Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic and biliary carcinomas remain a challenge to clinicians and investigators, as diagnosis is rarely achieved while the tumor is still in a curative stage. Clinical symptoms and signs of these neoplasias are non-specific and heterogeneous. We review the clinical presentation of these tumors, with an emphasis on their pathophysiology and relationship with survival. Abdominal pain is the most common presenting complaint in pancreatic and biliary tract carcinomas, regardless of their size; although severe back pain usually indicates neural compromise, and is associated with a short survival. Jaundice may also be an early sign, in fact, pancreatic tumors that present as painless jaundice have been ascribed, a relatively more favorable prognosis. Weight loss is a common finding in most patients, being usually associated with malabsorption. These neoplasias may also present as diabetes, as an acute pancreatitis episode, with venous thrombosis or malignant thrombophlebitis, as a gastrointestinal hemorrhage, with mental disturbances, or skin manifestations.
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PMID:Vagaries of clinical presentation of pancreatic and biliary tract cancer. 1043 92

Weight loss late in the course of human immunodeficiency virus (HIV) disease is common and often multifactorial. Increased energy expenditure in response to opportunistic disease, as well as to HIV infection itself, can lead to protein-calorie malnutrition similar to that observed in starvation. Weight loss of as little as 5 percent in patients with HIV infection is associated with an increased risk of disease progression. Loss of body cell mass carries a particularly poor prognosis, and aggressive measures should be taken to stop such depletion. Patients exhibiting unexpected weight loss should be carefully examined to exclude decreased food intake, malabsorption, occult infection or neoplasm as the etiology of the weight loss. Early aggressive treatment of HIV disease and underlying opportunistic pathology, along with adequate pharmacologic, hormonal, nutritional and physical therapy, can often restore normal weight and body composition.
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PMID:Evaluation and treatment of weight loss in adults with HIV disease. 1049 11

Ileal Na+-dependent bile acid transporter (ISBT) constituting a gateway to enterohepatic circulation of bile acids occurs exclusively at the distal site of the small intestine. In the present study, we examined colonic tumorigenesis promoted by deoxycholic acid in relation to the expression of the ISBT. For this purpose, the small intestine of a Fischer-344 rat was resected a length of 20 cm above the ileo-cecal valve (ileal resection) or below the duodenum (jejunal resection). Then, rats were treated with an intraperitoneal injection of azoxymethane (15 mg/kg body wt.) once a week for 3 weeks and fed a 20% casein diet supplemented with 0.2% deoxycholate for 39 weeks. Northern blot analysis demonstrated that the ISBT mRNA was hardly detectable in ileum-resected rats. The excretion of fecal bile acids was 1.5-fold higher in the ileum-resected group than in the jejunum-resected group (P < 0.05). On the contrary, the serum bile acids concentration of ileal-resected rats was about one-half of that of jejunum-resected animals (P < 0.05). The tumor incidence and the total tumor number were significantly higher in the ileum-resected group than in the jejunum-resected one (P < 0.05). Interestingly, no tumor was found at the proximal colon in the jejunum-resected group while tumors developed frequently at the proximal site as well as mid and distal colon in the ileum-resected group. These observations demonstrate that malabsorption of bile acids owing to the lack of ISBT enhanced colon tumorigenesis.
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PMID:Elimination of Na+-dependent bile acid transporter from small intestine by ileum resection increases [correction of increase] colonic tumorigenesis in the rat fed deoxycholic acid. 1053 Jul 78

With modern forms of urinary diversion being widely employed during recent years, the awareness of possible complications and appropriate follow-up strategies gains rising importance and current follow-up strategies are reviewed herewith. Follow-up investigations after urinary diversion have to address possible surgical complications, metabolic changes as well as the risk of secondary malignancies in the incorporated bowel segments. The most important and possible deleterious surgical complication is upper tract dilation and obstruction following ureteroenteric anastomotic stenosis and occurs in 2-30% depending on the surgical technique and evaluated series. The most appropriate follow-up study to detect upper tract dilation is ultrasonography while the associated obstructional component can best be estimated by functional renographic studies (MAG(3) renal scan). The significance of reflux associated with urinary diversion remains controversial although experimental studies and clinical observations suggest a risk of renal functional deterioration associated with reflux which is certainly true in ureterosigmoidostomy following pyelonephritic changes. Possible metabolic changes include hyperchloremic metabolic acidosis and problems related to malabsorption due to bowel resection and incorporation of bowel segments into the urinary tract. The incidence of hyperchloremic acidosis is related to the form of urinary diversion, being higher in continent forms than in incontinent diversions, while hyperchloremic metabolic acidosis is most frequently encountered in ureterosigmoidostomy. While acute complications of metabolic acidosis may encompass hyperventilation as well as severe changes of serum electrolytes and acid base balance leading to cardiac arrhythmias necessitating immediate hospital treatment with intravenous alkalinizing, chronic acidosis may lead to osteopenia through hypocalcemia and stimulation of osteoclastic activity. Metabolic acidosis can be best detected by regular blood gas analysis. To prevent these complications prophylactic administration of alkalinizing agents (e.g. potassium citrate) should be readily performed. Malabsorption of bile acid strongly correlates with the length of ileum resected and can induce both chologenic diarrhea and malabsorption of liposoluble vitamins (A, D, E, K). Vitamin B(12) is exclusively absorbed in the distal ileum, serum levels therefore may be reduced following resection of distal ileum. This will not occur during the first 3-5 years following diversion because B(12) deposits usually will last for this period. Later, however, serum levels of vitamin B(12) should be checked annually while others favor routine substitution of this vitamin. The incidence of cancer occurring at the ureterointestinal anastomosis seems to be highest in patients with ureterosigmoidostomy varying between 2 and 29% with polypoid benign lesions being more frequent. The most common type of tumor is adenocarcinoma which has also been reported in colonic and ileal conduits as well as augmentation cystoplasty using either colon or ileum. Since the time interval between surgery and cancer occurrence is longer than 10 years, the newer forms of continent diversion theoretically also inherit the risk of tumor formation, which, however, has yet to be established because these diversions are only in wide use since 10 years. Currently, annual endoscopic controls are recommended in those patients with diversions where feces and urine are in contact with urothelium starting 5 years after surgery. Although formal guidelines for follow-up after urinary diversion have not yet been established by the working group on oncology of the German urological association, this paper suggests a follow-up strategy addressing surgical complications, metabolic changes and the risk of secondary malignancies.
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PMID:Follow-up after urinary diversion. 1059 89

There is a definite increase in combined-modality treatment of malignancies. Surgery, radiation therapy and/or chemotherapy often are combined. A disadvantage is the increased risk for short- and long-term complications, especially radiation-induced damage to normal healthy tissue such as intestine and bone. Brachytherapy and intraoperative radiotherapy are new radiation techniques with the potential to increase the radiation dose to the tumor while reducing the radiation dose to surrounding normal tissues. The surgical transposition of organs outside the pathway of the ionizing beam is a new surgical technique often used in the pelvis. Radiation damage to the gastrointestinal tract is often mentioned. Fibrosis and obstruction may occur as a result of stricture formation or fibrinous adhesions. Ischemic necrosis of the bowel wall may lead either to perforation or fistulae. Mucosal damage and lymphatic obstruction can cause malabsorption. These complications are difficult to manage and should be treated in specialized centers.
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PMID:Surgical Prevention and Treatment of Late Normal Tissue Injury. 1071 98

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

A component of ATP, phosphate is at the hub of the energy-related mechanisms operative in muscle cells. Together with calcium, phosphate is involved in bone tissue mineralization: thus, a chronic alteration in the metabolism of phosphate can induce bone and joint disorders. Diagnosis of chronic hypophosphatemia. Serum phosphate, calcium, and creatinine should be assayed simultaneously. Serum calcium is increased in hypophosphatemia caused by hyperparathyroidism and decreased in osteomalacia. Urinary phosphate excretion should be measured in patients with a normal serum calcium level and a serum phosphate level lower than 0.80 mmol/L. A decrease in urinary phosphate excretion to less than 10 mmol/24 h strongly suggests a gastrointestinal disorder, such as malabsorption, antacid use, or chronic alcohol abuse. In patients with a urinary phosphate excretion greater than 20 mmol/24 h, the maximal rate of tubular reabsorption of phosphate (TmPO4) and the ratio of TmPO4 over glomerular filtration rate (GFR) should be determined to look for phosphate diabetes. Manifestations and causes of phosphate diabetes in adults. Moderately severe phosphate diabetes in adults manifests as chronic fatigue, depression, spinal pain, and polyarthralgia, with osteoporosis ascribable to increased bone resorption. Although many cases are idiopathic, investigations should be done to look for X-linked vitamin D-resistant rickets missed during childhood, a mesenchymatous tumor, or Fanconi's syndrome with renal wasting of phosphate, glucose, and amino acids. Management of phosphate diabetes. Phosphate supplementation and, in patients with normal urinary calcium excretion, calcitriol produce some improvement in the symptoms and increase the bone mineral density. Whether dipyramidole is clinically effective remains unclear.
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PMID:Phosphate, the renal tubule, and the musculoskeletal system. 1139 20

It is generally accepted that the abdominal angina develops only when at least two of the three splanchnic vessels-mesenteric arteries and the celiac trunk exhibit a critical obstruction. That common opinion does not, however, take into account anatomical variants of arteries supplying the blood to the intestines. We present a case of a wasted, 40 year old male with a wide spread arteriosclerosis and postprandial pain. The ultrasound examination revealed total occlusion of the superior mesenteric artery (SMA). Celiac trunk (CT) and inferior mesenteric artery (IMA) were patent. The ultrasound indicated that only one splanchic vessel was obstructed; the systemic disorder, the neoplasm, as well as the malabsorption were ruled out. An arteriography of the abdominal aorta and of splanchnic arteries confirmed patency of CT and IMA, also lack of flow in the SMA. Atypical origin of the middle colic artery originating from the bed of CT was also shown. Lack of collaterals between IMA and SMA, typically conducting a sufficient blood flow, resulted in a fully symptomatic abdominal angina. Symptoms were relieved following surgical revascularization.
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PMID:[Advanced abdominal angina due to atherosclerosis with atypical celiac arteries]. 1142 65

Diencephalic syndrome (DS) is a complex of signs and symptoms related to hypothalamic dysfunction. Its main features are emaciation despite normal energy intake and an alert appearance. This syndrome has been described in association with space-occupying lesions of the hypothalamic-optic chiasm region, mainly low-grade glioma, and less often with tumors in the proximity of the IV ventricle. Two patients with DS are reported. The first patient was an 8-month old boy with classical features of DS. Extensive investigation of malabsorption revealed no abnormalities and the first neurologic sign was a rotatory nystagmus. Magnetic resonance imaging (MRI) showed evidence of a hypothalamic tumor, which was identified after surgical resection as a pilocytic astrocytoma. The second patient was an adolescent boy who presented a 20-kg weight loss over a 6-month period and psychological disturbances. Gastrointestinal disease was ruled out as a cause of malnutrition. Because of a polydipsia-polyuria syndrome, manifest while the patient was hospitalized with a suspected diagnosis of anorexia nervosa, MRI of the brain was performed. Multiple intracranial lesions were revealed, mainly in the hypothalamus, and were identified as a disseminated disgerminoma. No neurologic signs or symptoms were present. The patients died 2 years and 1 year after diagnosis, respectively. Although DS is rare, it should be considered in severe failure to thrive or emaciation despite adequate food intake and normal absorptive function of the small bowel.
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PMID:[Diencephalic syndrome: An uncommon cause of malnutrition]. 1204 23

Intraductal papillary mucinous neoplasms are rare pancreatic exocrine tumors with distinct clinicopathologic features. They usually present with a long history of chronic pancreatitis-like symptoms, which are often associated with weight loss, diarrhea, and malabsorption. We report a case of benign intraductal papillary mucinous neoplasm with focal squamous metaplasia presenting as acute necrotizing pancreatitis. The clinicopathologic features are discussed in a brief review of the literature.
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PMID:Intraductal papillary mucinous neoplasm of the pancreas presenting as acute pancreatitis. 1204 14


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