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PubMed1985

[Patient with familial Mediterranean fever and amyloidosis].

A patient is described, with genetic form of amyloidosis with family Mediterranean fever. The secondary amyloidosis, that developed as a complication, has been preceded by attacks of acute articular and abdominal pains of several years. Elevated level of ethicholanolon in urine was established as well as extremely high values of serum fibrinogen, admitted to be pathognomonic signs of family Mediterranean fever. The eposition of amyloidosis is confirmed via rectal and renal punch biopsy. In spite of the diffuse character of the deposited amyloid in the renal tissue, there were still no signs of glomerular sclerosis and clinicalf--normal depuration renal function was observed, with normal creatinine clearance and normal nitrogenous bodies in serum. A favourable effect of colchicine therapy was observed in the patients both as regards the acute attacks of the disease and as regards the renal involvement.

Adult↗
PubMed1965

Amyloidosis in captive anseriformes.

During the period 1945-1962, percentage deaths of anserine birds (ducks, geese and swans) did not vary remarkably from year to year even though the population has more than quadrupled during the same period. The number of deaths with amyloidosis has increased significantly even though the death rate did not change. The number of deaths due to tuberculosis, mould, renal diseases, hepatitis and infection accompanied by amyloidosis also increased, especially during the second half the study period. Cases of known secondary amyloidosis accounted for 71.4% whereas 28.6% of the remaining cases were classified as "doubtfully" primary. Sites of deposition amyloid in the two categories were the same and it has never been observed in the heart. The amyloid deposits in the birds did not differ from those in man when examined by number of histochemical methods.

Amyloidosis↗
PubMedDate not supplied

Amyloidosis in Reiter's syndrome.

A patient with a 27-year-history of chronic relapsing Reiter's syndrome who developed secondary amyloidosis is described. While there are only 2 reports of this association in the English literature, additional cases are suggested in the light of our present concepts. The patient represents the only case of clinically apparent secondary amyloidosis among 158 patients with HLA B27 associated arthropathies currently followed at our institution. Our patient's amyloidosis was treated for nearly 1 year with colchicine without response.

Adult↗
PubMed1980

Rapidly progressive glomerulonephritis and possible amyloidosis.

In two patients with crescentic glomerulonephritis, coexistence of amyloidosis was considered. In one, electron microscopy failed to show amyloid fibrils despite positive staining and history suggestive of amyloidosis. Glomeruli of the second patient contained amyloid-like fibrils in absence of clinical amyloidosis and with only equivocal or negative stains.

Amyloid↗
PubMed1984

Hepatic amyloidosis. A histopathologic analysis of primary (AL) and secondary (AA) forms.

The liver is a major site of amyloid deposition. The spectrum of histopathologic changes in the liver was studied in 38 patients with systemic amyloidosis (25 with primary or myeloma-associated amyloidosis [AL] and 13 with secondary, reactive [AA] amyloidosis). Overall architectural distortion, alterations of portal triads, as well as predilection for topographic deposition in the parenchyma and/or blood vessel walls were noted. Significant histopathologic differences in AL or AA amyloid liver involvement included 1) portal fibrosis, seen in 7 of 25 (28%) AL patients and 8 of 13 (62%) AA patients (P = 0.05), 2) parenchymal amyloid deposition in 25 of 25 (100%) AL amyloid and 10 of 13 (77%) AA amyloid patients (P = 0.04), and 3) vascular amyloid deposition found in 17 of 25 (68%) with AL amyloid and 13 of 13 (100%) patients with AA amyloid (P = 0.02). These data vary from the widely held concept that deposition of amyloid is predominantly vascular in the AL form and parenchymal in amyloid AA. Clearly, however, in individual cases significant overlap occurred, and characterization of amyloid types based on morphologic distribution of amyloid deposits may be possible in only a minority of cases. In most cases, differentiation of amyloid AL and amyloid AA forms requires clinical, histochemical, immunochemical, and sometimes more elaborate laboratory amino acid sequence studies for accurate identification.

Amyloid↗
PubMed1978

Spontaneous amyloidosis in LLC mice.

Practically all low leukocyte count (LLC) mice over 1 year of age develop renal amyloidosis. Renal amyloid is deposited in the glomeruli and in the interstitium between the convoluted as well as collecting tubules, with consequent development of cysts and necrosis. LLC mice die of chronic renal failure. Electron microscopic studies reveal amyloid fibrils in the mesangium, a thickening of the basement membranes, and fusion of the foot processes in the glomeruli. Massive amounts of amyloid fibrils are also present in the interstitium, where intracellular fibrils in the fibroblasts as well as in the tubular epithelium cells are found. Vesicles, which are probably formed from membrane disruption, and amorphous materials are seen along the basement membranes. LLC mouse amyloidosis is discussed with regard to its potential as a model for studies on amyloidosis as well as the etiology and origin of amyloid fibrils.

Amyloid↗
PubMedDate not supplied

Soft tissue uptake of bone seeking radionuclide in amyloidosis.

The diagnosis of amyloidosis is often difficult due to variable clinical manifestations and the need for biopsy confirmation. We evaluated the use of bone scanning radionuclides in an effort to delineate soft tissue amyloidosis. Three of 7 patients with proven amyloid reviewed retrospectively, and 3 of 17 studied prospectively had abnormal soft tissue uptake of radionuclide, most commonly diffuse hepatic uptake. Amyloidosis should be considered in any patient with diffuse hepatic uptake or other soft tissue uptake of bone seeking radionuclides. A mechanism for the abnormal uptake (increased calcium content of the involved tissue) is postulated based on in vitro tissue analysis for calcium.

Adult↗
PubMed1983

Iatrogenic, insulin-dependent, local amyloidosis.

Human and experimental amyloidosis can occur either as a generalized widespread deposit of various proteins or a localized deposit. We looked for local amyloidosis caused iatrogenically under clinical and experimental conditions. Subcutaneous tissue from one diabetic patient and six Wistar rats, which had received a continuous local infusion of 1.2 iu of insulin daily for 6 weeks, was examined histologically. In all cases the development of granulation tissue around the tip of the catheter was observed. In addition, inhomogenous extracellular deposits showing green birefringence under polarized light when stained Congo red were seen. Immunohistologically, they displayed binding of anti-insulin antibody. Electron microscopy demonstrated a typical spear-like fibrillar structure with a fibril diameter of 60 to 80 A. These findings confirmed that the deposited substance was amyloid. Iatrogenically administered protein produced in vivo amyloidosis at the site of its entry. Insulin can lead to the formation of amyloid fibrils not only in vitro but also in vivo.

Amyloid↗
PubMed1983

Amyloidosis (AL). Clinical and laboratory features in 229 cases.

At the Mayo Clinic from 1970 to 1980, 229 patients with primary systemic amyloidosis (AL) were examined. Nephrotic syndrome, congestive heart failure, orthostatic hypotension, carpal tunnel syndrome, and peripheral neuropathy were often associated features. Electrophoresis of the serum revealed a spike in only 40%, but immunoelectrophoresis disclosed a monoclonal protein in 68%. Eighty-nine percent of patients in whom it was sought had a monoclonal protein in the serum or urine. The diagnosis of amyloidosis was made before death in 96% of the patients. The preferred sites for biopsy were the bone marrow, rectum, kidney, carpal ligament, liver, small intestine, skin, and sural nerve. The median survival of the 229 patients was 12 months. The median survival of the 77 patients with congestive heart failure was 6 months after the onset of symptoms. Congestive heart failure or arrhythmias accounted for death in 40%. Treatment for amyloidosis is unsatisfactory but includes melphalan, prednisone, colchicine, and dimethyl sulfoxide.

Adult↗
PubMed1983

Protein AA in primary and myeloma associated amyloidosis.

Protein AA, the main fibril constituent in secondary systemic amyloidosis, was demonstrated by the peroxidase-anti-peroxidase method in kidney sections from five out of 14 cases of primary and myeloma associated amyloidosis, all having an immunoglobulin light chain derived protein as a major subunit. In three of these cases, protein AA was also demonstrated in double immunodiffusion of dissolved amyloid preparations. The protein had the characteristics of protein AA in elution position, immunodiffusion and isoelectric focussing pattern. The significance of protein AA in primary and myeloma associated amyloidosis is unknown.

Amyloid↗
PubMed1984

[Differential diagnosis between constrictive pericarditis and cardiac amyloidosis by computerized M-mode echocardiography].

A diastole is a non specific haemodynamic syndrome which may result from constrictive pericarditis or from a restrictive cardiomyopathy. The aim of this study was to differentiate these two types of condition by analysis of computerised M mode recordings of the left ventricle. Three groups of patients were studied: 5 cases of confirmed cardiac amyloidosis (Am); 5 cases of constrictive pericarditis confirmed surgically (CP) and 10 normal subjects (NL). The study was based on analysis of parameters of ventricular filling and of diastolic thinning of the LV free wall. A significant difference was observed between AM and CP but not between PC and NL. Amyloidosis was characterised by a reduction in the maximum velocity of endocavitary diameter lengthening (AM 0,84 +/- 0,56 cir/sec; PC 3,95 +/- 0,77, p less than 0,01), prolongation of the rapid filling phase (AM 0,42 +/- 0,17 sec; PC 0,16 +/- 0,06 sec, p less than 0,02) and a decrease in maximum velocity of free wall thinning (AM 0,45 +/- 0,23 th/syst/sec; PC 4,79 +/- 2,1, p less than 0,01). The diastolic thickness of the free wall was greater in the amyloidosis group (AM 1,73 +/- 0,61 cm; PC 1,05 +/- 0,21, p less than 0,05) and correlated with the reduction of maximum velocity of free wall thinning. Parameters of global diastolic filling did not distinguish the two conditions. The M mode recordings were therefore digitalised to provide graphs of chamber filling and wall thinning and their derivatives.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Characterization of spontaneous amyloidosis of Syrian hamsters using the potassium permanganate method.

Amyloid from 16 Syrian hamsters with spontaneous age-related systemic amyloidosis retained affinity for Congo red dye after treatment with potassium permanganate. Serum electrophoresis showed a slight rise in gamma globulins without a monoclonal spike. Bence-Jones proteins were not present in the urine. There was no histological evidence of plasmacytosis. Amyloidosis could not be associated with chronic inflammation. The lack of apparent etiology of this amyloid and its resistance to potassium permanganate treatment suggests that it is a primary non-AA amyloid. This finding varies with a report suggesting that the spontaneous amyloidosis of aged Syrian hamsters is associated with the AA fibril.

Amyloid↗
PubMed1984

Amyloidosis in six dairy cows.

Amyloidosis was diagnosed in 6 Holstein cows that were examined because of chronic intractable diarrhea. Besides diarrhea, the chief finding was a nephrotic-like syndrome, in that there was edema, hypoproteinemia, and proteinuria. Other consistent clinicopathologic abnormalities were hyperfibrinogenemia, low-normal serum calcium content or hypocalcemia, hypomagnesemia, prolonged bromosulphalein half time, high serum urea nitrogen concentration, high serum creatinine concentration, and low urine specific gravity. Foci of inflammation including traumatic reticuloperitonitis, traumatic pericarditis, salpingitis, mastitis, and metritis were found. There was histologic evidence of amyloid in the kidneys, liver, adrenal glands, and spleen. The iodine-sulfuric acid test for amyloid was positive in 2 cows. The Congo red dye test for amyloid was positive in 2 other cows. In spite of supportive care, all the cows either died naturally or were euthanatized. Because foci of inflammation were found in each cow, it was concluded that the most likely classification of amyloidosis in these cases would be reactive systemic amyloidosis and that the major amyloid fibril protein would be type AA.

Amyloid↗
PubMed1984

[Intestinal pseudo-obstruction in primary amyloidosis of the intestinal tract].

In an 80-year-old patient who had recurrent attacks of subileus over three years, a complete large bowel ileus finally developed. At laparotomy, massive dilatation and extreme fragility of the large bowel was found. Subtotal colectomy was performed, within 24 h of which the patient died. The surgical specimen and autopsy revealed primary amyloidosis (A light chain type) confined nearly exclusively to the intestinal tract. Pseudoobstructive ileus in amyloidosis can be chiefly accounted for by the heavy amyloid infiltration of the tunica muscularis of the bowel wall. Amyloidosis of the arteries and nerve plexus may be contributory factors.

Aged↗
PubMed1984

Behcet's disease associated with amyloidosis.

The association of Behcet's disease and amyloidosis is relatively rare. We present two patients with Behcet's disease who developed amyloidosis during the course of their illness. The relation of amyloidosis with Behcet's disease is not clear. We discuss the possible etiopathogenetic factors.

Adult↗
PubMed1983

Bleeding manifestations in 100 patients with amyloidosis.

Focal or generalized hemorrhage is a commonly encountered clinical problem in patients with amyloidosis. In 100 patients with amyloidosis, 41 patients experienced one or more bleeding episodes: petechiae and ecchymoses (23), gastrointestinal tract bleeding (18), bleeding after a diagnostic procedure (eight), hematuria (three), hemoptysis (two), and miscellaneous (four). Severe hemorrhage was the cause of death in three patients. Bleeding occurred frequently in the absence of abnormalities of clotting tests, suggesting that hemorrhage in amyloidosis is most often due to amyloid infiltration of blood vessels. In this group of patients, an isolated factor X deficiency was not observed.

Amyloidosis↗
PubMed1983

Primary amyloidosis presenting as Sjögren's syndrome.

A patient had severe sicca complex. Histopathologic and immunologic examination of the salivary glands showed amyloid fibril infiltration, type A lambda VI. To our knowledge, this is the first documentation of immunologically characterized primary amyloidosis causing the sicca complex. The sicca complex is usually associated with Sjögren's syndrome and the presence of autoantibodies to SSA and SSB. These antibodies were absent in our patient, despite the severity of the sicca syndrome. The clinician should consider more unusual causes of the sicca complex, eg, amyloidosis, particularly if the serologic markers of antibodies to SSA and SSB are absent. Tissue typing the amyloid protein diagnosed primary amyloidosis, obviating the need to search for underlying disease.

Amyloidosis↗
PubMed1983

Resistance of Rowett athymic (nude) rats to casein-induced amyloidosis.

Rowett athymic (nude) rats (n = 18) were injected subcutaneously (36 to 86 injections) or intraperitoneally (10 to 56 injections) with 10% casein solution to attempt to induce amyloidosis. Neither the injected nor the control rats had gross or microscopic evidence of amyloid deposition. Serum beta- and gamma-globulin concentrations were significantly higher in the injected rats than in the control rats. There were no significant changes in blood urea nitrogen or serum alanine aminotransferase values of the experimental groups compared to the control groups. The relationship of amyloidosis to deficient cell-mediated immunity and the use of the nude rat for the study of the pathogenesis of amyloidosis are discussed.

Amyloidosis↗