses may be
reasonably proposed in order to avoid the development of a
Wemicke syndrome which is potentially lethal in a short time
if not recognized and corrected in time.
Optic neuropathy from thiamine deficiency in a
patient with ulcerative colitis
Van Noort B.A.A.; Bos P.J.M.; Klopping C.; Wilmink J.M.
Department of Ophthalmology, G2N, A.M.C., University of
Amsterdam, 1105 AZ Amsterdam Netherlands
Doc. Ophthalmol. (Netherlands), 1987, 67/1-2
(45-51)
A 35-year-old man with ulcerative colitis who was receiving
parenteral feeding with large amounts of glucose, suddenly
developed severe optic neuropathy and oculomotor palsy. The
visual acuity fell bilaterally to 0. Although it was stated
that thiamine has been regularly suppleted in the preceding
period, high doses of vitamin B1 were given. Visual acuity
promptly returned to 1.0 but large visual field defects
persisted. Later on it appeared that erroneously no vitamin B1
has been given before.
Vitamin D status in Crohn's disease: Association
with nutrition and disease activity
Harries A.D.; Brown R.; Heatley R.V.; et al.
Department of Gastroenterology, University Hospital of Wales,
Cardiff United Kingdom
Gut (England), 1985, 26/11 (1197-1203)
Forty patients with Crohn's disease were divided into
undernourished (18) and well nourished (22) groups depending
on whether their midarm circumference was below or above 90%
of the ideal standard. Plasma 25-(OH)D3 and the dihydroxylated
metabolites, 24,25-(OH)sub 2D3 and 1,25-(OH)sub 2D3 were
measured in the summer. Results were related to clinical and
biochemical parameters and also compared with results from
patients with ulcerative colitis and healthy subjects who
served as controls. Plasma 25-(OH)D3 was reduced in the
undernourished Crohn's group compared with the well nourished
Crohn's group, who did not differ from the controls. Over 50%
of the undernourished Crohn's group had evidence of secondary
hyperparathyroidism and raised alkaline phosphatase
concentrations, although concentrations of 1,25-(OH)sub 2D3
were normal. The low 25-(OH)D3 concentrations related to
disease activity. It is suggested that undernourished Crohn's
patients who have high levels of disease activity are at risk
of vitamin D deficiency, and attempts should be made to
improve their vitamin D nutrition.
Zinc and vitamin A deficiency in patients with
Crohn's disease is correlated with activity but not with
localization or extent of the disease
Schoelmerich J.; Becher M.S.; Hoppe-Seyler P.; et al.
Department of Internal Medicine, University of Freiburg,
Freiburg Germany, West
Hepato-Gastroenterol. (Germany, West), 1985, 32/1
(34-38)
A study of serum zinc and plasma vitamin A concentrations
in 54 patients with Crohn's disease was performed. Compared
with controls the patients had significantly lowered zinc and
vitamin A concentrations. There was a marked correlation
between zinc and vitamin A and the activity of the disease, as
measured by the Crohn's disease activity index, and a weaker
correlation with serum proteins considered to be indicators of
disease activity. No correlation was found to vitamin B12
absorption, to the localization of the disease, or to previous
ileal resection. The results suggest that zinc and vitamin A
deficiency occurs in patients with active Crohn's disease and
is not primarily caused by absorption abnormalities.
Substitution might be helpful or even necessary in patients
with highly active disease.
The prevalence of vitamin K deficiency in chronic
gastrointestinal disorders
Krasinski S.D.; Russell R.M.; Furie B.C.; et al.
USDA Human Nutrition Research Center on Aging at Tufts
University, Boston, MA 02111 USA
Am. J. Clin. Nutr. (USA), 1985, 41/3 (639-643)
Vitamin K deficiency results in the appearance of abnormal
prothrombin, deficient in gamma-carboxyglutamic acid, in the
blood. The presence of abnormal prothrombin can be eliminated
or lowered by the administration of vitamin K. Since the
abnormal prothrombin antigen assay is approximately 1000-fold
more sensitive than the prothrombin time for the diagnosis of
vitamin K deficiency, this assay was used to evaluate patients
with intestinal abnormalities. Vitamin K deficiency was found
in 18 of 58 patients (31%) with chronic gastrointestinal
disease and/or resection. All patients with vitamin K
deficiency had either Crohn's disease involving the ileum or
ulcerative colitis treated with sulfasalazine or antibiotics.
Abnormal prothrombin levels returned toward normal in patients
treated with vitamin K but not in patients who were not
treated with vitamin K. The mean plasma vitamin E level in
patients with vitamin K deficiency was significantly lower
than in vitamin-K sufficient patients (p<0.01). We conclude
that certain chronic forms of gastrointestinal disorders are
associated with vitamin K deficiency.
Vitamin serum levels (Bsub 1sub 2 folic acid,
25-OH-Dsub 3) in Crohn's disease and ulcerative colitis
Dageforde J.; Otte M.; Normann D.; et al.
Klinik fur Innere Medizin der Medizinischen Hochschule
Lubeck, D-2400 Lubeck Germany, West
Arztl. Lab. (Germany, West), 1985, 31/3
(100-102)
Decreased serum levels of 25-OH-vitamin Dsub 3 are a not
uncommon finding in ulcerative colitis and Crohn's disease.
Exogenous factors, in particular a lack exposure, are the main
causes. Vitamin Bsub 1sub 2 levels are only decreased in some
Crohn patients with involvement of the ileum. This is
explainable by malabsorption. Absorption of folic acid is
reduced in both diseases through the interaction with
salazosulfaphyridine. Organic malabsorption probably plays a
minor role. Elimination of the deficiency states be means of
solar irradiation and substitution therapy is necessary.
Sulfasalazine inhibits the absorption of folates in
ulcerative colitis
Dept. Int. Med., Univ. California, Davis, CA 95616 USA
N. Engl. J. Med. (USA), 1981, 305/25 (1513-1517)
Folate deficiency, a common occurrence in patients with
inflammatory bowel disease, has been ascribed in part to the
therapeutic use of sulfasalazine. However, a clear relation
between the use of sulfasalazine (salicylazosulfapyridine) and
the development of folate malabsorption and deficiency has not
been shown. The authors designed studies to evaluate the
relation of the use of sulfasalazine to folate malabsorption
and deficiency in patients with ulcerative colitis. They
compared the incidence of low serum folate levels in patients
who were using sulfasalazine and those who were not. In a
selected group of patients, the intestinal-perfusion method
was used to study the effects of graded concentrations of
sulfasalazine at the site of jejunal hydrolysis and luminal
disappearance of folates. The data indicate that sulfasalazine
inhibits the hydrolysis of polyglutamyl folate and also
decreases the absorption of both polyglutamyl and monoglutamyl
folates.
Clinical-pharmacological aspects, application and
effectiveness of total parenteral nutrition in surgical
patients
Dionigi R.; Guaglio R.; Bonera A.; et al.
Inst. Clin. Surg., Univ. Pavia Italy
Int. J. Clin. Pharmacol. Biopharm. (Germany, West), 1979,
17/3 (107-118)
The term 'total parenteral nutrition' (TPN) refers to the
maintenance of an adequate nutritional status, normal body
weight and positive nitrogen balance solely by intravenous
means. It requires solutions providing calories, amino acids
and other nutrients in amounts much greater than those
indicated for maintenance of normal body weight. Nutrient
solutions have been studied, selected and prepared in our
Hospital Pharmacological Service utilizing a sterile closed
system, which allows large-volume filtering, sterilizing and
bottling devices. For maintenance of weight gain in adults, a
basic formula is employed, which provides 1,100 Kcal/l with
pure crystalline amino acids mixed with 50% anhydrous dextrose
in water in a ratio of 5.8:1 (160 Kcal:1 g nitrogen). Minerals
and vitamins are added to the base solution prior to use and
may be increased or decreased by simple addition or omission
depending on the patient's condition. This paper is based on
192 surgical patients who received TPN and have been followed
in strict cooperation between the Hospital Pharmacological
Service and the Surgical Department. The patients, ranging
from 23 to 79 years of age, with life threatening diseases and
unable to maintain adequate nutrition by the oral route,
received TPN through a central catheter inserted via
subclavian puncture (146 cases) or through a surgically
created internal A-V fistula (46 cases). The condition of the
patients generally improved within a few days after starting
TPN; and weight gain, wound healing general improvement and a
shorter period of hospitalization were observed. TPN could be
efficiently combined with oncologic treatment, and a
significant improvement of the patients' performance status
and decrease of toxic side-effects due to chemotherapeutic
agents were observed. TPN has been successfully applied also
in patients with fistulas of the alimentary tract obtaining
spontaneous closure and in patients with ulcerative colitis,
showing its beneficial effect in allowing complete bowel rest
for healing. No major complications or deaths could be
attributed to TPN or to the route of administration.
Iron deficiency in inflammatory bowel disease.
Diagnostic efficacy of serum ferritin
Thomson A.B.R.; Brust R.; Ali M.A.M.; et al.
Dept. Med., Univ. Alberta, Edmonton Canada
Am. J. Dig. Dis. (USA), 1978, 23/8 (705-709)
The prevalence of iron-deficiency anemia was defined in 105
patients with inflammatory bowel disease and an appraisal made
of the diagnostic value of serum ferritin for the assessment
of iron stores. Iron deficiency, defined by the absence of
bone-marrow hemosiderin was found with anemia in 36% of 41
patients with ulcerative colitis (UC) and 22% of 64 patients
with Crohn's disease (CD). Iron deficiency without impaired
erythropoiesis was detected in an additional 32% of patients
with UC and 2% with CD. Anemia with plentiful bone-marrow iron
was present in 33 (51%) of patients with CD, only one of whom
had vitamin Bsub 1sub 2 deficiency. Red blood cell morphology,
RBC indices, serum iron, and percent transferrin saturation
correlated poorly with stainable marrow iron. Serum ferritin,
assayed in samples from 45 patients, was <18 ng/ml in 4/12
with iron-deficiency anemia and 0/5 with absent marrow iron
and a normal hemoglobin level; values >55 ng/ml were
invariably associated with the presence of marrow hemosiderin.
Based on a lower normal limit of 18ng/ml, the serum ferritin
had an excellent predictive value (100%) but a high predictive
error (32%) in the diagnosis of iron deficiency in
inflammatory bowel disease. Serum ferritin >55 ng/ml ruled
out iron deficiency as the basis for anemia.
Ascorbic acid metabolism in ulcerative colitis of
bacterial origin (Russian)
Husainov O.H.
Kaf. Infekts. Bol., Tadzhik. Medinst., Dushanbe USSR
Zdravookhr.Tadzh. (USSR), 1973, 20/4 (10-12)
Investigation of 39 patients suffering from acute bacterial
dysentery and 25 with an exacerbation of the chronic form
revealed disturbances of the vitamin C metabolism in all
cases, manifested by a low content of the vitamin in the blood
and its low excretion in the urine. The degree of the changes
depended on the clinical manifestations of the disease.
Administration of vitamin C in therapeutic doses corrected the
vitamin deficiency in acute bacterial dysentery. In patients
with exacerbations of chronic dysentery the indices of the
ascorbic acid metabolism failed to reach the normal values,
thereby indicating more prolonged and massive vitamin
therapy.
Selenium supplementation in the diets of patients
suffering from ulcerative colitis
Stedman J.D.; Spyrou N.M.; Millar A.D.; Altaf W.J.; Akanle
O.A.; Rampton D.S.
J.D. Stedman, Department of Physics, University of Surrey,
Guildford, Surrey GU2-5XH United Kingdom
Journal of Radioanalytical and Nuclear Chemistry (Hungary),
1997, 217/2 (189-191)
Ulcerative colitis (UC) is a type of inflammatory bowel
disease (IBD) in which there is recurrent inflammation of the
mucous membranes of the colon. Inflammation is accompanied by
the production of reactive oxygen species (ROS) including,
amongst others, hydrogen peroxide. Selenium in the form of the
selenoprotein glutathione peroxidase (GSH-Px) acts as a
catalyst in the reaction which reduces hydrogen peroxide to
watch. It may therefore beneficial to supplement the diets of
patients who suffer from UC with selenium. In this preliminary
study nine patients suffering from moderate UC were
supplemented with selenium-beta tablets (300 microg Se per
tablet) twice daily. Blood samples were taken at the start of
the trial and at 1, 2 and 4 week intervals. Freeze-dried serum
samples were analysed for their selenium content using the
technique of instrumental neutron activation analysis (INAA).
Samples were also analysed by particle induced X-ray emission
(PIXE) to monitor other trace elements levels. Selenium
concentrations were found to increase during supplementation
and iron concentrations to decrease. Stool frequency was also
found to improve suggesting that ROS may be important in the
pathogenesis of UC.
Nutrition and ulcerative colitis
Burke A.; Lichtenstein G.R.; Rombeau J.L.
Prof. J.L. Rombeau, Department of Surgery, Hospital
University of Pennsylvania, 3400 Spruce Street, Philadelphia,
PA 19104 USA
Bailliere's Clinical Gastroenterology (United Kingdom), 1997,
11/1 (153-174)
The role of diet in the aetiology and pathogenesis of
ulcerative colitis (UC) remains uncertain. Impaired
utilization by colonocytes of butyrate, a product of bacterial
fermentation of dietary carbohydrates escaping digestion, may
be important. Sulphur-fermenting bacteria may be involved in
this impaired utilization. Oxidative stress probably mediates
tissue injury but is probably not of causative importance.
Patients with UC are prone to malnutrition and its detrimental
effects. However, there is no role for total parenteral
nutrition and bowel rest as primary therapy for UC. The
maintenance of adequate nutrition is very important,
particularly in the peri-operative patient. In the absence of
massive bleeding, perforation, toxic megacolon or obstruction,
enteral rather than parenteral nutrition should be the mode of
choice. Nutrients may be beneficial as adjuvant therapy.
Butyrate enemas have improved patients with otherwise
recalcitrant distal colitis in small studies, Non-cellulose
fibre supplements are of benefit in rats with experimental
colitis. Eicosapentaenoic acid in fish oil has a
steroid-sparing effect which, although modest, is important,
particularly in terms of reducing the risk of osteoporosis,
but it seems to have no role in the patient with inactive
disease. gamma-Linolenic acid and anti-oxidants also are
showing promise. Nutrients may also modify the increased risk
of colorectal carcinoma. Oxidative stress can damage tissue
DNA but there are no data published at present on possible
protection from oral anti-oxidants. Butyrate protects against
experimental carcinogenesis in rats with experimental colitis.
Folate supplementation is weakly associated with decreased
incidence of cancer in UC patients when assessed
retrospectively. Vigilance should be maintained for increased
micronutrient requirements and supplements given as
appropriate. Calcium and low-dose vitamin D should be given to
patients on long-term steroids and folate to those on
sulphasalazine.
An enteral formula containing fish oil,
indigestible oligosaccharides, gum arabic and antioxidants
affects plasma and colonic phospholipid fatty acid and
prostaglandin profiles in pigs
Campbell J.M.; Fahey G.C. Jr.; Lichtensteiger C.A.; Demichele
S.J.; Garleb K.A.
G.C. Fahey Jr., Division of Nutritional Sciences, Department
of Animal Sciences, University of Illinois, Urbana, IL 61801
USA
Journal of Nutrition (USA), 1997, 127/1
(137-145)
Evidence supports a pathogenic role of arachidonic
acid-derived inflammatory mediators within the
gastrointestinal tract of patients with inflammatory bowel
disease. The purpose of this study was to assess the effects
of an ulcerative colitis nutritional formula (UCNF) containing
oligosaccharides, fish oil, gum arabic and antioxidants on
plasma and colonic phospholipid fatty acid and prostaglandin
profiles in pigs. Twenty-four growing barrows in two
replications were equally randomized among four killing times
(d 0, 7, 14 and 21), and one of two diets, a control and the
UCNF. Diets contained comparable levels of protein, fat, and
nonstructural carbohydrate and met 100% of the energy
requirements of the pig. Intake and body weight were recorded
daily while blood, urine and tissue samples were collected at
time of kill. Within 1 wk of ingestion of the UCNF, the
composition of plasma phospholipid fatty acids showed an
increase in 20:5(n- 3) and 22:6(n-3) (P < 0.0001) and a
decrease in 20:4(n-6) and 18:2(n-6) (P < 0.0001). Similar
effects were observed for the phospholipids in the colonic and
cecal mucosa. Plasma prostaglandin E was unaffected by
treatment, whereas thromboxane B2 and 6-keto-prostaglandin
F(1alpha) levels were significantly decreased after 7 d of
UCNF ingestion. Ingestion of the UCNF resulted in a
suppression in the synthesis of proinflammatory prostaglandins
by cecal and colonic mucosal cells. Levels of colonic and
cecal prostaglandin E, 6- ketoprostaglandin F(1alpha) and
thromboxane B2 were significantly decreased after 7 d of UCNF
ingestion. These changes may have been mediated by rapid
increases of (n-3) fatty acids into cellular phospholipids.
Dietary supplementation with the UCNF may prove beneficial for
patients with ulcerative colitis by modulating colonic
prostaglandin synthesis.
The effect of folic acid supplementation on the
risk for cancer or dysplasia in ulcerative colitis
Lashner B.A.; Provencher K.S.; Seidner D.L.; Knesebeck A.;
Brzezinski A.
USA
Gastroenterology (USA), 1997, 112/1 (29-32)
Background and Aims: Two case-control studies have shown
that folate may protect against neoplasia in ulcerative
colitis. This historical cohort study was performed to better
define this association. Methods: The records of 98 patients
with ulcerative colitis who had disease proximal to the
splenic flexure for at least 8 years were reviewed. Documented
folate use of at least 6 months was deemed a positive
exposure. Results: Of the patients, 29.6% developed neoplasia
and 40.2% took folate supplements. The adjusted relative risk
(RR) of neoplasia for patients taking folate was 0.72 (95%
confidence interval (CI), 0.28-1.83). The dose of folate
varied with the risk of neoplasia (RR, 0.54 for 1.0 mg folate;
RR, 0.76 for 0.4 mg folate in a multivitamin compared with
patients taking no folate). Folate use also varied with the
degree of dysplasia (RR for cancer, 0.45; RR for high-grade
dysplasia, 0.52; RR for low-grade dysplasia, 0.75 compared
with patients with no dysplasia) (P = 0.08). Conclusions:
Although not statistically significant, the RR for folate
supplementation on the risk of neoplasia is <1 and shows a
dose-response effect, consistent with previous studies. Daily
folate supplementation may protect against the development of
neoplasia in ulcerative colitis.
The value of an elimination diet in the management
of patients with ulcerative colitis
Candy S.; Borok G.; Wright J.P.; Boniface V.; Goodman
R.
Gastro-intestinal Clinic, Department of Medicine, Groote
Schuur Hosp., Univ. Cape Town, Cape Town South Africa
South African Medical Journal (South Africa), 1995, 85/11
(1176-1179)
Debate exists about the role of diet in both the aetiology
and the management of ulcerative colitis. To examine the
latter, a group of patients with documented ulcerative colitis
was studied at the Groote Schuur Hospital Gastro-intestinal
Clinic. A total of 18 subjects, 9 female and 9 male, were
randomised into active or control groups and followed up
weekly for 6 weeks. Subjects in the control group were asked
to document but not alter their intake of food and drink.
Those in the experimental group had their diets systematically
manipulated to exclude foods that appeared to provoke
symptoms. The symptoms, sigmoidoscopy and biopsy findings of
all subjects were compared before and after. 'Remission' was
defined as the passage of normal stools with absence of rectal
bleeding. 'Improvement' was defined as a decrease in the
number of diarrhoeal stools and/or a diminution of rectal
bleeding. At the end of the trial the diet group displayed
significantly fewer symptoms than did the controls (P = 0.009;
Fisher's exact test). Sigmoidoscopic findings improved in 8
subjects in the diet group compared with 2 of the controls.
Histological findings improved in 3 of the diet group as well
as in 3 of the controls. There were no foods that provoked
symptoms in all patients, though spiced and curried foods and
fruits, especially grapes, melon and the citruses, commonly
caused diarrhoea. In only 2 patients were symptoms reproduced
consistently on reintroduction of a particular food, pork in 1
case and yellow cheese in another.
Efficacy of glutamine-enriched enteral nutrition in
an experimental model of mucosal ulcerative colitis
Fujita T.; Sakurai K.
First Department of Surgery, Jikei University School of
Medicine, 3-25-8 Nishishinbashi, Minato-ku, Tokyo 105
Japan
British Journal of Surgery (United Kingdom), 1995, 82/6
(749-751)
Intact intestinal epithelium and associated lymphatic
tissue act as body defences against luminal toxins. This
barrier may become threatened or compromised in inflammatory
bowel disease, leading to an increase in mucosal permeability
and subsequent translocation of endotoxins. The effect of oral
glutamine on gut mucosal ornithine decarboxylase activity and
on endotoxin levels in portal vein blood was studied in a
guinea-pig model of carrageenan- induced colitis. Despite
failure to show induction of ornithine decarboxylase activity
by glutamine administration, the mean endotoxin level of
portal vein blood in guinea-pigs fed a glutamine-enriched
elemental diet was 25.3 pg/ml compared with 71.2 pg/ml in
animals given a standard elemental diet (P<0.01). A
glutamine-enriched elemental diet may be therapeutically
beneficial in patients with inflammatory bowel disease.
Influence of nutrition in ulcerative colitis - The
significance of nutritional care in inflammatory bowel
disease
Nagel E.; Bartels M.; Pichlmayr R.
Klinik fur Abdominal, Transplantationschirurgie,
Konstanty-Gutschow-Stras se 8, D-30625 Hannover Germany
Langenbecks Archiv fur Chirurgie (Germany), 1995, 380/1
(4-11)
Nutritional therapy for ulcerative colitis (UC) is
controversial. Studies are usually designed to investigate
total parenteral (TPN) or total enteral nutrition (TEN), and
before these can be compared it is necessary to differentiate
between the different therapeutic aims. The aims of artificial
nutritional support in patients with UC are the readjustment
of the nutritional status, possible remission of disease
activity, and decrease in the incidence of surgical
intervention or postoperative complication. Owing to the
heterogeneity of the results published so far, it is still
difficult to compare studies. Nevertheless, they indicate that
the extent and severity of the colitis and the patient
selection are of paramount importance in the implementation of
nutritional therapy. Positive effects of TPN reported from
non-controlled studies were not confirmed by controlled
trials. Moreover, TPN was no more effective than an oral diet.
Regarding remission rates or operative interventions needed,
TPN had more side effects than and no defined advantages over
TEN. TEN seems to be useful for certain patients. In some
patients with UC, it seems to be accompanied by fewer
postoperative complications. However, a definitive conclusion
on the effects of TEN or TPN is not yet possible. In this
context, certain fatty acids may have an important role in the
treatment of UC. In prospective, randomized and controlled
studies omega-3 fatty acids were found to be therapeutically
useful. A reduction of the steroid doses needed is
particularly important. Another therapeutic approach in distal
UC is seen in the rectal administration of short chain fatty
acids.
Soy fiber delays disease onset and prolongs
survival in experimental Clostridium difficile
ileocecitis
Frankel W.L.; Choi D.M.; Zhang W.; Roth J.A.; Don S.H.;
Afonso J.J.; Lee F.- H.; Klurfeld D.M.; Rombeau J.L.
Harrison Department of Surgery, University of Pennsylvania
Hospital, 34th and Spruce Street, Philadelphia, PA 19104
USA
J. Parenter. Enter. Nutr. (USA), 1994, 18/1
(55-61)
Clostridium difficile colitis is a disabling complication
in critically ill patients who commonly receive broad-spectrum
antibiotics and liquid diets. To date, there is no
experimental model specifically designed to investigate the
effects of liquid diets on this type of colitis. The addition
of fiber to liquid diets normalizes gut structure and improves
absorptive function in selected conditions of intestinal
dysfunction. The purposes of this study were the following:
(1) to develop a reproducible model to examine the interaction
of acute C difficile-induced colitis and liquid diets, (2) to
determine whether the addition of soy fiber to a liquid diet
improves disease, and (3) to investigate possible mechanisms
of fiber-mediated disease improvement. Syrian hamsters were
pair-fed with either a polymeric liquid diet or the same diet
with 1.4% soy fiber for 10 days. Animals were given either
clindamycin and C difficile (to produce ileocecitis), or
equivalent volumes of saline. Mean survival time and
systematic stool examinations for C difficile toxin
positivity, liquidity, and percent water were performed to
determine the effect of soy fiber on disease. Survival time
was prolonged by 34% (p < .05), and C difficile toxin
positivity and stool liquidity were significantly reduced (p
< .05) with fiber. Additional animals were studied to
determine possible mechanisms for improved survival in
fiber-supplemented animals. Cecal histology, colonic water
absorption, cecal microflora, and gastric to anus transit time
were measured in these animals. Colonic water absorption and
gastric to anus transit time were significantly increased (p
< .05) and decreased (p < .05) with fiber, respectively.
A hamster model of C difficile ileocecitis has been designed
to investigate the effects of liquid diets. Fiber
supplementation prolongs survival in this model due in part to
a delay in onset of C difficile infection and improved colonic
water absorption.
Influence of intravenous n-3 lipid supplementation
on fatty acid profiles and lipid mediator generation in a
patient with severe ulcerative colitis
Grimminger F.; Fuhrer D.; Papavassilis C.; Schlotzer E.;
Mayer K.; Heuer K.-U.; Kiss L.; Walmrath D.; Piberhofer S.;
Lubbecke F.; Kramer H.-J.; Stevens J.; Schutterle G.; Seeger
W.
Department of Internal Medicine, Justus-Liebig-University,
Klinikstrasse 36, D-6300 Giessen Germany
Eur. J. Clin. Invest. (United Kingdom), 1993, 23/11
(706-715)
N-3 fatty acids were supplied to a 36-year-old female
patient suffering from ulcerative colitis and severe steroid
side-effects, in a sequence of parenteral and enteral
administration. During a moderately active period of disease,
200 ml d-1 fish oil-derived lipid emulsion (eicosapentaenoic
acid (EPA), 4.2 g; docosahexaenoic acid (DHA), 4.2 g) was
infused for 9 days, in parallel with rapid tapering of the
steroid dose. Disease activity declined rapidly, and the
patient was subsequently provided with 16 fish oil capsules
per day (EPA, 2.9 g; DHA, 1.9 g) for 2 months. At the end of
this period of therapy, severe colitis recurred with
intestinal and extraintestinal manifestations. The n-3 lipid
emulsion was then used for intravenous alimentation (29 days,
maximum dose 300 ml per day); during this time, marked
improvement of the inflammatory bowel disease was noted.
During both periods of parenteral n-3 lipid administration,
total plasma EPA and DHA contents increased several-fold,
surpassing that of arachidonic acid; this plasma n-3 fatty
acid enrichment was only maintained to a minor extent during
the intermediate period of dietary fish oil supplementation.
The intravenously administered EPA-containing triglycerides
were rapidly hydrolyzed, as evidenced by the appearance of
substantial quantities of EPA in the plasma free fatty acid
fraction. Platelet and neutrophil total membrane content of
EPA and DHA as well as n-3 fatty acid/AA membrane ratios
similarly increased during the periods of intravenous n-3
lipid administration and declined during oral fish oil uptake.
In contrast, erythrocyte membrane enrichment in EPA and DHA
occurred only after the prolonged (2 month) period of dietary
n-3 lipid supplementation. Ex vivo stimulation of neutrophils
with A23187 showed progressive increase in 5-series
leukotriene- and 5-HEPE-generation during both periods of n-3
lipid infusion, in parallel with the rise of plasma EPA
contents. Maximum 5-series/4-series leukotriene ratios
surpassed 0.25. Similarly, ratios of thromboxane B3/B2
liberated from ex vivo stimulated platelets surpassed 0.4
during ongoing n-3 lipid infusion. The profound changes in
fatty acid profiles and lipid mediator generation may be
related to the reduction in colitis activity observed during
the periods of intravenous n-3 lipid supplementation.
The role of marine fish oils in the treatment of
ulcerative colitis
Ross E.
Department of Internal Medicine, Tufts University School of
Medicine, Boston, MA 02111 USA
Nutr. Rev. (USA), 1993, 51/2 (47-49)
Recent studies suggest that marine fish-oil supplements,
which are rich in n-3 fatty acids, may reduce the inflammation
associated with ulcerative colitis. Fish oils may exert their
beneficial effects by shifting eicosanoid synthesis to less
inflammatory species or by modulating tissue levels of certain
cytokines.
Localized deficiencies of folic acid in
aerodigestive tissues
Heimburger D.C.; Colby F.; Benitez L.; Raiten D.J.;
Butterworth C.E.
Department of Nutrition Sciences, University of Alabama,
Birmingham, AL 35294 USA
Ann. New York Acad. Sci. (USA), 1992, 669/-
(87-96)
The notion that requirements for folic acid may be higher
in some tissues than others, resulting in localized
deficiencies in spite of blood levels in the normal range was
first suggested by the observation of megaloblastic changes in
the cervical epithelium that responded to folate
supplementation. Theoretically, such deficiencies may arise
from elevated folate turnover in response to rapid tissue
proliferation or repair; inactivation or alteration of its
function by external agents such as tobacco, alcohol, or
drugs; or altered metabolism or tissue uptake caused by an
inborn error. Marginal dietary intake could aggravate these
effects on cells at risk. Evidence for the possible existence
of localized folate deficiencies in the aerodigestive tract
includes lower circulating folate levels in smokers as
compared with nonsmokers; yet lower circulating levels in
smokers with bronchial metaplasia; lower folate levels in
scrapings of the buccal mucosa of smokers than non-smokers;
apparent improvement in bronchial atypical metaplasia in
smokers supplemented with folic acid; lower erythrocyte folate
levels and higher prevalence of cellular features compatible
with folate deficiency in geographic areas and individuals in
South Africa at high risk for esophageal cancer; and a trend
toward a lower prevalence of colonic dysplasia in ulcerative
colitis patients who use folic acid supplements. These
observations, as well as animal and in vitro studies, also
suggest that folate deficiency may be co-carcinogenic. Further
research in this area will be aided by the development of
animal models of localized folate deficiency and of
methodologies capable of measuring folate levels in minute
quantities of tissues and exfoliated cells.
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