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)

A patient with hypercalcemia and newly diagnosed multiple myeloma developed acute pancreatitis. Other etiologic factors for pancreatitis were excluded. Hypercalcemia secondary to hyperparathyroidism is associated with acute pancreatitis. In English literature, only one other case has been published where the hypercalcemia of multiple myeloma may have caused pancreatitis. Pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea/vomiting, and abdominal pain.
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PMID:Acute pancreatitis in a case of multiple myeloma with hypercalcemia. 248 50

A case of multiple myeloma (Bence Jones, lambda) associated with alcoholic liver cirrhosis is reported. A 56-year-old Japanese male died of hepatic failure and hypercalcemia. Autopsy revealed alcoholic liver cirrhosis and plasma cell myeloma. Immunoelectrophoretic analysis of his reserved serum disclosed the presence of M component of lambda Bence Jones protein. IgA and lambda light chain were demonstrated in the cytoplasm of the myeloma cells. Complications such as generalized amyloidosis, metastatic calcification, myeloma kidney and hemorrhagic pancreatitis were noted. The coexistence of multiple myeloma and liver cirrhosis has rarely been reported. On the basis of a review of the reported cases, a possible association between both diseases was discussed.
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PMID:Multiple myeloma in alcoholic liver cirrhosis. 265 75

Amylase-producing tumors are mainly adenocarcinomas and, in rare instances, multiple myelomas. We describe here a first case of amylase-producing Bence Jones type myeloma with pancreatitis-like symptoms and the second in a Caucasian patient. The finding of salivary-type hyperamylasemia in a 72-year-old female with a possible pancreatitis made us suspect the diagnosis. Amylase production was observed in bone marrow cultures in which 96% of cellularity was composed of plasmablasts. Serum amylase level decreased when chemotherapy was given.
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PMID:Amylase-producing Bence Jones multiple myeloma with pancreatitis-like symptoms. 750 60

There are three types of interferons (IFN), alpha, beta and gamma. IFN-alpha is produced in the leukocytes infected with virus, while IFN-beta is from fibroblasts infected with virus. IFN-gamma is induced by the stimulation of sensitized lymphocytes with antigen or non-sensitized lymphocytes with mitogens. It is believed that IFN-alpha and beta originated from the same ancestral gene, whereas IFN-gamma did not. IFN has not only an antiviral activity, but also various kinds of biological activities including cell growth inhibition, immunosuppressive effects, enhancement of macrophage, natural killer (NK) cell, killer (K) cell and neutrophil functions, and cell differentiation-inducing activity. IFN also shows the antitumor activity resulting from the integration of the above-mentioned biological activities. IFN is also deeply involved in the pathogenesis of various diseases, e.g., collagen diseases such as SLE and rheumatoid arthritis, insulin-dependent diabetes mellitus, fulminant hepatitis, severe pancreatitis, nephritis, multiple sclerosis, allergic diseases, and atherosclerosis. At present, IFN is clinically used in therapy against virus infections such as hepatitis B and C, and for malignancies such as renal cell carcinoma, multiple myeloma, malignant melanoma, glioblastoma, skin cancers, malignant lymphoma and chronic myelogenous leukemia.
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PMID:[Interferon-alpha, beta, gamma]. 799 28

62-year-old female, who had been under observation for an indolent myeloma for six years without therapy, was admitted because of left flank pain. Various imaging modalities disclosed left pleural effusion, and a huge abdominal tumor involving the left crus of the diaphragm, spleen, stomach, pancreatic tail, left adrenal gland, left kidney and left posterior abdominal wall. Morphological and immunological examinations revealed extensive proliferation of more anaplastic myeloma cells within the tumor and in the pleural effusion than those in bone marrow on admission or at the beginning of the period of observation. Chemotherapy reduced serum M-protein, but LDH, the volume of the pleural effusion, and the size of the tumor increased. She died of pancreatitis associated with massive bleeding from the gastric tumor. Renal function was well preserved until her terminal phase. The clinical course showed the progression of indolent myeloma into an aggressive one without chemotherapeutic intervention, implying a rare subtype in terms of the natural history of multiple myeloma.
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PMID:[Aggressive transformation of an indolent myeloma with abdominal extramedullary plasmacytoma after 6-year period of observation]. 802 86

Elevated phospholipase A2 activities in serum were measured in patients suffering from acute pancreatitis or various inflammatory diseases. The photometric phospholipase A assay of Hoffmann & Neumann (Klin. Wochenschr. 67 (1989) 106-109) was combined with immunoabsorption by different monoclonal antibodies directed against pancreatic phospholipase A2. Pancreatic phospholipase A2 was purified from human duodenal juice. Monoclonal antibodies were prepared by fusion of spleen cells from immunized mice with P3X63-Ag8-653 myeloma cells. Samples with phospholipase A2 activity were incubated in monoclonal antibody-coated microtitre plates. Phospholipase A2 activities were determined in the monoclonal antibody-treated samples as well as in control samples. The method allows the determination of the fraction of human phospholipase A2 isoenzymes in various biological materials. For pancreatic phospholipase A2 the specific binding capacity was about 60-80%, the unspecific binding was 5-30%. Practically no cross-reactivity was seen with partially purified serum phospholipase A2, with recombinant platelet phospholipase A2, or with the sera of patients with non-pancreatic diseases. In conclusion, the present study confirmed the presence of pancreatic phospholipase A2 in human duodenal juice and in the ascites of necrotizing pancreatitis. However, pancreatic isoenzyme was absent in non-pancreatic inflammatory diseases. Therefore, elevated phospholipase activities in non-pancreatic inflammatory diseases cannot be attributed to the pancreas.
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PMID:Differentiation of human phospholipase A2 isoenzymes in serum and other body fluids with use of monoclonal antibodies. 831 67

Acute pancreatitis is a very uncommon presenting feature of multiple myeloma. We report an elderly non-alcoholic man presenting with acute abdominal pain and rapidly progressing renal failure. Investigations revealed lytic lesions in the vertebrae and skull, M band on urine electrophoresis, and radiological and biochemical evidence of acute pancreatitis. The patient died despite conservative management of the pancreatitis.
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PMID:Multiple myeloma presenting as acute pancreatitis. 1040 73

For a long time fibrinopeptide A(FPA), fibrinopeptide B(FPB), D-dimer, FM test, serum FDP, and thrombin anti-thrombin complex(TAT) are being used as molecular markers to for sure diagnose hypercoagulable state and thrombus formation. Indeed these molecular markers are very useful for diagnosing thrombus formation, disseminated intravascular coagulation(DIC), and the indicator of treatment of DIC. But these molecular parameters are not enough and difficult for prognosis of the disease or predicting the complication of patients as the most important subject for clinicians. The soluble fibrin monomer-fibrinogen complex (SF) is a complex coupling fibrin monomer and fibrinogen molecules to be formed in the early-activated state of blood coagulation. Thus such a molecular complex is expected to serve as a parameter for the diagnosis of thrombus formation and DIC, in particular its early stage. The aim of the present study is to evaluate a potential usefulness of a newly developed SF test utilizing an SF specific monoclonal antibody (IF-43). We measured SF together with established other parameters in 195 patients with DIC, subclinical DIC/hypercoagulable state, and non-DIC. The diagnosis of DIC was made based on a modified version of the criteria established by the Ministry of Health, Labor and Welfare of Japan. Underlying disease includes leukemia, malignant lymphoma, myelodysplastic syndrome (MDS), multiple injury, giant ovarian tumor, prostatic cancer with multiple bone metastasis, lung cancer, breast cancer with multiple lung and bone metastasis, severe pneumoniae, sepsis, hemophagocytic syndrome (HPS), and rheumatoid arthritis. The SF levels in DIC patients were significantly higher than those in the subclinical DIC/hypercoagulable state, and the non-DIC patients. Receiver operating characteristic (ROC) analysis shows that the specificity and sensitivity of the SF assay appears to be satisfactory. As the level of SF reflects the thrombin generation activity in plasma, it would serve as a strong tool to selectively kick up the state of thrombin generation. These results indicate that the SF could be a specific and reliable parameter for the diagnosis of DIC and contribute to legitimate managements of patients with DIC. The excessive life response to serious clinical insults, such as sepsis, severe pancreatitis, trauma and shock, is called systemic inflammatory response syndrome (SIRS). Once SIRS occurs, people may often die from serious complications such as adult respiratory distress syndrome (ARDS), acute lung injury (ALI), disseminated intravascular coagulation (DIC) and multiple organ failure (MOF). Especially, ALI followed by pneumoniae associated with SIRS could depend on patient's prognosis and life. That is to say, it seems to be urgent for clinicians to make differential diagnosis between Pneumoniae associated with SIRS and Coagulopathy (PASC) and Simple Pneumoniae (SP). Soluble fibrin monomer-fibrinogen complex(SF) is formed in the early-activated state of blood coagulation. Thus such a molecular complex is expected to serve as a parameter for the diagnosis of coagulopathy, in particular its early stage. The aim of the present study is to make differential diagnosis between Pneumoniae associated with SIRS and Coagulopathy (PASC) and Simple Pneumoniae(SP) by using a newly developed SF test utilizing an SF specific monoclonal antibody (IF-43). We measured SF together with established other parameters, hemogram, blood laboratory items in 7 patients with PASC and 17 patients with SP. The diagnosis of Pneumoniae was defined according to the criteria: clinical symptoms abnormal shadow in both Chest X-p and Chest CT, increased level of CRP, number of WBC. The diagnosis of SIRS was based on the criteria established by American College of Chest Physicians (ACCP)/Society of Critical Care Medicine (SCCM) Consensus Conference held in August of 1991 in Northbrook, IL (USA). Underlying disease includes leukemias, malignant lymphoma, myelodysplastic syndrome (MDS), multiple myeloma, idiopathic thrombocytopenia purpura(ITP), multiple injury (bone fracture), cerebral hemorrhage, enterocolitis, Appendicitis, lung cancer, larynx cancer, bronchiolitis obliterans organizing pneumonia(BOOP), chronic obstructive pulmonary disease(COPD), sepsis. The SF levels in PASC patients are significantly higher than those in SP patients (p < 0.001). Otherwise, there is no significant difference of the CRP levels between in PASC group and SP group (p < ns). There is no co-relationship between SF level and D-dimer level. Receiver operating characteristic (ROC) analysis shows that the specificity and sensitivity of the SF assay appears to be quite satisfactory. As the level of SF reflects the thrombin generation activity in plasma, it would serve as a strong tool to selectively kick up the state of thrombin generation. These results indicate that the SF could be a specific and reliable parameter for the diagnosis of PASC and contribute to legitimate managements of patients with PASC.
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PMID:[A novel molecular marker for thrombus formation and life prognosis--clinical usefulness of measurement of soluble fibrin monomer-fibrinogen complex (SF)]. 1516 5

Well over six decades since its first description, the Rheumatoid Factor (RF)-autoantibodies recognizing Fc (constant) portion of IgG through their own Fab (antigen binding variable segments)-is believed to have come of age. Autoimmune pancreatitis is a unique form of pancreatitis, biologically characterized by an elevated serum IgG4 concentration. Given the fact that IgG4 myeloma proteins can act as RF, we initially hypothesized that IgG4 in autoimmune pancreatitis might do likewise, hence potentially contributing to disease pathogenesis. Indeed Western blotting clearly showed that IgG4 binds to IgG1 kappa, IgG2 kappa, IgG3 kappa myeloma proteins, as well as to IgG Fc, in line with a typical RF activity. Further experiments however unraveled the unexpected fact that unlike hitherto known RF, IgG4 does not engage IgG Fc through its Fab, but its very own Fc. These data therefore collectively describe a Novel RF (NRF) in autoimmune pancreatitis. In the future, the relevance of NRF, beyond autoimmune pancreatitis, in both diagnosis/prognosis as well as pathophysiology of autoimmune and other systemic diseases where IgG4's role seems paramount, needs to be systematically assessed.
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PMID:A novel immunoglobulin-immunoglobulin interaction in autoimmunity. 1829 31

The proteosome inhibitor bortezomib is used in the treatment of patients with multiple myeloma. Proteosomes are responsible for the degradation of I-kappaB, the inhibitory protein of transcription factor nuclear factor kappa B (Nf-kappaB). The heat shock protein (HSP) inducing effect of bortezomib is also documented. The aim of our work was to test the anti-inflammatory effect of bortezomib in cholecystokinin-octapeptide (CCK-8)-induced acute pancreatitis. Male Wistar rats were divided into three groups (n=8 in each). Group P received an i.p. injection of physiological saline (p.s.) 60 min. before the induction of acute pancreatitis by three hourly s.c. injections of 100 microg/kg CCK-8. Group BP received 1 mg/kg bortezomib dissolved in p.s. 1 h previous to pancreatitis induction. Group C was treated with the vehicle (p.s.). Animals were exsanguinated 4 h after the last injection of CCK-8. Bortezomib pre-treatment significantly reduced the pancreatic weight/body weight ratio, and improved the histology by decreasing the extent of vacuolization and infiltration. Bortezomib pre-treatment inhibited I-kappaBbeta degradation, and induced the synthesis of HSP72. The results confirmed the anti-inflammatory effect of bortezomib in acute experimental pancreatitis. This effect of the drug is presumably mediated by the inhibition of Nf-kappaB activation and induction of HSP synthesis.
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PMID:Simultaneous proteosome inhibition and heat shock protein induction by bortezomib is beneficial in experimental pancreatitis. 1948 1


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