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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The short bowel syndrome is the result of a congenital or acquired loss of a large part of the small intestine. The most frequent causes of surgical resection of the intestine in infants are arterial or venous thrombosis, intestinal volvulus, necrotizing enterocolitis, and Crohn's disease. Symptoms include nutrient and electrolyte malabsorption, steatorrhea and diarrhea, which can result in failure to thrive. The consequences of extensive small bowel resections consist of nutritional deficiencies, gastric acid hypersecretion, nephrolithiasis, cholelithiasis and lactic acidosis. Of these, D-lactic acidosis is an infrequent but important complication because of the symptoms that it can produce. D-lactic acid in the human organism is generated by intestinal bacteria, D-lactate ingestion, or endogenous production in the methyl glycoxylase pathway. Neurological symptoms such as somnolence, ataxia or altered behavior in a patient with short bowel syndrome should make us think of D-lactic acidosis caused by bacterial overgrowth. We present the case of an 11-year-old boy with short bowel syndrome secondary to multiple resections during the postnatal period who was admitted to hospital for episodes of confusion and altered behavior. The diagnosis was lactic acidosis. Outcome was favorable due to prompt instauration of treatment.
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PMID:[D-lactic acidosis in an 11-year-old patient with short bowel syndrome]. 1660 77

Surgical intervention has become an accepted therapeutic alternative for the patient with medically complicated obesity. Multiple investigators have reported significant and sustained weight loss after bariatric surgery that is associated with improvement of many weight-related medical comorbidities, and statistically significant decreased overall mortality for surgically treated as compared with medically treated subjects. Although the Roux-en-Y gastric bypass (RYGB) is considered an acceptably safe treatment, an increasing number of patients are being recognized with nephrolithiasis after this, the most common bariatric surgery currently performed. The main risk factor appears to be hyperoxaluria, although low urine volume and citrate concentrations may contribute. The incidence of these urinary risk factors among the total post-RYGB population is unknown, but may be more than previously suspected based on small pilot studies. The etiology of the hyperoxaluria is unknown, but may be related to subtle and seemingly subclinical fat malabsorption. Clearly, further study is needed, especially to define better treatment options than the standard advice for a low-fat, low-oxalate diet, and use of calcium as an oxalate binder.
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PMID:Nephrolithiasis after bariatric surgery for obesity. 1835 97

Bariatric surgery is now recognized as a sure and effective way for weight reduction in morbid obesity. However some procedures induce intestinal malabsorption leading to enteric hyperoxaluria. So bariatric surgery could place these patients not only at risk for nephrolithiasis but also for oxalate induced nephropathy and chronic renal failure. Because of the growing incidence of obesity worldwide, physicians and patients should be aware of such potential complications. There is no mean to discuss this treatment because of its spectacular efficiency on obesity and its comorbidities. But it is necessary to choose the surgical technique according to the risk factors of the patients. Following surgery, preventive treatment strategies are indicated, such as modified dietary lifestyle and specific drugs as we suggested to limit or even avoid these complications. However observance could fail in the long term. In case of oxalate nephropathy, surgery may be proposed to restore the intestinal tract but with the risk of overweight relapse. To illustrate this matter, we report here significant observations of three patients, which, having successfully benefited from the same bariatric surgery, have presented lithiasic complications for two of them and oxalate nephropathy leading to chronic renal failure and hemodialysis for the third.
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PMID:[Bariatric surgery, calcium oxalate urinary stones and oxalate nephropathy]. 2113 57

Renal stone disease may ensue from either derangements of urine biochemistries or anatomic abnormalities of kidneys and urinary tract. Genetic, environmental and dietary factors may also cooperate in the pathophysiology of nephrolithiasis. An adequate metabolic evaluation should focus on the urinary excretion of promoters and inhibitors of stone formation as well as on the occurrence of systemic diseases potentially related to secondary nephrolithiasis (i.e., endocrine disturbances, malabsorption, bone diseases). Moreover, metabolic investigations should provide reliable information on patient's dietary habits, guide towards the best therapeutic approach and enable the physician to verify patient's compliance to prescribed therapies.AN EXTENSIVE METABOLIC EVALUATION IS RECOMMENDED IN PATIENTS WITH ACTIVE STONE DISEASE (NAMELY, AT LEAST ONE NEW STONE WITHIN THE LAST TWO YEARS), OR IN THOSE HAVING HAD A SINGLE STONE EPISODE OCCURRED IN PECULIAR CONDITIONS: familial history of disease, childhood, menopause, pregnancy, systemic diseases. Simplified protocols may be adequate in non-active nephrolithiasis or in patients with single stone and no relevant risk factors.In our Stone Centre, a so-called "first level screening" is performed by routine, in order to assess urinary supersaturation with stone forming salts and evaluate the excretion of dietary-related metabolites in urine. Relative blood and urine determinations are reported below.IN VENOUS BLOOD: urea, creatinine, uric acid, Na, K, total and ionised Ca, Mg, P, Cl, alkaline phosphatase, gas analysis. In 24-hr urine samples: urea, creatinine, uric acid, Na, K, Ca, Mg, P, Cl, oxalate, inorganic sulphate, citrate, pH, ammonia and titratable acidity. IN FASTING URINE SAMPLES: Ca, citrate, creatinine, hydroxyproline, Brand's test for cistinuria, urine sediment, urine culture. If the first-level evaluation suggested an abnormal bone turnover, then further determinations are warranted, namely, calciotropic hormones (blood Vitamin D and PTH), markers of bone resorption (urine pyridinium crosslinks, serum crosslaps) and formation (serum osteocalcin) bone mineral density.EVENTUALLY, MORE SOPHISTICATED INVESTIGATIONS ARE REQUIRED TO IMPROVE THE DIAGNOSIS OF PECULIAR DISEASES: serum oxalate and glycolate, urine glycolate and L-glycerate, hepatic AGT activity (primary hyperoxalurias); genetic tests (hereditary nephrolithiasis); acidification tests (renal tubular acidosis).
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PMID:Biochemical evaluation in renal stone disease. 2246 Sep 94

Decreased kidney function from kidney deposition of calcium oxalate has been described previously in inflammatory bowel disease and after jejuno-ileal and Roux-en-Y gastric bypass surgeries. Although celiac disease is the most prevalent bowel abnormality associated with intestinal malabsorption, its relationship to high kidney oxalate burden and decreased kidney function has not been established. We report a case of subclinical celiac disease and hyperoxaluria that presented with loss of kidney function as a result of high oxalate load in the absence of overt diarrhea, documented intestinal fat malabsorption, and nephrolithiasis. Subclinical celiac disease is commonly overlooked and hyperoxaluria is not usually investigated in kidney patients. We propose that this entity should be suspected in patients with chronic kidney disease in which the cause of kidney damage has not been clearly established.
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PMID:Subclinical celiac disease and crystal-induced kidney disease following kidney transplant. 2273 30

Ileal pouch-anal anastomosis (IPAA) following total proctocolectomy has become the surgical treatment of choice for ulcerative colitis patients who have medically refractory disease or neoplasia. Unfortunately, various metabolic complications have been reported with this surgical procedure, including anemia, vitamin B(12) deficiency, bile salt and fat malabsorption, vitamin D deficiency, bone loss, and nephrolithiasis. Recognition and early diagnosis of these complications are important when managing IPAA patients.
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PMID:Adverse metabolic sequelae following restorative proctocolectomy with an ileal pouch. 2293 64

Mounting evidence correlate vitamin D3 (cholecalciferol) supplementation or higher serum levels of vitamin D (25(OH)D) with a lower risk of developing multiple sclerosis (MS), reduced relapse rate, slower progression or fewer new brain lesions. We present here the case of a woman who was diagnosed with MS in 1990. From 1980 to 2000, her ability to walk decreased from ~20 to 1 km per day. Since January 2001, a vitamin D3 supplement was ingested daily. The starting dose was 20 mcg (800 IU)/day and escalated to 100 mcg (4000 IU)/day in September 2004 and then to 150 mcg (6000 IU)/day in December 2005. Vitamin D3 intake reduced muscular pain and improved ambulation from 1 (February 2000) to 14 km/day (February 2008). Vitamin D intake over 10 years caused no adverse effects: no hypercalcaemia, nephrolithiasis or hypercalciuria were observed. Bowel problems in MS may need to be addressed as they can cause malabsorption including calcium, which may increase serum PTH and 1,25(OH)2D levels, as well as bone loss. We suggest that periodic assessment of vitamin D3, calcium and magnesium intake, bowel problems and the measurement of serum 25(OH)D, PTH, Ca levels, UCa/Cr and bone health become part of the integral management of persons with MS.
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PMID:Effect of high-dose vitamin D3 intake on ambulation, muscular pain and bone mineral density in a woman with multiple sclerosis: a 10-year longitudinal case report. 2320 62

Five children with glucose-galactose malabsorption (GGM) are presented. Two infants from Saudi Arabia were first-degree relatives, the third infant was unrelated and the other two were of Yemeni and Syrian origin, respectively. All the infants had chronic diarrhoea and four had failed to thrive since early infancy. All had stools positive for reducing substances, and sugar chromatography showed glucose and galactose malabsorption. Small bowel biopsies were normal in all. One infant developed gangrene of both legs as a complication of hypernatraemia and dehydration, necessitating bilateral amputation. Two infants had nephrolithiasis. All the infants responded well to fructose-based formulae. GGM should be considered in the differential diagnosis of chronic diarrhoea in infants breastfed or artificially fed from early life.
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PMID:Five Arab children with glucose-galactose malabsorption. 2392 85

Over the past 10 years, major progress has been made in the knowledge of urinary lithogenesis, including the potential pathogenetic role of Randall's plaques and renal tubular crystal retention. Urine supersaturation is the driving force of this process and can be induced by some risk factors, including low urine volume, high urinary excretion of calcium oxalate and uric acid and low urinary excretion of citrate. Primary hypercalciuria can be due to intestinal overabsorption renal leak and bone reabsorption of calcium. Prophilaxis is mainly conducted with thiazides and low calcium diet which is indicated only in the intestinal form. Primary hyperoxaluria is treated with pyridoxine and may require in the severe forms simultaneous renal and liver transplantation. Enteric hyperoxaluria is secondary to fatty acids malabsorption and requires diet, oral calcium and cholestiramine. Hyperuricosuria is caused by diet endogenous overproduction, mainly due to enzymatic defects or high renal excretion of uric acid. Urine alkalinization with K or K and Mg citrate can prevent stone formation even in idiopathic uric acid nephrolithiasis, in which a defect of urine acidification is supposed to be the main abnormality, and in hypocitraturic patients. Cystinuria is a rare inherited defect with an intense clinical impact. It can be classified in three forms and urinary stone formation is the role. Increased solubility and conversion of cystine in a more soluble form are the main goals of the prophylaxis which includes K citrate and thiol agents administration. Tiopronin is preferred to D-penicillamine due to its lower side effects.
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PMID:[Nephrolithiasis: metabolic defects and terapeutic implications]. 2474 15

Obesity is a significant health concern and is associated with an increased risk of nephrolithiasis, particularly in women. The underlying pathophysiology of stone formation in obese patients is thought to be related to insulin resistance, dietary factors, and a lithogenic urinary profile. Uric acid stones and calcium oxalate stones are common in these patients. Use of surgical procedures for obesity (bariatric surgery) has risen over the past two decades. Although such procedures effectively manage obesity-dependent comorbidities, several large, controlled studies have revealed that modern bariatric surgeries increase the risk of nephrolithiasis by approximately twofold. In patients who have undergone bariatric surgery, fat malabsorption leads to hyperabsorption of oxalate, which is exacerbated by an increased permeability of the gut to oxalate. Patients who have undergone bariatric surgery show characteristic 24 h urine parameters including low urine volume, low urinary pH, hypocitraturia, hyperoxaluria and hyperuricosuria. Prevention of stones with dietary limitation of oxalate and sodium and a high intake of fluids is critical, and calcium supplementation with calcium citrate is typically required. Potassium citrate is valuable for treating the common metabolic derangements as it raises urinary pH, enhances the activity of stone inhibitors, reduces the supersaturation of calcium oxalate, and corrects hypokalaemia. Both pyridoxine and probiotics have been shown in small studies to reduce hyperoxaluria, but further study is necessary to clarify their effects on stone morbidity in the bariatric surgery population.
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PMID:Stone formation and management after bariatric surgery. 2585 Jul 90


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