Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Problems in the management of abdominal tuberculosis are discussed with reference to 300 surgically verified cases. The protean clinical manifestations depend on the site and extent of the disease, and its complications. Operation was resorted to for complications when diagnosis was in doubt and when intrinsic intestinal disease was proved. Surgery was preceded by antituberculous drugs whenever possible. At operation, the disease was found to involve the alimentary canal in 196 cases; in the remaining 104, only the lymph nodes and/or the peritoneum were affected. Intestinal resection was carried out in 100 cases. Emergency surgery carries a high mortality (18/76) because of toxemia, hypoproteinemia, anemia, etc. Positive histology was obtained in 229 cases. One hundred and seventy-nine cases showed evidence of caseation. Caseation and peritoneal tubercles (103 cases) differentiate intestinal tuberculosis from Crohn's disease. Despite considerable progress made in therapy and prophylaxis during the last quarter of the century, tuberculosis of various sites continues to be a major health hazard in India. The precise prevalence of Koch's disease of the abdomen has not been determined due to lack of a survey in random samples of population. This common malady, however, with its protean profiles and varied complications continues to challenge the diagnostic acumen and therapeutic skill of clinicians practicing various discplines of medicine.
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PMID:Abdominal tuberculosis. Experiences with 300 cases. 87 48

Twelve patients who underwent laparotomy for suspected acute appendicitis were found to have Crohn's disease of the terminal ileum. Appendectomy was performed in all although in only four patients was the appendix grossly inflamed. Postoperative complications, either abscess or fistula, developed in four patients (33%). Careful investigation of the records revealed some preoperative diagnostic clues: a history of recurrent abdominal pain and/or diarrhea (83%), physical examination revealing normal temperature (50%), and laboratory results compatible with a chronic process such as microcytic anemia (33%) and hypoproteinemia/hypoalbuminemia/hypocholesterolemia (50%). As the differential diagnosis between Crohn's disease and appendicitis is difficult and the surgical approach to the appendix in the presence of Crohn's disease is controversial, we illuminate some practical points in the preoperative evaluation of these patients and deal with the question of whether appendectomy should be performed in these patients.
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PMID:Preoperative clues to Crohn's disease in suspected, acute appendicitis. Report of 12 cases and review of the literature. 129 36

A female patient with Crohn's disease was assessed by laboratory evaluation for multiple sclerosis. Because of her hypoproteinemia, she was given an albumin infusion, which caused immunoglobulin concentrations to fall below the normal limit. Based on a cerebrospinal fluid (CSF) sample drawn after infusion, she was found to have an abnormally high IgG index and a high intrathecal IgG synthesis rate. However, clinical correlations ruled out demyelinating disease. Various equations used for the calculation were examined and found to yield false positive results with values of serum IgG below the reference range. Only the Ohman formula provided the correct prediction in this patient. Although hypo- or hyper-albuminemia have little effect on these equations, they may escalate the impact of hypoimmunoglobulinemia. Thus, interpretation of laboratory data under these conditions must be exercised with care.
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PMID:Effect of hypoimmunoglobulinemia on laboratory evaluation of multiple sclerosis. 151 21

We report an unusual case of Crohn's disease. Our subject, a 43-yr-old lady, presented with severe iron deficiency anemia, hypoproteinemia and lymphocytopenia, but without any clinical manifestations of Crohn's disease either at presentation or during follow-up. She had recurrent episodes of severe iron deficiency anemia, repeatedly requiring blood transfusions (28 units in 20 months). She was found to have a short stricture with ulceration in the ileum due to Crohn's disease, and a blind loop with bacterial overgrowth above it. Resection of the affected area prevented further recurrence of anemia and corrected hypoproteinemia. We postulate that her anemia and hypoproteinemia were due to blood and protein (lymph) loss from the ulcerated area in the ileum. Such a presentation has not been described before.
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PMID:Atypical presentation of Crohn's disease: severe, recurrent iron deficiency anemia dependent on blood transfusions. 827 77

Protein-losing enteropathy (PLE) is a rare but severe complication of Crohn's disease (CD) and hypoalbuminemia can be one of the presenting symptoms of this illness. The diagnosis of PLE can only be made after exclusion of malnutrition and liver or kidney failure. Significant intestinal leakage can be caused by mucosal injury, increased lymphatic pressure or dilated lymphatics and has been reported in a large number of diseases. The protein-losing can be diagnosed by assessing the excretion of different radiolabeled macromolecules in the faeces or by the clearance of alpha-1-antitrypsine in stools. The primary approach should be the optimization of the nutritional status. Medical treatment of the underlying disease is primordial. In other cases surgical resection of the most affected areas is inevitable. We report a case of a 21-year-old male with a 4 year history of CD, who developed significant hypoproteinemia with pitting oedema, initially in the absence of any other sign of severe disease activity. A "Cr-chloride albumin excretion confirmed our hypothesis of protein-losing enteropathy. Because of sub-obstruction signs some months later, a laparotomy was performed which revealed a severely affected loop with dilatation of the proximal jejunum. Interestingly, multiple large lymph nodes and dilated lymphatics were seen. A partial jejunal resection was performed for stricturing Crohn's disease. Histology showed severe mesenteric granulomatosis, dilated lymph vessels and granulomatous vasculitis. After the resection our patient improved without further albumin infusions and the oedema resolved.
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PMID:Protein-losing enteropathy in Crohn's disease. 1734 81

Intestinal lymphangiectasia in the adult may be characterized as a disorder with dilated intestinal lacteals causing loss of lymph into the lumen of the small intestine and resultant hypoproteinemia, hypogammaglobulinemia, hypoalbuminemia and reduced number of circulating lymphocytes or lymphopenia. Most often, intestinal lymphangiectasia has been recorded in children, often in neonates, usually with other congenital abnormalities but initial definition in adults including the elderly has become increasingly more common. Shared clinical features with the pediatric population such as bilateral lower limb edema, sometimes with lymphedema, pleural effusion and chylous ascites may occur but these reflect the severe end of the clinical spectrum. In some, diarrhea occurs with steatorrhea along with increased fecal loss of protein, reflected in increased fecal alpha-1-antitrypsin levels, while others may present with iron deficiency anemia, sometimes associated with occult small intestinal bleeding. Most lymphangiectasia in adults detected in recent years, however, appears to have few or no clinical features of malabsorption. Diagnosis remains dependent on endoscopic changes confirmed by small bowel biopsy showing histological evidence of intestinal lymphangiectasia. In some, video capsule endoscopy and enteroscopy have revealed more extensive changes along the length of the small intestine. A critical diagnostic element in adults with lymphangiectasia is the exclusion of entities (e.g. malignancies including lymphoma) that might lead to obstruction of the lymphatic system and "secondary" changes in the small bowel biopsy. In addition, occult infectious (e.g. Whipple's disease from Tropheryma whipplei) or inflammatory disorders (e.g. Crohn's disease) may also present with profound changes in intestinal permeability and protein-losing enteropathy that also require exclusion. Conversely, rare B-cell type lymphomas have also been described even decades following initial diagnosis of intestinal lymphangiectasia. Treatment has been historically defined to include a low fat diet with medium-chain triglyceride supplementation that leads to portal venous rather than lacteal uptake. A number of other pharmacological measures have been reported or proposed but these are largely anecdotal. Finally, rare reports of localized surgical resection of involved areas of small intestine have been described but follow-up in these cases is often limited.
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PMID:Intestinal lymphangiectasia in adults. 2136 42

Amyloidosis is a clinical entity that results from deposition of an extracellular protein material that causes disruption in normal architecture and impairs function of multiple organs and tissues. Secondary amyloidosis (AA) is a rare but serious complication that occurs in the context of cancer, chronic inflammation and chronic infectious diseases, including inflammatory bowel disease, mainly long-standing Crohn's disease. Renal failure is the most common clinical presentation of AA, ranging from nephrotic syndrome and impaired renal function to renal failure, with a potential for high morbidity. The incidence of the association of secondary amyloidosis in patients with Crohn's disease has been reported to be 0.5%-8%. We present a case of a 39-year-old male patient diagnosed with Crohn's disease at age 21 and submitted to right hemicolectomy because of ileus 17 years before. Thereafter, he was treated with corticosteroids for 15 years and with azathioprine for a short period; in the last three years he was on therapy with mesalazine alone. He was hospitalized due to worsening clinical condition and re-evaluation of the underlying disease. Physical examination revealed marked peripheral edema in both lower extremities. Endoscopic and radiographic examinations confirmed the underlying disease activity. Laboratory tests showed an increase of inflammatory reactants, anemia, hypocalcemia, and severe hypoalbuminemia and hypoproteinemia. He had proteinuria over 24 g/L and creatinine clearance of 66 mL/min, falling within second grade of chronic kidney disease. Renal biopsy was performed for evaluation of renal insufficiency with nephrotic range proteinuria. Congo red staining showed the presence of characteristic amyloid deposition; deposits immunoreacted with the antibody against amyloid A protein, confirming the diagnosis of secondary amyloidosis. The patient was suggested active induction treatment with corticosteroids and azathioprine to achieve remission of Crohn's disease, thereafter treatment with infliximab, but he did not consent with this therapy at that time. Studies with infliximab have demonstrated a decrease in SAA circulating levels and proteinuria, as well as stabilization of renal function. Amyloidosis is frequently described as a major cause of death in patients with Crohn's disease, with long-term mortality between 40% and 60%. Various therapeutic attempts such as azathioprine, colchicine, dimethyl sulfoxide, infliximab, and elemental diets have been tried but there is no definite treatment for secondary amyloidosis in Crohn's disease. Kidney transplantation may offer the best prospects for patients with Crohn's disease who develop amyloidosis and end-stage renal failure.
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PMID:[Secondary (AA) amyloidosis in Crohn's disease]. 2235 96

The objective of this article is to report improvement of nutritional status by protein supplements in the patient with protein-losing enteropathy. The patient was a female whose age was 25 and underwent medical treatment of Crohn's disease, an inflammatory bowl disease, after diagnosis of cryptogenic multifocal ulcerous enteritis. The weight was 33.3 kg (68% of IBW) in the severe underweight and suffered from ascites and subcutaneous edema with hypoalbuminemia (1.3 g/dL) at the time of hospitalization. The patient consumed food restrictively due to abdominal discomfort. Despite various attempts of oral feeding, the levels of calorie and protein intake fell into 40-50% of the required amount, which was 800-900 kcal/d (24-27 kcal/kg/d) for calorie and 34 g/d (1 g/kg/d) for protein. It was planned to supplement the patient with caloric supplementation (40-50 kcal/kg) and protein supplementation (2.5 g/kg) to increase body weight and improve hypoproteinemia. It was also planned to increase the level of protein intake slowly to target 55 g/d in about 2 weeks starting from 10 g/d and monitored kidney load with high protein supplementation. The weight loss was 1.0 kg when the patient was discharged from the hospital (hospitalization periods of 4 weeks), however, serum albumin was improved from 1.3 g/dL to 2.5 g/dL and there was no abdominal discomfort. She kept supplement of protein at 55 g/d for 5 months after the discharge from the hospital and kept it at 35 g/d for about 2 months and then 25 g/d. The body weight increased gradually from 32.3 kg (65% of IBW) to 44.0 kg (89% of IBW) by 36% for the period of F/u and serum albumin was kept above 2.8 g/dL without intravenous injection of albumin. The performance status was improved from 4 points of 'very tired' to 2 points of 'a little tired' out of 5-point scale measurement and the use of diuretic stopped from the time of 4th month after the discharge from the hospital owing to improvement in edema and ascites. During this period, the results of blood test such as BUN, Cr, and electrolytes were within the normal range. In conclusion, hypoproteinemia and weight loss were improved by increasing protein intake through utilization of protein supplements in protein-losing enteropathy.
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PMID:A case of protein supplement effect in protein-losing enteropathy. 2343 Mar 93

Protein-loosing enteropathy in patients with inflammatory bowel diseases (IBDs) is an uncommon complication, but should be considered in any patient with hypoproteinemia in whom other causes have been excluded such as concomitant hepatic disease, severe malnutrition or proteinuria. The diagnosis is based on determination of fecal alpha-1 antitripsin clearance and stool analysis. Prognosis depends upon the patient and the disease location, severity and complication. Treatment is directed at control of the underlying IBDs but also includes albumin infusion in the most severe cases of hypoalbuminemia and fluid retention, dietary modifications for recovery and maintenance of nutritional status and supportive care to prevent further complication like deep venous thrombosis. Surgery is not curative in Crohn's disease patients, but in severe protein-loosing enteropathy with severe disease, not responding to conventional therapy, it may be the best choice.
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PMID:Protein-losing enteropathy in inflammatory bowel diseases. 2644 87

Duodenal injury is a serious abdominal organ injury. Duodenal fistula is one of the most serious complications in gastrointestinal surgery, which is concerned for its critical status, difficulty in treatment and high mortality. Thoracic and abdominal compound closed injury and a small part of open injury are common causes of duodenal injury. Iatrogenic or traumatic injury, malnutrition, cancer, tuberculosis, Crohn's disease etc. are common causes of duodenal fistula, however, there has been still lacking of ideal diagnosis and treatment by now. The primary treatment strategy of duodenal fistula is to determine the cause of disease and its key point is prevention, including perioperative parenteral and enteral nutrition support, improvement of hypoproteinemia actively, avoidance of stump ischemia by excessive separate duodenum intraoperatively, performance of appropriate duodenum stump suture to ensure the stump blood supply, and avoidance of postoperative input loop obstruction, postoperative stump bleeding or hematoma etc. Once duodenal fistula occurs, a simple and reasonable operation can be selected and performed after fluid prohibition, parenteral and enteral nutrition, acid suppression, enzyme inhibition, anti-infective treatment and maintaining water salt electrolyte and acid-base balance. Double tube method, duodenal decompression and peritoneal drainage can reduce duodenal fistula-related complications, and then reduce the mortality, which can save the lives of patients.
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PMID:[Diagnosis and treatment of duodenal injury and fistula]. 2833 58


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