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

The concentration in serum of cathodal trypsinogen has been studied in certain clinical and experimental situations. The concentration correlated with pancreatic amylase activity. Low levels were found in patients with malabsorption due to exocrine pancreatic insufficiency. The concentration rose after endoscopic retrograde cholangiopancreatographic examinations (ERCP). After ERCP, however, no trypsin was detected complexed with protease inhibitors, as is generally found in acute pancreatitis. The trypsinogen concentration in serum also rose in renal failure indicating a renal elimination route for the endogenous trypsinogen.
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PMID:Studies on the turnover of endogenous cathodal trypsinogen in man. 10 10

A series of 29 cases of amyloidosis of the alimentary tract is reported. Five cases (17%) were primary amyloidosis; 14 cases (48%) were amyloidosis secondary to other diseases (such as chronic inflammatory and neoplastic diseases); 10 cases (35%) were amyloidosis of the heredo-familial type connected with Familial Mediterranean Fever. In 23 patients (79%) the diagnosis was established by biopsies, and in 6 more cases on autopsy. Gastrointestinal involvement was found in all age groups. Gastro-enterologic complications observed in the present series include: diarrhea, malabsorption, ileus and gastrointestinal bleeding. In addition other conditions such as jaundice (3 cases), esophagitis and acute hemorrhagic pancreatitis were observed. In 22 patients proteinuria was observed and in 13 patients the nephrotic syndrome. Among 17 patients, in 11 the clinical picture before death was that of terminal renal failure. The survival after diagnosis among 14 patients reached 4 years in 9 cases, and 19 years in one case. The diagnostic value of the rectal biopsy is emphasized.
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PMID:[Gastrointestinal amyloidosis]. 18 89

Severe osteomalacia due to causes other than malabsorption and, where renal function was impaired, disproportionate to the degree of renal failure, is described in 15 adults. Only one was younger than 46 years, the median age being 59 years. The diagnosis was not made for months in most patients. After investigation, the patients were grouped as follows: nutritional three cases, "renal" six cases, hypophosphataemia three cases, neurofibromatosis and primary hyperparathyroidism one each. The last patient was poorly nourished and had taken anticonvulsants and analgesics. Most patients responded well to treatment with calciferol. These cases indicate the need to be aware that osteomalacia may occur in previously healthy middle-aged or elderly subjects.
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PMID:Osteomalacia due to unusual causes presenting in adults. 28 91

Intestinal malabsorption of calcium and the development of osteomalacia in conservatively treated renal failure is explained by a quantitative deficiency of 1,25-dihydroxycholecalciferol, which also contributes to the development of hypocalcaemia. Excess of 25-hydroxycholecalciferol can substitute for this deficiency. The presence and healing of azotaemic osteomalacia is unrelated to the prevailing plasma [Ca] x [P] product. The data suggest that "vitamin D" acts directly on bone mineralisation, but the claim that this apparent effect is normally due to 25-hydroxycholecalciferol is considered unproven. Most of the phenomena of azotaemic osteodystrophy are encountered in simple vitamin D deficiency; as in that condition, deficiency of 1,25-dihydroxycholecalciferol may be of primary significance in causing secondary hyperparathyroidism in renal failure.
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PMID:Vitamin D and the syndromes of azotaemic osteodystrophy. 36 40

Calcium and phosphate absorptions were studied by radiotracer techniques in 30 patients after successful cadaveric renal transplantation, and results were compared with those in a group of normal subjects and in groups of patients with chronic renal failure (CRF). Both calcium and phosphate absorptions were impared in patients with CRF, including those receiving haemodialysis. Abnormalities of calcium absorption, however, seemed to occur earlier in the course of advanced renal failure than abnormalities in phosphate absorption. Calcium absorption improved dramatically after successful renal transplantation, while phosphate absorption remained the same. A dissociation between calcium and phosphate absorptions is not often seen clinically, and the mechanisms for it are unknown. Phosphate malabsorption may be a further contributing factor in the development of persistent hypophosphataemia after transplantation.
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PMID:Dissociation of absorptions of calcium and phosphate after successful cadaveric renal transplantation. 37 43

A microbiologic technique for the assay of methotrexate (MTX) in urine, serum, erythrocytes, feces, and skin is described. The accuracy of the method equals that of routine microbiologic assays of folic acid. Important differences in serum MTX levels in psoriatic patients during the 24 hours after standardized intravenous and intramuscular administration were demonstrated. Repeated intravenous doses tended to be cleared from the blood univormly. After oral doses many patients achieved peak serum levels within 2 hr. with fall of level by 4 hr. Others achieved lower levels and responded less well clinically. Persistence of high serum levels at 24 and 48 hr did not confer obvious clinical benefit or necessarily give rise to by renal function when the creatinine clearance was greater than 50 ml/min. However, impaired renal function was clearly correlated with slow clearance. Routine measurement of MTX blood levels is of value in patients with suspected malabsorption or partial renal failure.
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PMID:Assay of therapeutic doses of methotrexate in body fluids of patients with psoriasis. 112 53

Synthetic 1alpha-hydroxycholecalciferol (1alpha-OH-D3) was given intravenously in a dose of 2.5-10 mug per day to three patients with chronic renal failure. As little as 10 mug of 1alpha-OH-D3 daily for a week improved intestinal calcium absorption to a normal level, raised serum calcium, and reduced serum alkaline phosphatase. Severe rickets which had not responded to large amounts (greater than 200 mg in total) of vitamin D2 was markedly cured with 2.5 mug of 1alpha-OH-D3 given daily for 3 weeks. These clinical data hold promise that is certainly useful in the improvement of intestinal malabsorption of calcium and bone diseases in renal failure.
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PMID:Curative effects of 1alpha-hydroxycholecalciferol on calcium metabolism and bone disease in patients with chronic renal failure. 121 80

Ninety systemic sclerosis (SSc) patients, all females, none of them suffering from either renal failure or intestinal malabsorption, and 90 sex and age matched controls were investigated for bone mineral content (BMC) by dual photon-absorptiometry (Am 241, I 125) (Osteoden P, NIM) evaluated at two sites of the nondominant radius. BMC as well as bone density (BD) were found to be significantly lower in the patients than in the controls. No alteration of calcium metabolism was detected in the patients, neither were we able to find any relationship between osteopenia and the extent of the involvement of the skin or of any internal organ. We observed, however, that the percentage of the patients in menopause was significantly greater than that of the controls (p less than .001). Furthermore, menopause had occurred in the patients significantly earlier than in the controls (p less than .001). Therefore, earlier menopause can play a role in the induction of osteopenia in systemic sclerosis. Further prospective studies are needed to check the hormonal status of SSc patients.
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PMID:Osteopenia in systemic sclerosis. Evidence of a participating role of earlier menopause. 206 1

Home parenteral nutrition has prevented malnutrition in patients who cannot maintain adequate nutrition by enteral feedings alone. The risk of bone and mineral abnormalities in these patients is significant for several reasons. Pre-existing skeletal disease can occur from factors known to affect the population at large as well as from malnutrition, malabsorption, and corticosteroid use related to the underlying disease process. Long-term use of infused nutrients and potential toxins can further alter bone turnover. Hypercalciuria is frequently present during HPN, yet its etiology is poorly defined. Parenteral nutrition admixture concentrations of calcium, phosphorus, protein, sodium, and dextrose may all play a role. Any development of acidosis can certainly aggravate hypercalciuria, which may be an indirect marker of abnormal bone turnover. Although increased protein intake can promote the development of acidosis-induced calciuresis, infused phosphorus and acetate can help reduce calcium excretion. Parenteral nutrition contamination by aluminum can cause a spectrum of osteomalacic bone disease similar to aluminum-associated changes seen in renal failure patients. Even with recent attempts to remove aluminum from the parenteral admixture, low-turnover bone disease can still occur. At present, HPN-related bone disease is a poorly understood entity because of its multifaceted nature. Patients receiving long-term parenteral nutrition should be considered to have an increased risk for the development of metabolic bone disease. Early monitoring for and treatment of bone disease should be considered in all patients receiving HPN.
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PMID:Long-term parenteral nutrition and metabolic bone disease. 211 69

Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.
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PMID:Acute deterioration of renal function associated with enteric hyperoxaluria. 222 62


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