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PubMed1997

A randomized, double-blind study of the effect of olestra on disease activity in patients with quiescent inflammatory bowel disease. Olestra in IBD Study Group.

PURPOSE: To determine the effects of olestra, a zero-calorie fat substitute that is neither digested nor absorbed, on the well-being and disease state of persons with chronic inflammatory bowel disease (IBD) in remission. PATIENTS AND METHODS: Eighty-nine patients with mild to moderate ulcerative colitis (n = 43) or Crohn's disease (n = 46) in remission, with a history of disease of 2 years or longer, were enrolled in this prospective study from nine private practices, three university-based medical centers, and one Veterans Administration medical center in the United States. Forty-four patients were randomly assigned to receive olestra and 45 to receive triglycerides in chips or cookies daily for 4 weeks. At Week 4, patients were classified as in remission, worsened, or relapsed according to an investigator's global assessment based on sigmoidoscopy (for ulcerative colitis) or the Crohn's disease activity index, laboratory findings, and clinical course. RESULTS: At Week 4, the olestra and triglyceride groups did not differ significantly with respect to the percentages of patients who relapsed (P = 0.494; difference = 2.4%; upper 95% CL = 8.8%) or with respect to the percentages of patients who experienced any worsening of their symptoms (P = 0.630; difference = 0.2%; upper 95% CL = 13.3%). Of evaluable patients, 90% (37 of 41) given olestra remained in remission with no worsening, compared with 90% (38 of 42) given triglycerides. Gastrointestinal symptoms were comparable between the treatment groups, and there were no treatment-related laboratory abnormalities. Six patients were excluded from analysis for reasons unrelated to treatment. CONCLUSION: Olestra did not affect the activity of quiescent mild to moderate IBD.

Abdominal Pain↗
PubMedDate not supplied

Inflammatory bowel disease and endothelin-1: a review.

Inflammatory bowel disease (IBD) appears to be an inappropriate response to an antigen that leads to chronic inflammation rather than repair. This review looks at the role of endothelin-1 (ET-1) as a proinflammatory agent in IBD. ET-1 antagonists in animal models reduce the incidence and severity of IBD. These antagonists may be useful for treatment of IBD in humans.

Animals↗
PubMed2003

Increased tissue protein synthesis during spontaneous inflammatory bowel disease in HLA-B27 rats.

Inflammatory bowel diseases (IBDs) are associated with an increased whole-body protein turnover. In certain drug-induced experimental models of IBD, disturbances of protein synthesis in tissues have been reported recently, but it is unclear if similar disturbances occur in other chronic intestinal diseases. Therefore we investigated changes in protein synthesis in different tissues of HLA-B27 (human leucocyte antigen B27) transgenic rats that develop spontaneously chronic inflammation, with major involvement of the colon. Protein synthesis rate in HLA-B27 rats was shown to be higher in nine different tissues compared with control (Fisher 344) rats. The absolute rate of protein synthesis was highly stimulated at the main inflammatory site (+290% in the colon). However, liver, muscle and skin appeared to be major contributors to the increased protein synthesis observed at the whole-body level. Despite the increased protein synthesis, HLA-B27 rats presented a marked atrophy of muscles, which suggests an increased proteolysis. These results contrast with metabolic disturbances described in acute inflammation and colitis induced by drugs (i.e. dextran sodium sulphate). The present study suggests that the modifications of protein metabolism are strongly influenced by the type of the inflammatory diseases and thus by the underlying mechanisms, which result in different metabolic adaptations and specific nutritional requirements.

Acute Disease↗
PubMed1998

Experimental immunomodulatory therapy of inflammatory bowel disease.

Crohn's disease and ulcerative colitis are chronic inflammatory bowel diseases (IBD) of unknown etiology but demonstrate a rising incidence in many western countries. Although little is known about inflammatory pathomechanisms which are specific to either Crohn's disease or ulcerative colitis, a distinction between both diseases can often be made by typical clinical manifestations, endoscopic appearance or histologic characteristics. The immunology if mucosal inflammation in both diseases is characterized by an overwhelming preponderance of pro-inflammatory cytokine expression with an apparent inability to adequately downregulate immune activation. Moreover, it appears that Crohn's disease does not describe a single clinical entity: The ability to develop certain disease characteristics (e.g. fistula or stenosis formation, respectively) varies between individuals and may be a constant characteristic not being altered in the natural course of disease. From clinical observations it can be therefore concluded that disease subgroups may exist which could be distinctly different in disease pathophysiology and treatment response. With the development of defined immune interventions single steps in the immune cascade can be targeted and evaluated for therapy. Humanized monoclonal antibodies have been engineered which bind with a high affinity to tumor necrosis factor-alpha, a pro-inflammatory cytokine with particular importance in the immunoregulation of inflammation. Although the precise mechanism of action is not completely understood, it appears that a single infusion of this monoclonal antibody (cA2) can induce remission in a high percentage of steroid dependent, chronic active patients with Crohn's disease. The parenteral administration of interleukin-10 (IL-10), a contra-inflammatory cytokine, which downregulates immune activation in most immune and non-immune cells, also induces improvement in this patient group. At present it is still unclear, how interleukin-10 needs to be administered: Studies using intravenous application of IL-10 lead to very promising results, whereas the subcutaneous administration induced a considerable less impressive therapeutic effect. New therapeutic principles are appearing on the horizon, which have not been evaluated in a critical number of patients yet but appear promising because of the concept. One strategy will be the use of anti-sense oligonucleotides. Anti-sense oligonucleotides in the appropriate chemical structure can penetrate cells and neutralize a complementary sense-mRNA of the target molecule. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules (ICAM-1) and pro-inflammatory signaling molecules (i.e. nuclear factor kappa B). The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of inflammatory bowel disease but will also open important new insights into a further understanding of inflammation pathophysiology.

Adjuvants, Immunologic↗
PubMed1973

Nyctohemeral growth hormone levels in children with growth retardation and inflammatory bowel disease.

Short stature is a common complication of inflammatory bowel disease. Recently McCaffery, Nasr, Lawrence, and Kirsner (1970) concluded, from blood growth hormone (GH) levels obtained during insulin-hypoglycaemic provocation, that GH deficiency contributed to the retardation in growth observed in subjects with inflammatory bowel disease. Although it was not possible to eliminate the possibility of partial hypopituitarism, this study does not confirm the existence of GH deficiency in six subjects with short stature complicating inflammatory bowel disease. The nyctohemeral (night and day) serum GH is described, and the insulin and glucose levels in these subjects and normal sleep-related GH rises in all are demonstrated. This finding is not compatible with growth hormone deficiency. In one subject the response to arginine provocation was blunted. Three subjects manifested hyperinsulinism and evidence for ;insulin resistance'. These findings are unexplained but suggest that insulin resistance may contribute to a blunted GH response to insulin-induced hypoglycaemia. Blunted GH response to both arginine and insulin-induced hypoglycaemia may also result from continuous secretion and reduced pituitary storage of growth hormone. This possibility is suggested by the pattern of raised blood GH levels in one of the subjects.

17-Ketosteroids↗
PubMed1993

The lung in inflammatory bowel disease.

Respiratory involvement in patients with inflammatory bowel disease (IBD) has been reported mainly since 1976. This form of involvement should clearly be separated from interstitial lung disease due to sulfasalazine or mesalamine, although the distinction may be difficult in some cases. We report the data of an ongoing Registry containing 33 cases (23 cases receiving no drug therapy) with ulcerative colitis or, less often, Crohn's disease, who developed varied bronchopulmonary problems. In several cases, the exact diagnosis and the relation of the bronchopulmonary disease to IBD had not been established for many years, thus delaying effective treatment with steroids. In most cases (28/33), respiratory involvement followed the onset of IBD (8 of these 28 cases were postcolectomy), and in the remainder, respiratory manifestations predated the IBD. Patterns of involvement included: 1) Airway inflammation, in the form of subglottic stenosis, chronic bronchitis, severe chronic bronchial suppuration, bronchiectasis, and chronic bronchiolitis. In cases with large airway involvement, endoscopy showed exuberant inflammatory tissue in the airways and narrowing of tracheal and/or bronchial lumen. Histologically, airways were heavily infiltrated by a dense aggregate of inflammatory cells, and there were mucosal ulcerations. 2) Varied patterns of interstitial lung disease, mainly bronchiolitis obliterans with organizing pneumonia, and pulmonary infiltrates and eosinophilia. (3) Miscellaneous other forms of involvement including striking neutrophilic necrotic parenchymal nodules (corresponding histologically to sterile aggregates of neutrophils), and serositis. Steroids were very effective in the majority of cases. Inhaled steroids were of durable benefit in patients with chronic bronchitis, but less often so in those with chronic bronchial suppuration, bronchiectasis, or chronic bronchiolitis. Steroids administered orally led to marked improvement in patients with interstitial lung disease and necrotic nodules, but lacked effectiveness in several patients with severe airway inflammation or chronic bronchiolitis. Intravenous steroids were required in the initial management of life-threatening complications such as asphyxiating subglottic stenosis or extensive interstitial lung disease. Bronchial lavages with methylprednisolone were effective in some patients with severe airway inflammation. Patients with IBD can develop varied inflammatory complications in the lung, and a sizable fraction of these complications is steroid-sensitive.

Adolescent↗
PubMed1980

The incidence and prevalence of inflammatory bowel disease in North Tees Health District.

The experience with inflammatory bowel disease in a stable, defined population in northeast England is described. In this population, the incidence of inflammatory bowel disease was higher than expected. In particular, a high incidence of colorectal and anal Crohn's disease was found. The literature is reviewed in order to identify some of the factors responsible for this unusual prevalence of inflammatory bowel disease in the study population. No explanation for our unexpected findings can be advanced.

Adolescent↗
PubMed1990

An epidemiologic study of inflammatory bowel disease in Rochester, New York. Hospital incidence.

The epidemiological understanding of inflammatory bowel disease has been limited by the referral bases of most inflammatory bowel disease studies. The Colitis-Ileitis Study Group of Rochester, N.Y., developed a community-wide, computerized cumulative registry of all inflammatory bowel disease patients hospitalized at the 8 community hospitals for 1973-86. Clinical data were abstracted from each of the 1651 identified hospital charts. All of these patients resided in Monroe County (city and suburbs) and the 5 contiguous counties (Genesee/Finger Lakes Region, population 1,030,640). Of the 1651 hospital patients identified in the study, 1358 resided in Monroe County (Rochester and its immediate suburbs, population 702,238). Incidence, defined as time of onset of symptoms of inflammatory bowel disease, rose from baseline rates in the 1930s to peak in 1980 (Crohn's disease = 50.29/10(5) per decade, ulcerative colitis = 35.12/10(5) per decade) and declined through 1986. For Crohn's disease, the age-specific incidence rates peaked in the 20-29-yr-old group in each of the 5 decades studied. Ulcerative colitis seems to occur at all ages and may have a bimodal distribution. There was a period effect, with the 1970s having the highest incidence of Crohn's disease and ulcerative colitis for each age group. However, the age-specific incidence rate for Crohn's disease showed a 40% decrease in the 1980s compared with the 1970s in the 10-39-yr-old group (p less than 0.001). The age-specific incidence rate for ulcerative colitis showed a 50% decrease in the 1980s compared with the 1970s in the 10-49-yr-old group (p less than 0.001).

Age Factors↗
PubMed1992

Medical treatment of inflammatory bowel disease.

Advances in the drug treatment of inflammatory bowel disease include the development of site-specific delivery systems for 5-aminosalicylate (5-ASA), topically active corticosteroids with minimal systemic bioavailability, and a variety of antagonists to specific inflammatory mediators. These novel therapeutic approaches have emerged from pharmaceutical improvements on traditional drugs and also from an improved understanding of the mucosal immune system and the pathogenesis of inflammatory bowel disease.

Adjuvants, Immunologic↗
PubMed2005

Intraperitoneal cytokine productions and their relationship to peritoneal sepsis and systemic inflammatory markers in patients with inflammatory bowel disease.

PURPOSE: This prospective, blinded study was designed to assess intraperitoneal cytokine productions and their relationship to clinical presentations and systemic inflammatory markers in patients with inflammatory bowel disease. METHODS: Fifty patients who required abdominal surgery for active inflammatory bowel disease (ulcerative colitis, 27; and Crohn's disease, 23) were investigated. Interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha levels in intraperitoneal fluid (obtained by intraoperative lavage) and plasma were measured by enzyme-linked immunosorbent assay. To compare intraperitoneal cytokine productions between diseases with a different degree of inflammation, intraperitoneal cytokine measurement also was performed for patients who required surgery for colorectal cancer (n = 25) and acute appendicitis (n = 25). RESULTS: The median intraperitoneal cytokine (interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha) levels were significantly higher in patients with inflammatory bowel disease than in patients with colorectal cancer and acute appendicitis. In patients with inflammatory bowel disease, intraperitoneal cytokine levels were significantly higher in patients with intraperitoneal sepsis (abscess/fistula) than in patients without intraperitoneal sepsis at laparotomy. Intraperitoneal cytokine levels did not correlate with type of disease (ulcerative colitis/Crohn's disease), age, gender, duration of disease before surgery, preoperative medical treatment, and the extent or site of disease. There were no significant correlations between intraperitoneal cytokine levels and the following systemic inflammatory markers: plasma cytokine levels, white blood cell count, platelet count, erythrocyte sedimentation rate, and C-reactive protein levels. Postoperative intraperitoneal septic complications (anastomotic leak/abscess/enterocutaneous fistula) more frequently occurred in patients with higher intraperitoneal cytokine levels. CONCLUSIONS: Intraperitoneal cytokine productions were greatly elevated in patients with inflammatory bowel disease, and their levels correlated with the presence of intraperitoneal sepsis at laparotomy and development of postoperative intraperitoneal septic complications. Intraperitoneal cytokine levels showed no correlations with systemic inflammatory markers.

Adult↗
PubMed2006

Anti-calreticulin antibodies in patients with inflammatory bowel disease.

PURPOSE: Although the pathogenesis of inflammatory bowel disease (IBD) is unclear, autoimmune processes seem to play roles in IBD because several types of autoantibodies have been found in it. Calreticulin (CRT) is a soluble Ca2+ binding protein which is present in a wide variety of cells. CRT is localized mainly in the endoplasmic reticulum and is often a target for autoantibodies. The aim of this study was to evaluate the clinical significance of anti-CRT antibodies measured by enzyme-linked immunosorbent assay (ELISA) using the sera of patients with ulcerative colitis (UC) and Crohn's disease (CD). METHODS: We measured the serum anti-CRT antibodies of 31 Japanese patients with UC and 24 with CD by ELISA. The controls were 105 subjects: 30 healthy persons, 44 patients with primary biliary cirrhosis (PBC), 21 with systemic lupus erythematosus (SLE) and 10 with acute colitis (AC). RESULTS: The mean titer of anti-CRT antibodies was significantly higher in patients with UC than in healthy individuals (p <0.05). The prevalence of anti-CRT antibodies in these patients was significantly higher during the initial phase than during the passing phase (p <0.05). In patients with CD, the mean titer of anti-CRT antibodies was not significantly higher than in healthy individuals. The positivity for anti-CRT antibodies, however, was about 30% in those patients, which was as high as in patients with UC, SLE and PBC. In patients with AC, anti-CRT antibodies were all negative. CONCLUSIONS: The positivity of anti-CRT antibodies may have a diagnostic value for IBD, especially in the initial phase of UC.

Adolescent↗
PubMed2000

Instruments for quality of life assessment in patients with inflammatory bowel disease.

BACKGROUND: Health-Related Quality of Life is an important measure of illness perception on the part of the patient. In this review, the current status of the Health-Related Quality of Life assessment in studies concerning inflammatory bowel disease is examined and the various instruments proposed for this purpose are considered and compared. METHODS: A search was made of the Medline database, for relevant articles since 1980. Standard criteria were used for including studies for further evaluation. RESULTS: All studies on measuring Health-Related Quality of Life in inflammatory bowel disease patients conclude that the instruments used were valid and reliable assessment tools. Valid instruments that have been proposed for the assessment of health-related quality of life are: the Inflammatory Bowel Disease Questionnaire, the Rating Form of Inflammatory Bowel Disease Patient Concerns, an Inflammatory Bowel Disease-specific questionnaire developed in Cleveland, the Ulcerative colitis and Crohn's disease Health Status Scales and a Disease-specific questionnaire developed in the University of Padova. CONCLUSIONS: Assessing health-related quality of life in inflammatory bowel disease patients is an ever-expanding practice, especially in clinical trials. The instruments that, currently, satisfy most demands for simplicity and validity are the Inflammatory Bowel Disease Questionnaire, reflecting primarily disease activity, and the Rating Form of Inflammatory Bowel Disease Patient Concerns which corresponds more to the psychological and social aspects of inflammatory bowel disease from the patient's point of view.

Health Status Indicators↗
PubMed2005

Defense mechanisms in inflammatory bowel disease.

BACKGROUND: Although psychiatric disturbances and personality features are possibly involved in inflammatory bowel disease, little attention has been given to the potential role of defense mechanisms in the formation, course, or prognosis of the disease. The purpose of the present study was to determine whether certain defense styles and ego mechanisms of defense are associated with inflammatory bowel disease, including both ulcerative colitis and Crohn's disease. METHODS: Seventy-six consecutive unselected outpatients participated in the study. The sample consisted of 39 patients with Crohn's disease, 33 with ulcerative colitis, and 4 with an intermediate form of inflammatory bowel disease. The Symptom Distress Checklist (SCL-90-R), Defense Style Questionnaire (DSQ), and Hostility and Direction of Hostility Questionnaire (HDHQ) were used. RESULTS: Crohn's disease patients presented a more immature defensive profile than ulcerative colitis patients, using a "maladaptive action" style, as well as "consumption" and "pseudo-altruism" defense mechanisms more often. These differences were statistically significant and they were independent of age, sex, educational level, disease extension, and pharmacologic treatment. A significant positive correlation was also found between disease activity and defensive profiles in both ulcerative colitis and Crohn's disease patients. In contrast, there was no statistically significant difference between ulcerative colitis and Crohn's disease patients in terms of psychiatric symptoms. CONCLUSIONS: Crohn's disease patients presented a different and more immature defensive profile than patients with ulcerative colitis. In addition, the more psychologically mature inflammatory bowel disease patients had lower rates of relapses and surgical operations, providing evidence that these aspects of personality are likely to influence the patients' adaptation to the disease.

Adolescent↗
PubMed1997

Inflammatory bowel disease and osteoporosis.

The relation between inflammatory bowel disease (IBD) and osteoporosis has received increasing attention during the past decade. The prevalence of low bone mass in patients with IBD has been reported to be more than 50%. The development of a quick non-invasive method to diagnose osteoporosis (dual-energy X-ray absorptiometry) provides a practical tool to identify the patient who needs special attention. The aetiology of the bone disease in patients with IBD has still not been elucidated, but corticosteroids may play a major role. Studies on the prevention/treatment of IBD-related osteoporosis are scarce. In a single uncontrolled study hormone replacement therapy proved effective in preventing bone loss in peri- and post-menopausal women with IBD. A placebo-controlled study showed that supplementation with calcium and vitamin D prevents bone loss in patients with Crohn's disease. The present paper reviews our current knowledge on the mechanisms and epidemiology of IBD-related bone disease.

Bone Density↗
PubMed2004

The histological diagnosis of dysplastic and neoplastic lesions in inflammatory bowel disease: a pathological perspective.

Patients with inflammatory bowel disease (IBD), both ulcerative colitis (UC) and Crohn's disease (CD), are at an increased risk for developing colorectal carcinoma (CRC). The accurate diagnosis of dysplasia in biopsies taken during periodic surveillance of long-standing IBD patients is most important in prevention of UC and CD related cancer. Distinction of low from high grade IBD-related dysplasia and differential diagnosis between IBD-related dysplasia and dysplasia in sporadic adenoma as well as distinction from pseudodysplastic lesions in inflammatory pseudopolyps or reparative lesions is often very subtle and difficult and demands expertise of second experienced gastrointestinal pathologist. Although surveillance colonoscopy with multiple biopsies does not reduce the cancer mortality, it offers a reasonable chance of detecting precancer and performed prophylactic colectomy. Novel methods of detecting dysplasia are continuously being evaluated, including chromoscopy and molecular biology markers. In the future, one may expect, from these new markers to detect the dysplasia in IBD patients before development of histological evidence of neoplastic changes.

Colon↗
PubMed2000

Inflammatory bowel disease.

Till about 3 decades ago, inflammatory bowel disease (IBD) was considered as non-existent in our country. However, since that time several reports of IBD, mainly ulcerative colitis have been published. More recently, Crohn's disease is also being reported from the country. This trend of UC appearing first in a population followed by CD also appears to be true in other developing nations. A substantial increase in the rates of CD over UC in the last few decades is reported from developed nations as well. Of the other epidemiological factors, an increased risk of CD and lower risk of UC in smokers is established in adults. However, it appears that smoking increases the risk of IBD in children. The etiology of IBD remains elusive. Within the triad of genetics, immunity and antigen responsible for the development of IBD, maximum advances have been made in the field of immune aberrations and this is being exploited to treat the disease. It is well established that IBD results from a disordered immune system in the gut, in response to an unidentified antigen in a predisposed individual. The immune response is enhanced and revolves around antigen-presenting cells, CD 4 T-lymphocytes and tumor necrosis factor alpha. CD results from an enhanced Th1 activity. The pathogenesis of UC is less clear but appears to be humoral. Advances in diagnostics include the availability of serology, ultrasound and nuclear scans, none of which have been tried in our setting where infectious diseases and tuberculosis is rampant. Growth failure and the importance of nutrition in IBD, especially CD, cannot be underemphasized. In many situations nutritional interventions have been used solely as a form of therapy for CD. Newer steroid molecules with minimal systemic effects are also being considered. Other treatment options highlighted are the use of immunosuppressive agents, biologic agents and role of surgery.

Adult↗
PubMed1995

Circulating soluble adhesion molecules in inflammatory bowel disease.

OBJECTIVE: To determine levels of soluble forms of the cell adhesion molecules (CAM), ICAM-1, E-Selectin and VCAM-1 in relation to prevalence, treatment and disease activity in inflammatory bowel disease. PATIENTS AND METHODS: Plasma was obtained from patients with ulcerative colitis (n = 49), patients with ulcerative colitis who had undergone restorative proctocolectomy (n = 32, eight of whom had a clinical pouchitis), Crohn's disease patients (n = 34) and 24 healthy controls. RESULTS: Plasma soluble ICAM-1 levels [medians (ranges in ng/ml)] were significantly higher in patients with active ulcerative colitis [270 (90-510)], pouchitis [415 (310-670)] and active Crohn's disease [305 (200-630)] than in those with inactive ulcerative colitis [225 (140-425), P = 0.031], non-inflamed ileoanal pouch [260 (140-380), P = 0.0004] and inactive Crohn's disease [245 (90-520), P = 0.045], respectively, and controls. The soluble E-Selectin levels were also significantly higher in patients with active ulcerative colitis [55 (40-140)], pouchitis [90 (45-145)], and active Crohn's disease [78 (30-115)] than in those with inactive ulcerative colitis [45 (20-80, P = 0.003], non-inflamed ileoanal pouch [45 (20-90), P = 0.001] and inactive Crohn's disease [48 (25-90, P = 0.020], respectively, and controls. CONCLUSIONS: The present study suggests that increased levels of soluble ICAM-1 and soluble E-Selectin occur during active inflammatory bowel disease and pouchitis, which may be used as sensitive markers of continuing inflammation.

Adult↗
PubMed2001

Iron and inflammatory bowel disease.

Both anaemia of iron deficiency and anaemia of chronic disease are frequently encountered in inflammatory bowel disease. Anaemia of iron deficiency is mostly due to inadequate intake or loss of iron. Anaemia of chronic disease probably results from decreased erythropoiesis, secondary to increased levels of proinflammatory cytokines, reactive oxygen metabolites and nitric oxide. Assessment of the iron status in a condition associated with inflammation, such as inflammatory bowel disease, is difficult. The combination of serum transferrin receptor with ferritin concentrations, however, allows a reliable assessment of the iron deficit. The best treatment for anaemia of chronic disease is the cure of the underlying disease. Erythropoietin reportedly may increase haemoglobin levels in some of these patients. The anaemia of iron deficiency is usually treated with oral iron supplements. Iron supplementation may lead to an increased inflammatory activity through the generation of reactive oxygen species. To date, data from studies in animal models of inflammatory bowel disease support the theoretical disadvantage of iron supplementation in this respect. The results, however, cannot easily be extrapolated to the human situation, because the amount of supplemented iron in these experiments was much higher than the dose used in patients with iron deficiency.

Administration, Oral↗