Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Strongyloides stercoralis is endemic in the southwestern islands Amami and Ryukyu in Japan. Systemic strongyloidiasis occurs in immunocompromised hosts. We report here on a 60-year-old patient with minimal-change nephrotic syndrome (MCNS) without eosinophilia or HTLV-I infection. She was treated with corticosteroid for MCNS and died of disseminated strongyloidiasis. The patient developed systemic purpura, ileus, respiratory distress, malabsorption, pancytopenia, pulmonary hemorrhage and sepsis due to Escherichia coli before death. Massive infestation with Strongyloides stercoralis was disclosed by autopsy, and the larvae was considered as a pathomechanism or exacerbating agent of nephrotic syndrome in endemic areas.
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PMID:Disseminated strongyloidiasis in nephrotic syndrome. 1203 2

Strongyloides stercoralis infestation is common in the tropics and is usually asymptomatic. Patients with immunocompromised states may develop hyperinfection and fulminant disease. It has been suggested that bacteria accompany S. stercoralis during its passage across the bowel wall, resulting in systemic sepsis. Herein is a report on a 30-year-old man with S. stercoralis infestation and small bowel bacterial overgrowth presenting as malabsorption syndrome. He developed extensive duodenojejunal ulceration, septicemia and fatal hypokalemia. Blood and jejunal fluid grew Escherichia coli with the same antibiotic sensitivity patterns. This supports the hypothesis of migration of bacteria from the intestinal lumen as a cause of septicemia in patients with fulminant S. stercoralis infestation.
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PMID:Strongyloides stercoralis infestation associated with septicemia due to intestinal transmural migration of bacteria. 1242 82

Reactive arthritis is associated with demonstrable infection at a distant site without evidence of sepsis at the affected joint(s). We present a rare case reactive arthritis where no bacterial or chlamydial infections could be established, rather larvae of Strongyloides stercoralis could be demonstrated in the stool and duodenal biopsy. Reactive arthritis, psoriasiform lesions and malabsorption with hypoproteinaemia, responded to successful treatment with antihelminthic drugs. Early recognition and adequate treatment for gastrointestinal infections and infestations before complications is important.
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PMID:Reactive arthritis, psoriasiform lesions and protein loosing enteropathy secondary to Strongyloidiasis. 1272 57

Azathioprine is commonly prescribed for autoimmune hepatitis and inflammatory bowel disease. An acute gastroenteritis-like syndrome has been ascribed to azathioprine use, but chronic diarrhea has not. We report a patient with autoimmune hepatitis who developed severe small-bowel villus atrophy and chronic diarrhea after azathioprine was initiated (50 mg/day). We present a case report of a patient followed up prospectively. Duodenal mucosal histology and expression of brush border enzyme dipeptidyl peptidase IV and peptide transporter PepT1 messenger RNA levels were determined before and after azathioprine discontinuation. Chronic diarrhea developed several weeks after the initiation of azathioprine and resulted in micronutrient depletion and severe protein-calorie malnutrition, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet. Severe malabsorption required parenteral nutrition support for longer than 1.5 years; this was complicated by unstable blood glucose control, acute calculous cholecystitis, catheter sepsis, and severe venous thrombosis. When the temporal association between azathioprine and diarrhea was identified, the drug was tapered while the patient consumed an unrestricted diet. Within 2 weeks after azathioprine was discontinued, diarrhea had completely resolved, and parenteral nutrition was discontinued. Mucosal biopsies obtained before and 4 months after azathioprine discontinuation showed complete reversal of severe duodenal villus atrophy and marked up-regulation of mucosal dipeptidyl peptidase IV and PepT1 messenger RNA. The patient has subsequently maintained normal liver function tests on low-dose prednisone alone, with normal stools and stable nutritional status for longer than 4 years. Azathioprine can induce severe small-bowel villus atrophy, diarrhea, and malabsorption that is reversible with drug discontinuation.
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PMID:Severe villus atrophy and chronic malabsorption induced by azathioprine. 1280 28

Enteral nutrition (EN) is the preferred and safe route of feeding in surgical patients incapable of self-nutrition. We describe three patients with severe brain insult and recurrent sepsis, who despite the early introduction of EN, remained hypoalbuminaemic, hypoproteinaemic and developed peripheral oedema. This state persisted, despite increasing the caloric and protein intake via the enteral route. However, after a short course of supplemental parenteral nutrition (PN), albumin and total protein levels improved, with resolution of peripheral oedema. We hypothesize that, in certain critically ill neurosurgical patients on EN, gastrointestinal malabsorption may underlie a persistently low serum albumin, total protein and peripheral oedema. A short course of supplemental PN may help to reverse this and a normal regimen of EN can then be continued.
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PMID:The role of parenteral nutrition as a supplement to enteral nutrition in patients with severe brain injury. 1463 48

A primary small intestinal natural killer (NK) cell lymphoma with pathologic features of enteropathy but lack of association with celiac disease is reported. A 37-year-old man presented with tarry stool, coffee-ground vomitus, and mild fever. He did not have chronic diarrhea or malabsorption. Segmental resection of the duodenum and jejunum showed multicentric transmural infiltration by medium-sized lymphoma cells expressing CD3, CD8, cytotoxic granules, and Epstein-Barr virus by in situ hybridization. The nontumorous mucosa away from the main tumor revealed enteropathy with villous blunting and increased intraepithelial lymphocytes sharing the same immunophenotype as the lymphoma cells. Both lymphoma and nontumorous areas were germline for T-cell receptor-gamma and immunoglobulin heavy chain gene rearrangement. Serologic test by ELISA was negative for anti-transglutaminase. The patient died of repeated gastrointestinal bleeding and sepsis at 2 months. Differential diagnosis of this unique nasal-type NK-cell lymphoma with enteropathy-associated T-cell lymphoma is discussed.
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PMID:Natural killer cell lymphoma of small intestine with features of enteropathy but lack of association with celiac disease. 1513 43

Intestinal failure is characterised by inability of the intestine to absorb sufficient nutrients to maintain the integrity and function of the body. This can be caused by malabsorption due to too short an intestine or an abnormality of the mucosa, or by a severe motility disorder. In addition to dietary measures, the prescription of total parental nutrition (TPN) at home is sometimes necessary. This treatment is a burden on the patient and the risk of complications must be reduced to a minimum. The risks of long-term parenteral nutrition can be limited and the quality of the provision of services can be increased if the co-ordination is in the hands of a centre for home parenteral nutrition. In the Netherlands there are two centres for home-TPN: the St Radboud University Medical Centre in Nijmegen and the University Medical Centre (AMC) in Amsterdam. In both children and adults, the most common indications are the short bowel syndrome and motility disorders. However, the syndromes that cause this are clearly different in the different age groups. Parenteral nutrition can be given for long periods of time. A large variety of complications can occur, related especially to the equipment or the nutrients. When the nutrition is given via a central venous catheter, then sepsis is a serious and possibly life-threatening complication. In case of administration via an arteriovenous shunt, thrombosis of the shunt is the most frequent problem. If the treatment by means of home-TPN fails, then transplantation of the small intestine should be considered.
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PMID:[Treatment of intestinal failure by total parenteral nutrition at home in children and adults]. 1575 16

Pompe disease, a disorder caused by a deficiency in the lysosomal enzyme acid alpha glucosidase, is frequently overlooked as a cause of floppy baby syndrome. The accurate diagnosis of floppy baby syndrome requires the sequential evaluation of medical causes (e.g., hypothyroidism, sepsis, malnutrition, malabsorption, congenital heart disease), neurologic etiologies (central [cerebral] and peripheral [lower motor unit]) and anatomic characteristics of the abnormality. Cardiomegaly on chest x-ray in a patient with floppy baby syndrome should alert the pediatrician to suspect Pompe disease. Based on this finding, further work-up or referral to a specialist can be considered. Pompe disease requires immediate attention. Symptomatic intervention of this disorder should be initiated at the earliest time possible to maximize the potential benefit from therapy and to prevent irreversible organ damage. Moreover, early diagnosis is important for providing parents with realistic information about their child's prognosis, and where appropriate, professional genetic counseling. Enzyme replacement therapy (ERT) with recombinant human GAA is currently being evaluated in clinical trials; the future availability of this option makes early identification of this condition even more critical. This article presents a unified view on the optimal approach to the accurate diagnosis of Pompe disease and to its recognition as one of the possible and treatable causes of floppy baby syndrome.
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PMID:Diagnostic challenges for Pompe disease: an under-recognized cause of floppy baby syndrome. 1670 78

Intestinal failure is a specific disease entity resulting from intestinal resection or disease-associated malabsorption and characterized by the inability to maintain protein-energy, fluid, electrolyte or micronutrient balance. We performed a MEDLINE search (1966-2006) to identify relevant articles, using keywords intestinal failure, parenteral or enteral nutrition, intestinal fistula and short bowel syndrome. Causes of intestinal failure are varied, with self-limiting or 'Type 1' intestinal failure occurring relatively commonly following abdominal surgery, necessitating short-term fluid or nutritional support. The rarer, 'Type 2' intestinal failure, is associated with septic, metabolic and complex nutritional complications, usually following surgical resection in patients with Crohn's or mesenteric vascular disease. A multidisciplinary approach to the management of patients with Type 2 intestinal failure is crucial: resolution of sepsis is required before adequate nutritional repletion can be achieved, and it is important to optimize nutritional status, not only through enteral or parenteral supplementation, but also by addressing complications of short bowel syndrome, before considering definitive surgical reconstruction. A structured approach to the management of Type 2 intestinal failure should reduce the likelihood of these complex patients developing 'Type 3' intestinal failure, which is characterized by the need for long-term parenteral nutrition.
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PMID:Review article: intestinal failure. 1680

This article presents a case study of a newborn with gastroschisis, followed by a retrospective analysis of gastroschisis cases admitted in a single tertiary neonatal intensive care unit over a 5-year period in terms of maternal age, prenatal diagnosis, type of repair, length of stay, and complications. Gastroschisis is an abdominal wall defect resulting from ischemia to blood vessels that supply the abdominal wall during the first trimester of pregnancy. The injury results in an opening in the abdominal wall that allows the abdominal contents, most often intestines and stomach, to develop outside the abdominal cavity. The incidence of gastroschisis is rising, primarily in young mothers aged 20 years or younger. Environmental factors including medication use and nutrition are proposed mechanisms for this association. Surgical management includes techniques for primary repair in which the intestinal contents are immediately closed inside the abdomen, or staged repair if the abdominal cavity is not able to accommodate the volume of intestine. Exposure of the fetal intestine to amniotic fluid can cause inflammation and damage, and significant gastrointestinal problems occur during the neonatal period after closure of the defect. Complications include prolonged ileus, sepsis, associated intestinal atresias, malabsorption, wound infection, and necrotizing enterocolitis.
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PMID:Gastroschisis: incidence, complications, and clinical management in the neonatal intensive care unit. 1730 69


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