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PubMed1981

Medication bezoar: intestinal obstruction by an isocal bezoar. Case report and review of the literature.

Medications may occasionally obstruct the gastrointestinal tract by virtue of their physical mass. Obturative obstruction of the alimentary tract is reportedly caused by an increasing number of medications, including hydroscopic bulk laxatives, cholestyramine, nonabsorbable antacids, and vitamin C tablets. Inspissated Isocal tube feedings caused jejunal obstruction in a postoperative patient. Medication bezoars are a rare cause of intestinal obstruction that may result in significant patient morbidity, including bowel necrosis, perforation, and peritonitis. The radiographic appearance may mimic an abdominal abscess.

Adult↗
PubMed1985

Indomethacin-induced intestinal ulcers in rats: effects of salicylazosulfapyridine and dexamethasone.

Characteristics of inflammatory bowel diseases have been hypothesized to resemble those of the syndrome of intestinal ulceration induced in the rat by non-steroidal anti-inflammatory compounds. However, no systematic studies have been undertaken to examine this possibility. Therefore, we have studied the influence of some pharmacological agents, such as steroids and salicylazosulfapyridine (SAS), which are clinically useful in the treatment of inflammatory bowel diseases, and to review published data on other pharmacological approaches commonly used for the therapy of inflammatory bowel diseases that have been shown to counteract indomethacin-induced intestinal toxicity. Orally administered SAS 100 to 800 mg/kg or dexamethasone 0.05 to 0.1 mg/kg exerted dose-related, anti-ulcer activity, with ED50 values and 95% confidence limits of 145 (95-222) mg/kg SAS and 0.184 (0.152-0.224) mg/kg dexamethasone. Other treatments, including cholestyramine, low-residue diets and antibiotics have also been reported to ameliorate clinical and experimental intestinal diseases. The clinical significance of present findings has been discussed.

Animals↗
PubMed1975

Effect of dietary fibre on gallstone formation in hamsters.

This study aimed at investigating the effect of different sources of dietary fibre on gallstone formation in hamsters. The substances studied were pectin, lignin and psyllium hydrocolloid. The two latter compounds protected hamsters against cholesterol gallstone formation. Lignin resulted in a decrease of the deoxycholic acid conentration and in a rise of the cholic/chenodeoxycholic acid ratio. These changes which are similar to those observed with cholestyramine suggest that lignin acts as a bile acid sequestrant. Psyllium hydrocolloid effected a similar shift of the cholic/chenodeoxycholic acid ratio but it also resulted in a rise of the deoxycholic concentration. This latter finding is not compatible with a bile acid sequestering role of this compound. The addition of alcohol to the drinking-water resulted in the formation of stones rich in pigment. Under these conditions the tendency to form such stones was not checked by either of the investigated substances.

Animals↗
PubMed1978

Diet and sterol biohydrogenation in the rat: occurrence of epicoprostanol.

The fecal sterols from rats fed several types of semipurified or commercial diets were analyzed by a combination of thin layer and gas liquid chromatography. In rats fed semipurified diets with lard, sucrose, and casein, increasing proportions of lard (0, 8, 20, 65%) enhanced the fecal coprostanol/coprostanol + cholesterol ratio (from 0.50 to 0.85). This ratio was reduced by replacing lard with triolein or a mixture of calcium oleate and linoleate (1:1) and did not change when trierucin was substituted. No coprostanol formation was observed in rats fed a diet with tripalmitin or tristearin. The addition of sodium hyodeoxycholate (0.5%) or cholestyramine (2%) to the basal diet was without effect on the coprostanol/coprostanol + cholesterol ratio in the feces. The addition of sodium taurocholate (0.2, 0.75, and 4%) strongly reduced coprostanol formation, while a chronic bile duct ligation led to an enhancement. Cholesterol feeding (0.05, 0.2, and 0.5% in the diet) slightly increased (from 51 to 66%) coprostanol formation. Trace amounts of epicoprostanol were generally found in the feces. However, in some cases a very high proportion (up to 60%) of this sterol was observed. Possible relationships between the presence of epicoprostanol and the nature of the diet are discussed.

Animals↗
PubMed1988

Induction of long-lasting hypercholesterolemia in the rat fed a cystine-enriched diet.

The influence of dietary excess (5%) of L-cystine on rat plasma lipoproteins was examined. After only one week of cystine feeding, an increase in the plasma cholesterol level and a decrease in triglyceride levels were observed. The increase in cholesterol level became greater when the duration of cystine-enriched diet increased until eight weeks (+131% after eight weeks), but no further increase occurred between 8 and 20 weeks. This change was essentially due to the progressive increase in cholesterol levels in high density lipoproteins (HDL) and in lipoproteins isolated between 1.040 and 1.063 g/ml, i.e., certain low density lipoproteins (LDL2), and containing mainly apoE-rich lipoproteins (HDL1). The decrease in plasma triglycerides resulted from that of chylomicrons and very low density lipoproteins (VLDL). The effects observed after four or eight weeks of cystine feeding were maintained for eight weeks after replacing the cystine diet by the standard diet. Ingestion of the standard diet containing either cholestyramine (2%) or probucol (0.25%) following eight weeks of cystine feeding significantly decreased plasma cholesterol levels. It is concluded that cystine-fed rats are a useful tool of investigation for understanding mechanisms leading to increased plasma cholesterol level and for hypocholesterolemic drug trials.

Animals↗
PubMed2002

Phase I clinical and pharmacokinetic trial of the cyclin-dependent kinase inhibitor flavopiridol.

PURPOSE: Flavopiridol (NSC 649890) is a synthetic flavone possessing significant antitumor activity in preclinical models. Flavopiridol is capable of inducing cell cycle arrest and apoptosis, presumably through its potent, specific inhibition of cyclin-dependent kinases. We conducted a phase I trial and pharmacokinetic study of flavopiridol given as a 72-h continuous intravenous infusion repeated every 2 weeks. METHODS: A total of 38 patients were treated at dose levels of 8, 16, 26.6, 40, 50 and 56 mg/m(2)/24 h. During the first infusion, plasma was sampled at 24, 48 and 72 h to determine steady-state concentrations, and peripheral blood lymphocytes were assessed by flow cytometry for evidence of apoptosis. Additional postinfusion pharmacokinetic sampling was done at the 40 and 50 mg/m(2)/24 h dose levels. RESULTS: Gastrointestinal toxicity was dose limiting, with diarrhea being the predominant symptom. Symptomatic orthostatic hypotension was also frequently noted. Several patients experienced tumor-specific pain during their infusions. The maximum tolerated dose (MTD) was determined to be 40 mg/m(2)/24 h. A patient with metastatic gastric cancer at this dose level had a complete response and remained disease-free for more than 48 months after completing therapy. Plasma concentrations at 24 h into the infusion were 94% of those achieved at steady state. Steady-state plasma flavopiridol concentrations at the MTD were 416.6+/-98.9 micro M. These concentrations are at or above those needed to see cell cycle arrest and apoptosis in vitro. The mean clearance of flavopiridol over the dose range was 11.3+/-3.9 l/h per m(2), similar to values obtained preclinically. Elimination was biphasic. The terminal half-life at the MTD was 26.0 h. No significant differences in pharmacokinetic parameters were noted between males and females. Patients taking cholestyramine to ameliorate flavopiridol-induced diarrhea had lower steady-state plasma concentrations. There was no significant change in the cell cycle parameters of peripheral blood lymphocytes analyzed by flow cytometry. CONCLUSIONS: The MTD and recommended phase II dose of flavopiridol given by this schedule is 40 mg/m(2)/24 h. The manageable gastrointestinal toxicity, early signs of clinical activity and lack of hematologic toxicity make further exploration in combination trials warranted.

Adult↗
PubMed1999

Erythropoietic protoporphyria with fatal liver failure.

A 33-year-old woman with a history of photosensitivity, persistent abdominal pain, and liver dysfunction was admitted to our department because of abdominal pain and progression of liver dysfunction. On admission, levels of protoporphyrin and coproporphyrin within erythrocytes were markedly increased. Autofluorescent erythrocytes were also detected, leading to a diagnosis of erythropoietic protoporphyria. A liver biopsy specimen revealed cirrhosis with dark brown granules filling hepatocytes, bile canaliculi, and bile ductules. Transfusion of washed erythrocytes, hemodialysis, and administration of cholestyramine and beta-carotene transiently improved levels of porphyrins and liver function. The patient died of rupture of esophageal varices followed by multiple organ failure. However, the treatments were believed to have extended survival.

Adult↗
PubMed2004

Debilitating diarrhoea and weight loss due to colitis in two RA patients treated with leflunomide.

Diarrhoea and weight loss are frequently reported adverse events in rheumatoid arthritis (RA) patients receiving the disease-modifying antirheumatic drug (DMARD) leflunomide. According to the available literature these side effects occur mostly during the first 6 months of treatment, are rather mild and rarely lead to treatment withdrawal. In this report, we describe the clinical, endoscopic and histologic findings in two RA patients with severe diarrhoea and important weight loss more than 12 months after starting treatment with leflunomide. In both cases the symptoms were caused by colitis, but one had ulcerative and the other microscopic colitis. Despite treatment with budesonide the complaints only improved after withdrawal of leflunomide, making a causal relationship between this drug and the pathogenesis of colitis probable. The heterogeneous histopathological findings in these two patients, however, do not allow us to draw any definitive conclusions about the mechanism by which leflunomide causes diarrhoea and weight loss in RA patients. We conclude that persistent diarrhoea or weight loss in patients taking leflunomide can be more serious than what is previously reported in the literature. In such cases leflunomide treatment should be stopped and an endoscopic examination of the colon is recommended. Given the long half-life of this drug a washout procedure with cholestyramine should be considered whenever the problem is severe or persistent.

Adult↗
PubMed2000

Lymphocytic and Collagenous Colitis.

Patients with symptomatic collagenous-lymphocytic colitis should eliminate dietary secretagogues such as caffeine- or lactose-containing food from their diet. When possible, use of nonsteroidal anti-inflammatory drugs should be discontinued. If steatorrhea is documented, a low-fat diet may be helpful. In the presence of bile salt malabsorption, binding resins such as cholestyramine might be useful. Nonspecific diarrheal agents such as loperamide hydrochloride, diphenoxylate hydrochloride and atropine, deodorized tincture of opium, or codeine might prove effective in some patients. Antibacterial agents such as bismuth subsalicylate (8 chewable 262-mg tablets daily) have been effective in symptom control. Metronidazole and erythromycin achieve response rates of 60%. Sulfasalazine, at the usual dose of 2 to 4 g daily, used in collagenous-lymphocytic colitis, demonstrated cessation of diarrhea in 1 to 2 weeks for 50% of patients. Other 5-aminosalicylic (5-ASA) compounds are preferred for patients with a history of sulfa allergy, and those who experience adverse reactions to sulfasalazine. Adrenocorticoid medication is reserved for patients whose conventional treatment with sulfasalazine or 5-ASA has failed. Resolution of diarrhea has been documented in 80% to 90% of patients within 1 week of treatment, however, in most patients, long-term therapy is required. Surgical management is reserved for those patients with disease refractory to medical therapy. Colectomy with ileostomy resulted in clinical and histologic resolution in small case series. If there is no abatement of symptoms, rule out other etiologies of diarrhea such as thyroid dysfunction, celiac disease, or bacterial overgrowth.

Journal Article↗
PubMed2001

Hyperlipidemia in Chronic Cholestatic Liver Disease.

Hyperlipidemia with a marked increase of low-density lipoprotein (LDL) and high- density lipoprotein (HDL) cholesterol levels is a common feature in patients with chronic cholestatic liver disease. Excess morbidity and mortality from cardiovascular disease has not been reported in these patients. This may be due to the particular lipoprotein pattern observed during chronic cholestasis, characterized by elevated serum HDL cholesterol, which may have a cardioprotective effect. However, in a subgroup of patients with chronic cholestasis, hyperlipidemia is characterized by markedly elevated LDL levels with normal or low HDL levels, probably reflecting hypercholesterolemia with coexisting familial and nutritional origins. Ursodeoxycholic acid, the only drug approved for the treatment of chronic cholestatic liver diseases, has been shown to slightly decrease serum cholesterol concentrations. However, the extent of LDL reduction by ursodeoxycholic acid may be insufficient to protect this subgroup of patients from increased cardiovascular risk. Patients in this subgroup probably would benefit from dietary modification, weight loss, and the administration of specific lipid-lowering drugs. Cholestyramine, which is the first-line treatment for pruritus in chronic cholestasis, may be also indicated for its cholesterol-lowering capacity in patients with hypercholesterolemia who complain of pruritus. Administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (simvastatin or pravastatin, 20 mg/d) should be limited to hypercholesterolemic patients with mild chronic cholestatic liver diseases in whom HDL serum levels are below the protective range or if additional risk factors for cardiovascular diseases are present.

Journal Article↗
PubMed2003

Treatment Options for Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis.

Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are chronic cholestatic liver diseases that affect 0.5 to 40 per 100,000 and 1 to 6 per 100,000 Americans, respectively. Prompt recognition and management of the clinical manifestations of these diseases is essential for the patients' well-being and ultimate outcome. Ursodeoxycholic acid (UDCA), 13 to 15 mg/kg per day, is the standard therapy for PBC and should be offered to every patient. It has been shown to slow progression of the disease and prevent the need for liver transplantation, which is the last recourse for patients with end-stage disease. However, there is no effective therapy for PSC yet. Patients are managed symptomatically, with surgical or endoscopic interventions as needed in cases of significant biliary obstruction. Complications of chronic cholestasis are seen in both PBC and PSC, with pruritus and fatigue being the most common complaints. The first choice for the treatment of pruritus is still cholestyramine, starting at 4 g/d. The pathogenesis of fatigue is poorly understood in this population; unrecognized hypothyroidism should be excluded. The use of antidepressants is currently under evaluation, but there is no specific therapy for fatigue as of yet. For prevention of severe osteoporosis, we recommend supplementation with 800 IU vitamin D and 1500 mg calcium/d. In patients with PBC and established osteoporosis, the use of alendronate and vitamin K appears to cause an increase in bone mineral density. Further studies are necessary before either of these drugs is routinely recommended. Finally, fat-soluble vitamin deficiencies are noted with more advanced disease. We recommend that serum levels be checked in high-risk patients, and that vitamins are replaced as appropriate with water-soluble supplements. However, other causes of malabsorption must be ruled out, including pancreatic insufficiency and celiac sprue.

Journal Article↗
PubMed2003

Intrahepatic Cholestasis of Pregnancy.

Intrahepatic cholestasis of pregnancy (or obstetric cholestasis) is a liver disorder that occurs in late pregnancy. Despite the potential adverse maternal and fetal/neonatal outcomes, cholestasis of pregnancy is often neglected and treated expectantly. More research is needed to improve the molecular and genetic understanding of the disease and to define a safe and effective medical treatment that improves clinical outcome. Ursodeoxycholic acid is considered to be a safe treatment option in the third trimester, but further randomized controlled trials are needed before ursodeoxycholic acid treatment can be generally recommended. Ursodeoxycholic acid is preferentially administered to patients with severe cholestasis (onset before week 33 or serum bile acid levels > 70 mmol/L) or to patients with a history of sudden fetal death, while maintaining close obstetric and regular biochemical surveillance (transaminases, bilirubin, and bile acid levels). Ursodeoxycholic acid can decrease pruritus and ameliorate liver tests, but effects on obstetric complications are ambiguous. S-Adenosylmethionine, dexamethasone, and cholestyramine can provide some relief of itching. Because none of these drugs have been shown to be harmful to mother or fetus, the individual woman and her clinician may decide whether to try one of the treatments described.

Journal Article↗
PubMed2003

Management of Primary Biliary Cirrhosis.

Primary biliary cirrhosis is a chronic, progressive disease for which there is no definitive treatment. Ursodeoxycholic acid, however, is of benefit for delaying progression to irreversible end-stage liver disease and prolonging survival free of transplantation. It is, therefore, the standard medical therapy for primary biliary cirrhosis. Orthotopic liver transplantation can be offered for patients with end-stage disease. Other important endpoints of treatment in this condition include management of the long-term complications of cholestasis such as pruritus, osteoporosis, and fat-soluble vitamin deficiencies. Pruritus is best treated with cholestyramine; rifampicin, antihistaminics, opioid-antagonists, and ondansetron can also be tried. Osteoporosis should be treated with calcium and vitamin D supplementation. Bisphosphonates or vitamin K2 may be of additional benefit to decrease the risk of fractures, but this is unproved as of yet. Deficiencies of vitamins A, D, E, and K should be treated with appropriate replacement. Finally, orthotopic liver transplant is indicated for cases of liver failure, intractable pruritus, or severe osteoporosis.

Journal Article↗
PubMed2004

Duodenogastric Reflux-induced (Alkaline) Esophagitis.

Duodenogastric reflux is the retrograde flow of duodenal contents into the stomach that then mix with acid and pepsin. These agents can reflux into the esophagus (ie, duodenogastroesophageal reflux ) and cause gastroesophageal reflux disease (GERD) and its complications, including stricture, Barrett's esophagus, and adenocarcinoma of the esophagus. Medical and surgical treatments of DGER can be difficult. Best medical treatment is proton-pump inhibitors, which decrease DGER by inhibiting both gastric acidity and volume, making less gastric contents available to reflux into the esophagus. The addition of the gamma-aminobutyric (GABA(B)) receptor agonist baclofen may further reduce DGER in patients not responding to proton-pump inhibitors. Bile acid-binding agents (aluminum-containing antacids, cholestyramine, sucralfate, urosodeoxycholic acid) have physiologic rationale, but their efficacy is unproven. Prokinetic agents can reduce DGER and its upper gastrointestinal symptoms by promoting increased gastric emptying. In patients with medically refractory symptoms, a Roux-en-Y diversion or duodenal switch operation may be helpful.

Journal Article↗
PubMed2005

Chronic Diarrhea.

Chronic diarrhea can be due to any of several hundred conditions. When investigation fails to uncover a specific cause that can be treated successfully, nonspecific therapy is implemented. This includes dietary alterations if specific aggravating foods can be identified, enteral or parenteral nutrition if nutritional status is compromised, and use of oral rehydration solutions if diarrhea produces volume depletion. Strategic use of dietary fiber can improve stool consistency and can be of special value when fecal incontinence is present concurrently. Medications of value include opiate antidiarrheal drugs, clonidine, octreotide, and bile acid-binding agents. Less potent opiates such as loperamide and diphenoxylate should be tried first, with more potent agents such as codeine, opium, and morphine used in refractory cases. Clonidine has both proabsorptive and motility effects that facilitate its antidiarrheal effect, but its antihypertensive action limits its utility. Octreotide is of great value in treating diarrhea due to endocrine tumors and dumping syndrome; its efficacy in other conditions or in nonspecific diarrhea is less well established. Bile acid binders such as cholestyramine or colestipol have several specific uses but have limited utility in nonspecific chronic diarrhea.

Journal Article↗
PubMed1999

Lymphocytic and Collagenous Colitis: Medical Management.

When possible, patients taking nonsteroidal anti-inflammatory medications should discontinue them when the diagnosis of microscopic colitis is made. Although there is no direct evidence of its efficacy, a trial of elimination of caffeine or lactose or both should be undertaken. Nonspecific antidiarrheal agents (eg, loperamide, diphenoxylate) may be administered, but appear to be largely ineffective in this population. An aminosalicylate should be initiated at full therapeutic dose (2 to 4 g daily) as the first-line therapy. Because sulfasalazine appears to be associated with a high incidence of adverse effects in patients with microscopic colitis, other derivatives of 5-aminosalicylate (5-ASA) are preferred. Bile salt-binding agents such as cholestyramine or colestipol appear to be effective alternatives for patients who are either unresponsive to or intolerant of aminosalicylates. Systemic corticosteroids are an effective treatment for microscopic colitis, but may offer only transient improvement in symptoms. Given their potential adverse effects, corticosteroids should be reserved for patients with refractory disease in whom aminosalicylates and bile salt-binding agents have failed. Other agents that may be effective include antibiotics, bismuth subsalicylate, budesonide, pentoxifylline, octreotide, and methotrexate. Although these agents can be considered in unusual cases, the cumulative clinical experience with them in this setting is relatively limited. Surgical intervention, with either fecal stream diversion or subtotal colectomy, shows promise as an intervention of last resort. In refractory cases of microscopic colitis, strong consideration should be given to excluding a concomitant diagnosis of celiac disease, bacterial overgrowth, or chronic infection.

Journal Article↗
PubMed1999

Pruritus.

The treatment of patients with pruritus of liver disease poses a challenge to the clinician. Resins (cholestyramine or colestipol) in quantities of 4 to 16 grams a day should be the initial agents used. In those who remain refractory, diphenhydramine should be added, although sedation may limit the use of higher doses. If symptoms still persist, rifampin up to 600 mg/day can be added to the above regimen with close monitoring of hepatic function. If, despite this combination, pruritus persists and quality of life remains poor, experimental therapies in the form of oral opioid antagonists, and orthotopic liver transplantation should be considered.

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