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 diagnosis of vertebral multiple myeloma, based on radiographic evidence of osteolytic lesions and the finding of monoclonal paraprotein and large numbers of plasma cells in bone marrow biopsies, was made in a mature Doberman Pinscher. The abnormal serum paraprotein was a cryoglobulin of the immunoglobulin A class. Neurologic signs associated with the tumor included pain, progressive pelvic limb paresis, and paraplegia that developed during a 6-week period.
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PMID:Neurologic complications of IgA multiple myeloma associated with cryoglobulinemia in a dog. 51 33

A case of multiple myeloma forming an intracranial mass which invaded the skull base was reported. A 72-year-old woman was admitted to the hospital because of left oculomotor paresis. Plain craniograms showed multiple punched out lesions. A CT scan demonstrated a mass lesion, which was homogeneously slightly enhanced with contrast medium, in the middle cranial fossa. MRI, both T1 and T2 weighted images, showed an isodensity mass. In the carotid angiograms the tumor was fed by the right branches of the cavernous portion of the internal carotid artery and the maxillary artery. Laboratory data were as follows: ESR: 132mm/30min, serum TP: 9.0g/dl, IgG: 4670mg/dl, IgA: 430mg/dl, and urinary Bence-Jones protein was detected. Bone marrow biopsy of the illiac bone demonstrated myeloma cells. During hospitalization oculomotor paresis disappeared, and the patient was treated with intramuscular interferon-alpha. Multiple myeloma which invades the skull base is rare, and only 10 cases have been reported since 1977. Moreover, the biclonal type is only 0.5% of all multiple myelomas.
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PMID:[A case of multiple myeloma (biclonal type) associated with an intracranial mass invading the skull base and oculomotor palsy]. 176 45

A patient with multiple myeloma developed gaze paresis to the left with slowed saccades and gaze-paretic nystagmus, which alternated with abduction palsy in the left eye (with preserved oculocephalic deviation) and dissociated adducting nystagmus in the right eye, suggesting so-called posterior internuclear ophthalmoplegia. At autopsy multiple small infarcts were found with partial destruction of the left paramedian pontine reticula formation (PPRF) extending towards the abducens nucleus, which was involved only in its inferior pole. The medial longitudinal fasciculus and other oculomotor structures were spared. It is suggested that slowing of all ipsilateral saccades with gaze-paretic nystagmus corresponded to partial destruction of the PPRF, and that intermitted abduction palsy in the ipsilateral eye with adduction nystagmus in the fellow eye was due to intermittant dysfunction of the abducens nucleus. Involvement of voluntary saccades, pursuit movements and vestibulo-ocular responses may be dissociated in partial lesions of the abducens nucleus.
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PMID:Paresis of lateral gaze alternating with so-called posterior internuclear ophthalmoplegia. A partial paramedian pontine reticular formation-abducens nucleus syndrome. 399 74

Although various studies supported the notion that leukemia cells in chronic myeloid leukemia (CML) may be recognized by the immune system, direct evidence showing the immunogenicity in vivo of proteins derived from the leukemia cells is lacking. In this study, we have constructed an expression cDNA library from the leukemia cells of a patient with CML and used the autologous serum to screen for high-titer IgG antibodies directed at the leukemia-derived proteins. We isolated eight distinct clones from the library, suggesting that multiple immune responses were elicited in the autologous host. Sequence analysis showed high degrees of homology to known gene sequences in six of the eight clones. Neither bcr-abl nor proteinase 3 sequences were isolated. Using Northern blot analysis, seven of the eight clones showed ubiquitous expression in normal bone marrow, leukemia cell lines, fresh leukemia cells, and normal tissues. However, clone no. 4 showed restricted mRNA expression, being only detected in some fresh leukemia cells, K562 cells, and normal testicular RNA. Using bacterial lysates in dot blot analysis, a panel of sera from normal individuals and patients with CML and other hematological malignancies were screened for high-titer antibodies against these eight clones. There were, among the CML patients, signficantly higher prevalence of antibodies against seven of the eight clones. They were observed even after omitting from the analysis patients with multiple myeloma whose associated immune paresis may impair immune responses to these proteins. Interestingly, antibodies against these proteins were also detected in a small number of normal individuals. Although the precise clinical significance of our findings remains to be determined, this study provides evidence in support of the potential immunogenicity of leukemia-derived proteins in the autologous host. It also provides basis for further investigations to characterize these proteins, especially clone no. 4, and determine their potential for immune targeting in CML.
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PMID:Prevalence of antibodies against proteins derived from leukemia cells in patients with chronic myeloid leukemia. 984 43

An association between mastocytosis and monoclonal gammopathy is a relatively rare but well recognized clinical finding. In the majority of cases, however, overt myeloma or lymphoma is not detectable morphologically. Here we describe the case of a 51 year-old male patient first presenting with paresis of the right facial nerve and the serological finding of IgM kappa paraproteinemia. The patient did not have organomegaly, lytic bone lesions, or urticaria pigmentosa-type skin lesions. Histological examination of a trephine biopsy specimen revealed the unusual coexistence of plasma cell myeloma and mastocytosis. Immunohistochemically, plasma cells were found to exhibit a monotypic staining for Ig heavy chain mu and Ig light chain kappa, thus confirming their neoplastic nature. Mast cells showed prominent spindling and formed dense multifocal infiltrates, thus enabling the diagnosis of bone marrow mastocytosis. Immunohistochemically, mast cells expressed tryptase, chymase, and KIT (CD117). In addition, aberrant expression of CD25 on mast cells was detected, confirming the coexistence of a neoplastic mast cell-proliferative disorder. According to the WHO proposal for classification of hematopoietic malignancies, this unique case, showing the association of two very rare haematologic neoplasms, can therefore best be referred to as bone marrow mastocytosis associated with IgM kappa plasma cell myeloma (SM-AHNMD).
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PMID:Bone marrow mastocytosis associated with IgM kappa plasma cell myeloma. 1516 Sep 59

Lytic lesions occurring in conjunction with plasma cell sarcoma (multiple myeloma) have rarely been reported in cats.A plasma cell sarcoma was diagnosed in a 13 year old castrated male Siamese cat with hind limb paresis resulting from osteolysis of the second lumbar vertebra. Serum electrophoresis showed a monoclonal gammopathy. A uniform population of plasma cells was found in and around the second lumbar vertebra and in the bone marrow of the femora, humeri, pelvis and the fifth lumbar vertebra. The neoplastic cells were identified as IgA and kappa chain specific by direct immunofluorescence.
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PMID:Plasma cell sarcoma in a cat. 1742 18

We report a case of IgG paraprotein cross-reactivity with IgM measurement in a patient with IgGkappa multiple myeloma and associated IgA and IgM immune paresis. IgM measurements using a Beckman-Coulter Synchron LX IgM reagent initially gave unmeasurably low IgM concentrations (<0.3 g/L) but IgM quantitation using later batches of reagent gave IgM concentrations of 13-42 g/L. Immunofixation confirmed the continued presence of the IgGkappa paraprotein band with suppression of IgA and IgM and analysis on the Behring BN2 and Beckman-Coulter Immage instruments showed IgM concentrations of <0.2 g/L. Immunofixation using the Synchron LX IgM reagent as antiserum confirmed binding of the Synchron LX IgM antiserum to the IgGkappa paraprotein. This case highlights the importance of checking all unexpected immunoglobulin measurements with previous results and immunofixation findings to avoid mistakes.
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PMID:Immunoglobulin G paraprotein cross-reactivity with immunoglobulin M measurement. 1858 33

An 11 years old Yucatan Pig with a Multiple Myeloma in the spinal cord, the sternum and the pelvis is described. The major clinical sign was a paresis of the hind limb. The most significant haematological change was a lymphopenia. The X-ray examination and computed tomography showed typical osteolytic changes in the skeleton. The histological examination of the bone marrow showed many, moderately well-differentiated plasma cells. Based on the collected findings and the exclusion of differential diagnoses, a Multiple Myeloma was diagnosed.
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PMID:[Multiple myeloma in a Yucatan Pig]. 2013 13

The paper describes a patient presenting with myeloma disease with concomitant macroglossia simulating a neoplasm in the bottom of the oral cavity and complicated by laryngeal paresis and the development of grade III stenosis. A brief characteristic of myeloma disease, amyloidosis, and macroglossia syndrome is provided. The authors focus attention on the main diagnostic criteria for this pathology and discuss possible diagnostic mistakes.
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PMID:[Myeloma disease with concomitant macroglossia: case report]. 2055 59

Bortezomib is a proteasome inhibitor demonstrating substantial activity in multiple myeloma. One of its key toxicities is peripheral neuropathy, which is reversible in most patients. The possibility that bortezomib might in rare cases induce severe neuropathies by auto-inflammatory mechanisms remains controversial. We report here the case of a 65-year-old female myeloma patient who was initially treated with bortezomib, doxorubicin, and dexamethasone (PAD). At the end of the second cycle of PAD, the patient presented with a rapid and severe onset of paresis of the left arm, accompanied by progressive sensory neuropathy and increasing neuropathic pain. After an extensive neurological work-up, including electrophysiological and laboratory evaluations as well as magnet resonance tomography imaging, we diagnosed an inflammatory autoimmune neuropathy, presumably induced by bortezomib, with accentuation of the left arm nerve plexus. We subsequently initiated regular treatment with polyvalent immunoglobulins, which gradually improved the neurological symptoms. In conclusion, the identification of an inflammatory autoimmune neuropathy, presumably associated with bortezomib, is a rare but important complication. An extensive neurological examination should be performed in patients who develop severe or unusual sensory or motor deficits under therapy with bortezomib, so as to differentiate autoimmune from toxic neuropathies, as therapeutic strategies differ for each.
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PMID:Inflammatory autoimmune neuropathy, presumably induced by bortezomib, in a patient suffering from multiple myeloma. 2155 20


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