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)

A patient with acquired immunodeficiency syndrome (AIDS) who required aggressive nutritional intervention via home parenteral nutrition therapy is described, and nutritional status, etiology and therapeutic management of AIDS-associated malnutrition, role of nutrition support, and factors for consideration in using parenteral nutrition in AIDS patients are discussed. Parenteral nutrition therapy was initiated in a 30-year-old AIDS patient with Kaposi's sarcoma lesions of the gastrointestinal tract because of rapid weight loss, low serum protein levels, and malnutrition. He had previously undergone a small-bowel resection and a jejunojejunostomy, and radiation and antineoplastic-drug therapy was planned. During parenteral nutrition therapy, the patient demonstrated increased physical strength and was able to care for himself during most of the time spent at home or in a long-term-care facility. Aggressive measures, including parenteral nutrition therapy, were discontinued 11 days before the patient's death. Complications of therapy included one episode of sepsis and a tear in the external catheter tubing. Malabsorption and diarrhea mainly caused by gastrointestinal disease, reduced food intake because of oral and esophageal infections, adverse effects from medication, and depression are factors that can contribute to AIDS-associated malnutrition. Also, hypermetabolism resulting from infections and fevers may contribute to malnutrition in AIDS. The extent to which this malnutrition affects the underlying immune dysfunction occurring in the syndrome and the response to other more direct drug therapies in AIDS is not known. Available methods for nutritional intervention are based on clinical experience and anecdotal reports. Because of gastrointestinal disease, an oral diet, supplements, and enteral tube feedings may not meet nutritional goals for an AIDS patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parenteral nutrition in the management of gastrointestinal Kaposi's sarcoma in a patient with AIDS. 313 64

Malnutrition and growth failure are frequent complications of inflammatory bowel disease in childhood owing to inadequate dietary nutrient intakes, excessive intestinal losses, malabsorption, and increased nutrient requirements. Aggressive nutritional therapy is indicated for primary and supportive management of disease activity, drug nutrient interactives, individual nutrient abnormalities, and the overall complications of inflammatory bowel disease, malnutrition, and growth failure. The prevention of nutritional disorders in inflammatory bowel disease is accomplished by monitoring anthropometric and biochemical indices and by instituting appropriate enteral or parenteral nutritional therapy when indicated.
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PMID:Nutritional management of inflammatory bowel disease. 392 33

On the basis of the already proposed distinction between "normal" and "pathological" aggression in laboratory animals, it is essayed an integration of the experimental findings derived from a specific animal model of aggression with the available clinical information on human violent behavior. The too disregarded importance of the role played by the inhibitory control of brain functions, appears instead reportedly essential in the regulation of emotions and behavior, and is of great relevance in explaining the behavioral changes that follow induced or spontaneous impairment of the serotonergic system of the brain. As a matter of fact, the numerous evidences indicate that genetic predisposition and induced or acquired defects of serotonergic inhibitory control greatly concur to precipitate anomalous strong aggression. Interestingly, the cluster of symptoms presented by laboratory rats in consequence of the serotonergic discontrol, has many unexpected similarities with several pathological conditions of man. This fact confers to laboratory experiments the value of a tool aimed at a better understanding of the biological mechanisms which underlie corresponding alterations of human conduct, with special reference to pathological aggression and violence. In this line, some specific nutrient defects and/or malabsorption conditions can be important in the facilitation or elicitation of mental illness including human aggression. In addition, the efficacy and neurochemical action of those substances capable to partially or completely block or prevent experimental aggression, will likely assume equal relevance in the management or prevention of human violent behavior.
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PMID:Reflections on experimental and human pathology of aggression. 638 39

A Bull Terrier that was continuously chasing its tail was examined clinically, electroencephalographically, and by computed tomography of the head. The dog was also given test treatments with an anticonvulsant (diazepam) and a pure opioid antagonist (naloxone). The dog appeared to be hysterical and dissociated from its surroundings. Electroencephalography revealed a seizure pattern that was most marked over the temporal lobe, and computed tomography revealed mild hydrocephalus. Diazepam effectively controlled tail chasing, whereas naloxone did not. The dog was discharged on anticonvulsant therapy but subsequently had to be euthanatized when aggression developed. Results of examination and treatment have led the investigators to propose a hereditary mechanism for tail chasing, perhaps related to zinc malabsorption.
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PMID:Tail chasing in a bull terrier. 845 9

Patients with Crohn's disease are at high risk for recurrent disease and often undergo multiple operations. Our aims were to evaluate surgical management and outcome of patients with Crohn's disease who develop short bowel syndrome (SBS) and to identify factors leading to this complication. We reviewed the records of 170 adult patients with SBS evaluated over a 20-year period. Thirty (18%) had Crohn's disease. SBS was defined as an intestinal remnant less than 180 cm with associated malabsorption. There were 20 women and 10 men ranging in age from 18 to 62 years. Eighteen (60%) presented initially with ileocolonic disease, seven (23%) with colonic disease, and five (17%) with small intestinal disease. The interval from initial diagnosis to development of SBS ranged from 2 to 32 years, with 21 patients (71%) having an interval greater than 15 years. The number of resections leading to SBS varied from 2 to 12 with 24 patients (80%) having four or fewer resections. Nineteen patients (63%) had an ostomy. Small intestinal remnant length was less than 60 cm in 10 patients, 60 to 120 cm in six patients, and greater than 120 cm in 14 patients. Only one patient underwent stricturoplasty before developing SBS. Five patients were initially diagnosed as having ulcerative colitis and underwent a pouch procedure, which was subsequently resected. Twenty patients (67%) required parenteral nutrition. Three patients have undergone reversed intestinal segment to slow intestinal transit. Two patients underwent intestinal transplantation. Two patients have died: one from parenteral nutrition-related liver failure and the other after intestinal transplantation. Crohn's disease remains a common cause of SBS. Aggressive resectional therapy, surgical complications, and errors in initial diagnosis contribute to development of SBS in these patients. Selected patients are candidates for surgical therapy for SBS.
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PMID:Short bowel syndrome and Crohn's disease. 1467 17

A double scenario characterizes the epidemiology of HIV infection in children. In countries where highly active antiretroviral therapy (HAART) is available, the pattern of HIV infection is evolving into that of a chronic disease, for which control strictly depends on patients' adherence to treatment. In developing countries with no or limited access to HAART, AIDS is rapidly expanding and is loaded with a high fatality ratio, due to the combined effects of malnutrition and opportunistic infections. The digestive tract is a target of the disease in both settings. Opportunistic infections play a major role in children with severe immune impairment, with Cryptosporidium parvum being the leading agent of severe diarrhea. Several therapeutic approaches are effective in reducing fecal output, but the eradication of the parasite is rarely obtained. Other opportunistic infections may induce severe and protracted diarrhea, including atypical mycobacteria and cytomegalovirus. Diagnosis of diarrhea should be individually tailored based on presenting symptoms and risk factors. A stepwise approach is effective in limiting patient discomfort and minimizing the costs of investigations, starting with microbiologic investigation and proceeding with endoscopy and histology. Aggressive treatment of infectious diarrhea is required in severely immunocompromised children. However, antiretroviral therapy prevents the development of severe cryptosporidiosis. The liver and pancreas are also target organs in HIV infection, although functional failure is rare. The digestive-absorptive functions are impaired, with steatorrhea, nutrient malabsorption, and increased permeability occurring in 20-70% of children. Intestinal dysfunction contributes to growth failure and further immune derangement, leading to wasting, the terminal stage of AIDS. Nutritional management is crucial in HIV-infected children and is based on aggressive nutritional rehabilitation through enteral or parenteral routes and micronutrient supplementation.HIV may play a direct enteropathogenic role and is implicated in both diarrhea and intestinal dysfunction. This explains the efficacy of antiretroviral therapy in inducing remission of diarrhea and restoring intestinal function. Gastrointestinal side effects of antiretroviral drugs are increasingly observed; they are often mild and transient. Severe reactions are rare but require the withdrawal of drugs. In conclusion, severe enteric infections and intestinal dysfunction characterize the intestinal involvement of HIV infection. This is more common in, but not limited to, children who do not receive effective antiretroviral therapy. Diagnostic approaches include microbiologic and morphologic examinations and assessment of digestive processes, but immunologic and virologic data should be also carefully considered. Treatment is based upon specific anti-infectious drugs, antiretroviral therapy, and nutritional rehabilitation.
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PMID:Management of gastrointestinal disorders in children with HIV infection. 1561 36

Malnutrition leading to growth failure is one of the main problems in maintainig children with chronic liver diseases. The pathogenesis of malnutrition is complex and includes reduced calorie intake, fat malabsorption, impaired protein metabolism and increased energy expenditure. The nutritional status is an important risk factor for survival post liver transplantation. Aggressive nutritional support with careful monitoring is essential, particularly where liver transplantation is considered. When the oral nutrition is inadequate, the enteral feeding with nocturnal intragastric tube should be started. In case of gastrointestinal intolerance, severe malnutrition and gastrointestinal bleeding, parenteral nutrition should be considered.
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PMID:Nutrition in pediatric patients before liver transplantation. 1771 Oct 99

Cystic fibrosis (CF) is mostly recognized for its pulmonary morbidity, but the earliest manifestations of the disease are related to its gastrointestinal and nutritional derangements. Destruction of acinar pancreatic tissue, pancreatic ductular obstruction, and lack of enzymatic activity lead to malabsorption (particularly of fats), diarrhea, and failure to thrive. A minority of CF patients carrying milder CF transmembrane conductance regulator (CFTR) mutations have preserved pancreatic secretory activity and are free from significant malabsorption early in life. However, these patients are at risk for losing pancreatic function over time. Nutritional status plays an important role in the progression of the pulmonary disease in CF. Further, CF patients with better nutritional status have a survival advantage. Several factors contribute to impaired nutritional status in CF (e.g., pancreatic insufficiency, chronic malabsorption, recurrent sinopulmonary infections, chronic inflammation, increased energy expenditure, suboptimal intake). Progressive lung disease further increases calorie requirements by increasing the work of breathing. Treatment programs that place an emphasis on higher caloric intake and more aggressive nutritional management in CF patients report better outcomes. Basic tenets of nutritional repletion in CF include the use of pancreatic enzyme replacement therapy and following a high calorie, high protein, unrestricted diet. At the Stanford Cystic Fibrosis Center, nutritional status is assessed on an ongoing basis through anthropometric parameters and annual assessment of body composition, bone density, glucose tolerance, and various biochemical and micronutrient levels. Based on the anthropometric data obtained on routine clinical encounters, patients are categorized as to their nutritional risk. This proactive approach for the early identification of nutritional risk has become a major theme within the network of US CF centers. Aggressive nutritional support with adequate pancreatic replacement management should lead to both normal growth and lung function preservation. In addition, nutritional status has to be monitored closely during routine encounters to allow for early intervention once derangements are noted. This will include increasing calories in the early stages of lung disease and being vigilant of gastrointestinal symptomatology and complications.
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PMID:Nutrition in cystic fibrosis. 1976 May 45

Pancreatoduodenectomy is one of the most invasive and complex procedures in gastrointestinal surgery. Perioperative nutritional management, particularly enteral nutrition, is essential for patients undergoing pancreatoduodenectomy to attenuate postoperative complications and avoid progression of malnutrition due to surgical stress. Early enteral nutrition including immunonutrition via catheter jejunostomy is recommended from the viewpoint of protection from postoperative complications. If inadequate caloric administration via enteral nutrition alone cannot be achieved, combined enteral and parenteral nutrition is warranted. Postoperatively, feeding can potentially be started in the very early phase, similar to oral intake after gastrectomy. If adequate caloric administration cannot be achieved via enteral nutrition alone, combined enteral and parenteral nutrition is also warranted in the postoperative period. A fat-restricted diet is preferable if pancreatic exocrine function is disturbed due to accompanying or chronic pancreatitis and the deterioration of the remnant pancreatic preserve. Aggressive administration of commercially available pancreatic exocrine enzymes is recommended to prevent malabsorption of dietary lipids in the subacute and chronic stages after pancreatoduodenectomy. Oral supplementation of n-3 polyunsaturated fatty acids can be used in postoperative pancreatic cancer patients.
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PMID:[Nutritional management in pancreatoduodenectomy patients]. 2015 18

A desmoid tumor, also known as aggressive fibromatosis, is a rare benign neoplasm that arises from fascial or musculoaponeurotic tissues. It can occur in any anatomical location, most commonly the abdominal wall, shoulder girdle and retroperitoneum. The typical clinical presentation is a painless mass with a slow and progressive invasion of contiguous structures. It is associated with a high local recurrence rate after resection. Many issues regarding the optimal treatment of desmoid tumors remain controversial. Aggressive surgical resection with a wide margin (2-3 cm) remains the gold standard treatment with regard to preserving quality of life. Radiotherapy alone has been shown to be effective for the control of unresectable or recurrent lesions. Desmoid tumors tend to be locally infiltrative, therefore, the fields must be generous to prevent marginal recurrence. The radiation dose appropriate for treating desmoid tumors remains controversial. We present a 25-year-old Caucasian man with local recurrence of a desmoid tumor after repeated surgical resection, treated with radiotherapy. The patient achieved complete tumor regression at 4 mo after radiotherapy, and he is clinically free of disease at 12 mo after the end of treatment, with an acceptable quality of life. The patient developed short bowel syndrome as a complication of second surgical resection. Consequently, radiotherapy might have worsened an already present malabsorption and so led to steatohepatitis.
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PMID:An unusual case of fatty liver in a patient with desmoid tumor. 2279 54


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