Gene/Protein Disease Symptom Drug Enzyme Compound
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Forty-five patients with proved gastrointestinal amyloidosis were examined to study the clinical and pathological features and to determine the correlation with amyloid fibril proteins. The examinations included physical examination, laboratory study, plain X-ray film of the abdomen, gastrointestinal radiography, gastrointestinal endoscopy, endoscopic biopsy, surgery, and autopsy. The results were as follows: 1) Amyloid fibril proteins consisted of amyloid light chain protein (AL) in 7 patients, amyloid A protein (AA) in 36, beta 2-microglobulin (AH) in one, and prealbumin (AF) in one. 2) At the time of examination, gastrointestinal symptoms were present in 43 (96%) of the 45 patients. The incidence of diarrhea and gastrointestinal bleeding was higher in patients with the AA type than in those with other types, whereas abdominal distension, nausea, and vomiting were more frequently evident in patients with the AL type. 3) The incidence of hypoalbuminemia, hypokalemia, and positive occult blood was higher in patients with the AA type, whereas abnormal electrocardiogram and cardiac failure were more frequently observed in patients with the AL type. The thyroid gland was enlarged in 7 patients with the AA type, and the macroglossia was evident in only 2 patients with the AL type. 4) The frequency of radiographic abnormalities in the gastrointestinal tract was as follows: 79% of the patients in the jejunum and ileum, 61% in the duodenum, 53% in the stomach, 32% in the colorectum, and 14% in the esophagus. Fine granular shadows were most frequently seen in patients with the AA type, whereas multiple polypoid protrusions and thickening of the folds were characteristic in patients with the AL type. 5) Endoscopic abnormalities were found as follows: 82% in the duodenum, 81% in the jejunum, 73% in the stomach, 42% in the colorectum, and 20% in the esophagus. Endoscopy revealed fine granular appearance in 31 (86%) of the 36 patients with the AA type, whereas multiple polypoid protrusions and thickening of the folds were evident in 5 (71%) of the 7 patients with the AL type. 6) On the histological examination of the biopsy specimens, amyloid deposition was found in the duodenum in 98% of the 45 patients studied, in the jejunum in 96% of the 26 patients, in the antrum in 93% of the 41 patients, and in the rectum in 86% of the 43 patients. 7) Histological findings of the biopsy and autopsy specimens revealed that the the degree of amyloid deposition was the highest in the duodenum and jejunum of the gastrointestinal tract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Diagnosis of gastrointestinal amyloidosis with special reference to the relationship with amyloid fibril protein]. 178 55

Eleven patients with rheumatoid arthritis that had been refractory to conventional drug therapy were treated with total lymphoid irradiation (TLI). Followup continued for 6 months in 9 patients, 12 months in 6 patients, and 24 months in 3 patients. At 6 and 12 months post-TLI, a significant improvement in clinical disease activity was demonstrated. Side effects noted during TLI included fatigue, nausea, diarrhea, and vomiting. One patient died of cardiorespiratory arrest, 2 patients died of kidney failure secondary to generalized amyloidosis, and 1 patient died of septic shock secondary to a multilocular septic arthritis. One patient experienced 2 episodes of septic arthritis; 2 patients manifested delayed wound healing. Immunologic assessments showed consistent lymphopenia in all patients. T lymphocyte subsets decreased after TLI, and showed a transient increase at 6 months post-TLI. The suppressed mitogen responsiveness, which was noted 2 months after irradiation, was found to increase almost to the pre-TLI levels at 12 months. The observed increase in morbidity and mortality after TLI is evidence that discourages the use of this therapeutic technique, at least in its present form.
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PMID:Total lymphoid irradiation in patients with refractory rheumatoid arthritis. 293 45

Intestinal pseudo-obstruction (IP) is an uncommon disorder of gut motility which must be differentiated from mechanical intestinal obstruction. We have seen 11 such patients over the last 5 years. Characteristic symptoms, shared by mechanical obstruction, include abdominal distention and pain, nausea, and vomiting. Radiologic studies reveal dilated loops of bowel with air fluid levels. In most patients a major differentiating feature from obstruction may be the presence of diarrhea rather than obstipation. Steatorrhea is secondary to an overgrowth of anaerobic bacteria in the motionless dilated loops of bowel. IP has been associated with various disorders: in our series two patients had scleroderma, one multiple small bowel diverticula, one systemic amyloidosis, one celiac disease, and one spinal cord injury; in only two patients was the disorder considered "idiopathic." Three patients had previously undergone a jejuno--ileal bypass for morbid obesity. During the acute episode, the patients were treated symptomatically with decompression by nasogastric or rectal tube with fluid and electrolyte replacement. Malabsorption treated with broad spectrum antibiotics reversing the steatorrhea but not episodes of pseudo-obstruction. Magnesium deficiency was present in seven patients and its correction resulted in amelioration of the symptom complex. In two patients episodes of pseudo-obstruction were markedly reduced by metoclopramide which was not effective in two others.
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PMID:Chronic intestinal pseudo-obstruction. 679 59

Continuous oral dimethylsulphoxide (DMSO) treatment (7-15 g/day) was given to 3 patients with amyloidosis of familial Mediterranean fever (FMF), 3 patients with idiopathic amyloidosis, and 7 patients with secondary amyloidosis. The nephrotic syndrome and various degrees of renal insufficiency were the major clinical manifestation in all case. Renal function was used as the main parameter for evaluation of therapy. DMSO treatment for 7-16 months produced no effect in the FMF patients and in the patient with idiopathic amyloidosis; they all ran the predictable clinical course of their disease and either died of cardiac failure or have been maintained on chronic haemodialysis. In the 7 patients with secondary amyloidosis an unequivocal improvement of renal function was observed following 3-6 months of DMSO treatment. It was shown by a 30-100% rise of creatinine clearance and a decline in proteinuria. This new equilibrium has been maintained as long as DMSO was administered. No serious side effects of DMSO wee encountered. Mild nausea and an unpleasant breath odour were the patients' main concern. We conclude that a therapeutic trial with oral DMSO is warranted in all patients with secondary amyloidosis. This treatment is unpleasant but bears no exceptional risks. It may significantly prolong life, though its effect on amyloid deposits themselves is doubtful.
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PMID:Prolonged dimethylsulphoxide treatment in 13 patients with systemic amyloidosis. 714 95

A 67 years old man was admitted on July 1979 for nausea, dysphagia and rectal pain. At age 64 he had undergone radiotherapy on the lower lip for an epidermoid carcinoma. He remained then healthy. His medical history was negative with the exception of chronic bronchitis. He had never been exposed to toxic agents or drugs and had never left Europe. A few days after admission he suffered acute intestinal obstruction but at laparostomy no etiology was found. At the same time the patient complained of pain in all four limbs and he was found to have diffuse wasting of muscles, areflexia and distal sensory loss. No sign of dysautonomia was present. Physical examination was negative with the exception of a cervical lymphadenopathy. The lymph node biopsy showed an undifferentiated metastatic carcinoma. Negative investigations included: blood cells count; serum ionogram and immunoelectrophoresis; thyroid function tests; serological test for Chagas' disease. The following abnormalities were found: ESR: 55-105; CSF protein: 145 mg/100 ml and 1 cell mm3; whole blood folic acid: 1,7 mg/ml; Hbs antigen was present in blood; EMG showed evidence of denervation but motor conduction velocities were normal. By September the patient's weakness had increased and complete intestinal obstruction persisted. At oesophageal, gastric and duodenal fibroscopy no contraction was visible, and biopsies were negative. The patient died of peritonitis on October 5th, 1979. At necropsy peritonitis secondary to multiple perforation of the large bowel was found. No recurrence of the lip carcinoma or metastase or evidence of a primary carcinoma was found. Light microscopy showed no evidence of amyloidosis or scleroderma. Examination of the alimentary tract showed abnormalities restricted to the myenteric plexuses which varied from one level to another. In the small bowel there was hyperplasia of the smooth muscle and the myenteric plexuses were enlarged by marked proliferation of Schwann cells. Severe neuronal loss and nodules of Nageotte were also noted. Schwann cells proliferation was less marked in the stomach and large bowel. Lympho-histiocytic infiltration strictly confined to the region of the myenteric plexuses was present in oesophagus, stomach, large bowel and rectum. Mild chronic inflammatory lesions were also found in anterior and posterior spinal roots and semi-lunar ganglia. The striking feature of this case is the association of an undifferentiated carcinoma and a polyradiculoneuritis with a complete alimentary tract palsy of rapid onset, secondary to lesions restricted to the myenteric plexuses. The low folate level was insufficient to explain the neuropathy. Investigations showed no evidence of the usual causes of intestinal pseudo-obstruction: muscular, dysautonomic, toxic, plexic (idiopathic, familial, inflammatory), Chagas' disease). The clinical course, the pathological pictures of the alimentary tract and spinal roots and the association with a carcinoma suggest that our case may represent a paraneoplastic syndrome...
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PMID:[Paralysis of digestive tract with lesions of myenteric plexuses. A new paraneoplastic syndrome (author's transl)]. 729 42

We herein report two cases of gastrointestinal amyloidosis, secondary to juvenile rheumatoid arthritis (JRA) in one, and rheumatoid arthritis (RA) in the other. A 21-year-old woman, who has been suffering from JRA for the past 12 years, was transferred to our hospital due to intense pain in the epigastrium and back, diarrhea, high fever, and paralytic ileus. Treatment by corticosteroid, antibiotics, protease inhibitor, and total parenteral nutrition was not effective. The laparoscopic surgery was performed because of repeated melena followed by an episode of hypovolemic shock. The resected specimen of the ileum showed histologically marked amyloid deposition in the arteriolar walls. A 83-year-old man with RA for 14 years, was admitted to our hospital with complaints of abdominal pain, nausea, and diarrhea. He underwent an emergency operation for perforation of the ileum. The resected specimen revealed amyloid deposition and non-caseating granulomas. The fragility and impaired blood supply caused by amyloid deposition in the vascular walls may have terminated in the severe intestinal lesion. Further clinicopathological studies along this line are keenly desired in order to establish therapeutic modalities for gastrointestinal amyloidosis.
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PMID:[Amyloidosis of the small intestine secondary to rheumatoid arthritis and juvenile rheumatoid arthritis: report of two cases]. 773 82

We studied the results of renal transplantation in 16 patients with renal amyloidosis and in 46 controls with primary glomerulonephritis. Amyloidosis was primary in five and secondary to familial Mediterranean fever (FMF) in 11. All patients received live related donor kidneys and the majority had one-haplotype HLA match. One- and 5-year graft and patient survival rates were comparable in both groups. Moreover, the frequency of acute rejection episodes and the mean serum creatinine values were not significantly different between members of the two groups. Significant gastrointestinal symptoms in the form of nausea, vomiting, abdominal pains, and diarrhoea occurred in seven of the patients with amyloidosis (43.7%) and in only one of the controls (2%) (P = 0.001). All seven recipients with amyloidosis who developed the gastrointestinal manifestations were receiving cyclosporin and six had FMF. Maintenance colchicine treatment prevented recurrence of FMF symptoms. In one patient discontinuation of colchicine was followed by recurrence of FMF symptoms. Recurrence of renal amyloidosis was not observed in five patients subjected to Trucut graft biopsies 1, 2, 3, 18 and 72 months post-transplantation. It is concluded that live-related donor kidney transplantation is a safe procedure in patients with amyloidosis and follows a course similar to glomerulonephritis patients.
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PMID:Study of live donor kidney transplantation outcome in recipients with renal amyloidosis. 797 Jan

A 63-year-old woman who started to have polyarthralgia in December 1993 has been diagnosed as rheumatoid arthritis (RA) and treated with muscular injection of gold sodium thiomalate. She began to have nausea, vomiting, anorexia and watery diarrhea in October 1995. A year later, she had to receive intravenous infusion on admission since more frequent watery diarrhea occurred more than ten times within a day. On admission in our hospital in December 1996, she had proteinuria in addition to gastrointestinal symptoms. The biopsy specimen from stomach, duodenum and kidney proved systemic amyloidosis associated with RA. In spite of steroid-pulse, dimethyl sulfoxide (DMSO) and colchicine therapy, profound proteinuria in nephrotic syndrome was continued in association with hypoproteinemia, anasarca and renal failure. She was treated on hemodialysis and intravenous hyperalimentation (IVH) until November 1997 when A-V shunt operation on left forearm was performed. However, the shunt was not available for HD and she suffered from septicemia and died on December 1997. This patient was a rare case of secondary systemic amyloidosis associated with RA in early clinical course.
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PMID:[A case of secondary systemic amyloidosis associated with rheumatoid arthritis after 3-year disease duration]. 1033 14

Dialysis-related amyloidosis (DRA) is one of the most serious complications interfering with rehabilitation in dialysis patients. Here, we report a case of beta2-microglobulin (beta2M)-related amyloidosis, in which the patient developed a severe intestinal pseudo-obstruction. The patient was a 42-year-old male who had been undergoing hemodialysis for 13 years, and who had no history of osteoarticular involvement of DRA. The first symptoms of the disease were severe abdominal fullness and nausea after meals. The whole intestinal wall biopsy revealed massive amyloid deposition in the propria muscularis. The patient became malnourished and died of acute subendocardial infarction 3 years after the onset. An autopsical examination revealed a massive deposition of amyloid, which was positively stained with anti-beta2M antibody but not AA amyloid, predominantly in the gastrointestinal muscular layer, including the tongue, esophagus, stomach, small intestines, colon, and rectum. These results suggest that the gastrointestinal involvement of beta2M-related amyloidosis might occur during the course of hemodialysis treatment, and that this possibility should be considered if patients suffer from intestinal pseudo-obstruction without osteoarticular symptoms.
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PMID:Chronic intestinal pseudo-obstruction due to dialysis-related amyloid deposition in the propria muscularis in a hemodialysis patient. 1130 14

Familial amyloidotic polyneuropathy (FAP), Portuguese type, is a hereditary amyloidosis caused by mutated transthyretin (ATTR) in which an exchange of valine for methionine at position 30 has taken place (ATTR Val30Met). Gastrointestinal complications, such as nausea, diarrhoea and malabsorption, have a significant impact on survival since the cause of death in the majority of cases is a consequence of extreme malnutrition due to dysmotility of the gastrointestinal tract. Recently, a role of the receptor for advanced glycation end products (RAGE) has been implicated in amyloid toxicity. Transthyretin (TTR) amyloid fibrils have been shown to have affinity for RAGE and subsequently induce NF-kappaB activation and apoptosis. Since gastrointestinal dysfunction plays an important role in FAP, we wanted to investigate if amyloid toxicity in the gastrointestinal tract is related to RAGE, NF-kappaB activation and apoptosis. Gastrointestinal tract autopsy samples were studied for the distribution of amyloid, RAGE, advanced glycation end products (AGE) and NF-kappaB. Furthermore, we examined the immunoreactivity of an apoptotic marker to investigate if an apoptotic pathway contributes to amyloid toxicity. The distribution of RAGE and AGE strongly correlated to that of amyloid deposits. Sequential immunofluorescence staining revealed a clear relationship between TTR, AGE and RAGE. No correlation between NF-kappaB, apoptotic marker and amyloid deposits was found. We conclude that RAGE-AGE or RAGE-TTR interaction might play important roles for gastrointestinal dysfunction and amyloid toxicity, although not through NF-kappaB activation and apoptosis.
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PMID:Advanced glycation end products (AGE) and the receptor for AGE are present in gastrointestinal tract of familial amyloidotic polyneuropathy patients but do not induce NF-kappaB activation. 1241 Mar 91


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