Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary localized amyloidosis was found in a family. A 66-year-old woman had suffered from hoarseness for 18 years. A biopsy specimen from the larynx showed amyloid deposits in the submucosal connective tissue. Her 40-year-old daughter noticed a subcutaneous nodule on her philtrum. Histologic examination showed the deposition of amyloid in the middle and lower dermis, which also encased the blood vessels and epidermal appendages. In both cases the amyloid deposits were positively stained with Congo red and the staining was resistant to potassium permanganate treatment. These amyloid deposits were strongly positive against the anti-amyloid antibody of the lambda light chain. These results indicate that the amyloid substance is derived from protein AL. There was no clinical or laboratory evidence of systemic amyloidosis or multiple myeloma in either patient.
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PMID:Primary localized amyloidosis in one family. 193 75

Three patients with vegetating iododerma as a result of potassium iodide therapy are presented. The first patient had polyarteritis nodosa, the second had monoclonal gammopathy of undertermined significance, and the third had multiple myeloma. Vegetating iododerma probably represents an idiosyncratic response to iodides; patients with polyarteritis nodosa and paraproteinemias may be predisposed.
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PMID:Vegetating iododerma with underlying systemic diseases: report of three cases. 182 51

We report a case of primary amyloid tumor (amyloidoma) of the left parotid gland. To the best of our knowledge this is the first case of this tumor in a parotid gland to be reported in the English literature. Congo red staining with prior potassium permanganate incubation confirmed the localized primary type of amyloid. Immunocytochemical studies demonstrated staining for immunoglobulin A, lambda and kappa light chains within the amyloid deposits and in the cytoplasm of the lymphocytes, and plasma cell aggregates. Ultrastructural examination showed characteristic findings of straight, nonbranching fibrils, measuring 80 to 100 A in length, that were diagnostic of amyloid. The patient had no symptoms and no clinical or laboratory evidence of systemic amyloidosis or multiple myeloma at a 1-year follow-up examination.
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PMID:Localized primary amyloid tumor of the parotid gland. 318 22

Two examples of localized primary amyloid tumor of the breast are presented, including one patient with metachronous bilateral lesions. Our findings and review of the literature indicate that this rare lesion occurs predominantly in elderly females and can be mammographically and clinically confused with carcinoma. Fine-needle aspiration biopsy can be a useful procedure to make a preliminary diagnosis. Congo red staining with prior potassium permanganate incubation confirmed the AL type of amyloid in our two cases; this might be the predominant type in the localized form involving the breast. Immunofluorescence studies demonstrated IgA, with kappa and lambda light-chain deposition within the amyloid foci in one case, and intracytoplasmic IgG with both light chains within plasma cells and amyloid deposits of the second case. Ultrastructural examination of one of the cases showed characteristic findings of straight, nonbranching fibrils of 4-9 nm, diagnostic of amyloid. From our findings and a review of the literature, we conclude that amyloid tumors of the breast can occur in three separate settings: secondary amyloidosis, systemic or multiple myeloma associated amyloidosis, and as a localized primary type having a benign course.
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PMID:Localized primary (AL) amyloid tumor of the breast. Cytologic, histologic, immunocytochemical and ultrastructural observations. 352 31

Amyloid bone lesions were found in 2 chronic hemodialysis patients presenting with pathologic hip fractures. These amyloid deposits were noted as lytic defects on plain skeletal radiographs. No evidence for disseminated amyloidosis was discovered on physical examination, skin biopsy, or bone marrow biopsy. Myeloma, other plasma cell dyscrasia, and preceding chronic inflammatory states were not found in either patient. The amyloid deposits had staining characteristics suggestive of secondary amyloid based on the potassium permanganate reaction. Isolated amyloid bone deposits should be included in the differential diagnosis of lytic bone lesions or pathologic fractures in chronic dialysis patients.
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PMID:Pathologic fractures associated with idiopathic amyloidosis of bone in chronic hemodialysis patients. 370 63

We present six patients with associated renal adenocarcinoma and systemic amyloidosis. In five of the patients amyloidosis showed clinical and organ distribution characteristics of reactive (secondary) amyloidosis. The amyloid deposits contained amyloid A protein as defined by potassium permanganate sensitivity and by reactivity with anti-amyloid A antiserum. Four of these patients had suffered from additional inflammatory diseases. In the sixth patient the amyloid disease had different clinicopathologic characteristics and was evidently of an immunoglobulin light-chain-derived type related to a concomitant multiple myeloma. Although renal carcinoma seems to be an effective stimulator of amyloid formation, the possible contributory influence of associated chronic inflammation deserves more careful appraisal.
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PMID:Renal adenocarcinoma and systemic amyloidosis. Immunohistochemical and histochemical studies. 388 41

An autopsy case of multiple myeloma (IgA-lambda) with extensive amyloid arthropathy of the systemic joints was described. Heavy deposits of amyloid (amyloidoma) were observed in the articular cavities of the joints. Furthermore, numerous amyloid deposits were found in the walls of small blood vessels in the general organs. Incubation of the paraffin sections of amyloid with potassium permanganate produced little loss of Congo red affinity and apple-green birefringence under polarized light. A crude preparation of amyloid protein was isolated from a frozen intra-articular mass, which had been obtained at necropsy, and injected into the footpads of BALB/c mice with complete Freund's adjuvant. The immune spleen cells were fused with myeloma cells (P3 X 63-Ag8.653) under the presence of polyethylene glycol. Hybridoma cell lines, producing supernatants which reacted not only with amyloid substances but also with normal human tissues, were omitted from the subjects of recloning, and one hybridoma cell line (Am-1) producing a specific monoclonal antibody (MAb) against the immunized amyloid substance was finally obtained. Using the indirect immunoperoxidase method, the specificity of MAb Am-1 was confirmed in the cryostat sections as well as in the formalin-fixed paraffin sections of various organs of the case from which the crude amyloid protein was obtained and used for immunization. Amyloid deposits in 25 cases with amyloidosis or amyloid deposits were examined with MAb Am-1, and 2 cases showed positive reactivity with Am-1. These 2 cases presented primary amyloidosis and focal amyloid deposits in the oral cavity, respectively; Congo red staining of amyloid in these cases showed resistance to treatment with potassium permanganate, as observed in the amyloid of the original case used for immunization. Trypsin treatment of the sections resulted in a loss of positive reactivity with MAb Am-1 in all these cases. This result indicates that Am-1 recognizes a substance composed of protein molecules. Furthermore, the immunohistochemical distribution of Am-1 positive reaction was consistent with the histological distribution of substance which could be stained by Congo red and showed apple-green birefringence under polarized light. These results have suggested that Am-1 reacts with a portion of amyloid protein which is resistant to treatment with potassium permanganate followed by Congo red staining.
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PMID:Production of monoclonal antibody against amyloid fibril protein and its immunohistochemical application. 391 46

A patient with progressive renal failure due to multiple myeloma presented with a mixed acid-base disorder (non-anion gap acidosis and respiratory alkalosis) with persistent severe hyperkalemia. Studies revealed an intact ability to lower urine pH during acid loading, markedly decreased plasma renin and aldosterone concentrations despite volume depletion, and an inappropriately low fractional excretion of potassium. Renal biopsy demonstrated plasma cell infiltration of the renal interstitium and typical proteinaceous intratubular casts. Both proximal and distal renal tubular acidification defects have been described previously in patients with multiple myeloma, but this is the first report of hyporeninemic hypoaldosteronism, hyperkalemia, and hyperchloremic metabolic acidosis in association with renal involvement in multiple myeloma.
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PMID:Hyporeninemic hypoaldosteronism in a patient with multiple myeloma. 638 30

Amyloid fibrils occurring in primary and myeloma-associated (AL), secondary (AA), and certain neuropathic hereditary forms of systemic amyloidosis can be distinguished biochemically or immunohistologically as being composed of immunoglobulin light chain, protein AA, or prealbumin respectively. All types of systemic and several localized forms of amyloidosis contain amyloid P component (protein AP). We studied formalin-fixed tissue from eight cases of lattice corneal dystrophy by the immunoperoxidase method using antisera to proteins AA and AP, to normal serum prealbumin and prealbumin isolated from a case of hereditary amyloidosis, and to light-chain determinants; additional cases were examined by indirect immunofluorescence of fresh-frozen material. We found weak (1:10 dilution) staining with anti-AP, but no reactivity with other antisera. Congo red staining was resistant to pretreatment of sections with potassium permanganate, a characteristic of non-AA amyloid. Two-dimensional gels of solubilized proteins from frozen tissue from two cases of lattice corneal dystrophy resembled those obtained from normal human cornea. Western blots of two cases of polymorphous amyloid degeneration and solubilized protein from normal cornea did not react with radioactive iodine-labeled anti-AA or anti-AP with purified protein AP and unfixed protein AA amyloid tissue as controls. We were unable to corroborate the presence of protein AA in the amyloid deposits of lattice corneal dystrophy. Although staining with antiserum to protein AP was demonstrable, the molecular configuration of this protein in stromal deposits remains to be defined.
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PMID:Lack of evidence for protein AA reactivity in amyloid deposits of lattice corneal dystrophy and amyloid corneal degeneration. 638 50

Total 105 Japanese cases of systemic amyloidosis were analysed in terms of Congo red staining with potassium permanganate, anti-amyloid serum staining by immunoperoxidase and the occurrence of monoclonal proteins (ie. plasma cell dyscrasia, PCD). Thirty three cases of primary type amyloidosis and 22 cases of myeloma-associated amyloidosis were mostly associated with PCD, with 3 exceptional cases without PCD. In contrast, 45 cases of secondary type amyloidosis were demonstrated as AA type, with no association of PCD. Predominance of lambda light chain in amyloidosis was contrasted to kappa chain predominance among the non-amyloidotic myeloma cases.
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PMID:Plasma cell dyscrasia in 105 Japanese patients with systemic amyloidosis. 686 4


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