(1) A reduced bone mineral density has been reported in inflammatory bowel disease (IBD). We studied in 90 patients (61 with Crohn’s disease, 22 with ulcerative colitis, 7 with indeterminate colitis), 45% 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 +/- 0.1 ng/ml). 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.
“Studies have shown that only 15% of patients seeing general doctors, and less than 40% of patients seeing specialists, are receiving any type of preventive therapy for steroid-induced bone loss. Doctors should realize that this is one of the most feared—and predictable—complications of chronic steroid use. We hope that this study and others like it will encourage both patients and physicians to pursue an appropriate course of action.”( SOURCE: The New England Journal of Medicine 1998;339:292-299.)
(2) Deficiencies were found in 85% of patients with Crohn’s disease vs 68% with ulcerative colitis during the course of the disease, predominantly a deficiency of iron and of calcium. Less frequently deficiencies of zinc, protein, cyanocobalamin, and folic acid were found.
(3) Malnutrition is observed frequently and is an important complication in patients with Crohn disease (CD). Serum concentrations of several nutrients (beta-carotene, vitamin C, vitamin E, selenium, and zinc) and activity of the enzyme glutathione peroxidase were also significantly lower in CD patients, as were antioxidant status and serum concentrations of magnesium and vitamin D. Percentage body fat and hamstring muscle strength were significantly lower in male CD patients than in control subjects, whereas muscle strength of the quadriceps was preserved.
(4) . The chief purpose of the gut is to digest and absorb nutrients in order to maintain life. Consequently, chronic gastrointestinal (GI) disease commonly results in malnutrition and increased morbidity and mortality. For example, studies have shown that 50-70% of adult patients with Crohn’s disease were weight-depleted. Weight loss of greater than 30% accompanying a variety of diseases was associated with a reduction in pancreatic enzyme secretion of over 80%, villus atrophy and impaired carbohydrate and fat absorption.
(5) Magnesium deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption.
(6) Patients with Crohn’s disease demonstrated significantly lower muscle
potassium content than did controls. Patients with extensive involvement
of the bowel tended to have lower muscle potassium content. Our results
indicate that potassium depletion is present in nonresected patients
with Crohn’s disease.One mechanism for fatigue may be the disturbance
of the potassium homeostasis.
(7) Hypomagnesemia is a cause of refractory hypocalcemia and
hypokalemia. Magnesium plays a key role in the metabolism of both calcium
and potassium, and must be considered in the evaluation of the hypocalcemic
patient.
(8) Patients with chronic intestinal disorders causing malabsorption,
nutritional losses through diarrhea, or catabolic illness would be expected
to have essential fatty acid (EFA) deficiency (EFAD). Compared with
control subjects, patients had (1) decreased polyunsaturated fatty acid
(PUFA) levels (43.7% v 50.4%, P < .0001), (2) increased monounsaturated
fatty acid (MUFA) levels (25.8% v 22.0%, P < .0001), (3) higher
ratios of mead(20:3 omega 9) to arachidonic (20:4 omega 6) acid (0.020
v 0.013, P < .04), and (4) lower concentrations of total (214
v 284 mg/dL, P < .01), saturated ([SFA] 63 v 75 mg/dL, P < .001),
MUFA (56 v 63 mg/dL, P < .001), and PUFA (93 v 143 mg/dL, P < .001).
Patients had metabolic shifts toward increased production of MUFA and an
increased ratio of derivatives to precursors of omega 6 fatty acids, shifts
that occur when cells are EFA-deficient. More than 25% of the patients
had biochemical evidence of EFAD according to at least one criterion. Patients
with chronic intestinal disease should be evaluated for likely EFA deficiencies
and imbalances, and treated with substantial amounts of supplements
rich in EFAs, such as oral vegetable and fish oils.
References:
1. ALTERED BONE METABOLISM IN INFLAMMATORY BOWEL DISEASE.
Bischoff SC; Herrmann A; Göke M; Manns MP; von zur Mühlen
A; Brabant G; Department of Gastroenterology & Hepatology, Medical
School of Hannover, Germany. Am J Gastroenterol, 1997 Jul, 92:7,
1157-63
2. NUTRITIONAL DEFICIENCIES AND COMPLICATIONS IN CHRONIC IBD Rath HC( herath@t-online.de ); Caesar I; Roth M; Schölmerich J; Klinik und Poliklinik fÂur Innere Medizin I, Klinikum, UniversitÂat Regensburg. Med Klin, 1998 Jan, 93:1, 6-10
3. COMPREHENSIVE NUTRITIONAL STATUS IN PATIENTS WITH LONG-STANDING CROHN DISEASE CURRENTLY IN REMISSION Geerling BJ; Badart Smook A; Stockbrügger RW; Brummer RJ; Department of Gastroenterology, University Hospital Maastricht, The Netherlands. bgee@sint.azm.nl Am J Clin Nutr, 1998 May, 67:5, 919-26
4. NUTRITION AND GASTROINTESTINAL DISEASE.
OKeefe SJ; Gastrointestinal Clinic, Groote Schuur Hospital, South Africa.
Scand J Gastroenterol Suppl, 1996, 220:, 52-9
5. MAGNESIUM AND INFLAMMATORY BOWEL DISEASE. Galland L; Magnesium, 1988, 7:2, 78-83
6. PLASMA AND SKELETAL MUSCLE ELECTROLYTES IN PATIENTS WITH CROHN’S
DISEASE.
Nyhlin H; Dyckner T; Ek B; Wester PO; J Am Coll Nutr, 1985, 4:5,
531-8
7. SYMPTOMATIC HYPOCALCEMIA WITH ORAL CLODRONATE. Johnson MJ; Fallon MT; Palliative Medicine, Huntershill Marie Curie Centre, University of Glasgow, Scotland, U.K. J Pain Symptom Manage, 1998 Feb, 15:2, 140-2
8. PREVALENCE OF ESSENTIAL FATTY ACID DEFICIENCY IN PATIENTS WITH CHRONIC GASTROINTESTINAL DISORDERS. Siguel EN; Lerman RH; Clinical Nutrition Unit, Evans Memorial Department of Clinical Research, Boston University Medical Center Hospital, MA, USA. Metabolism, 1996 Jan, 45:1, 12-23