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Biomedical subjects

U A Walker

Publications and source records attributed to U A Walker.

At least 19 recordsLinked to original sources
PubMed2006

99mTechnetium pyrophosphate scintigraphy in the detection of skeletal muscle disease.

We aimed to assess the specificity and sensitivity of (99m)technetium pyrophosphate muscle scintigraphy in the diagnostic workup of patients with suspected myopathy. We reviewed the charts of 166 patients; 52% of the subjects had myalgias, 36% had muscle weakness, 45% had an elevated serum creatine kinase (CK), and 49% had an increased C reactive protein (CRP). Scintigraphy was positive in 34 patients (20%). The test was more sensitive in the presence of muscle weakness, elevated CK, or increased CRP. The presence of myalgias did not influence the odds. Sensitivity was 60% in patients with the final diagnosis of polymyositis, dermatomyositis, or inclusion body myositis, and 70% in noninflammatory myopathies. Eight percent had false positive scintigrams. In individuals with biopsy-proven myopathy (51 subjects), the diagnostic sensitivity was 43%, and its specificity was 60%. Low positive and high negative likelihood ratios (5.0 and 0.65, respectively) document an only limited diagnostic efficiency of (99m)Tc-PYP scintigraphy in the evaluation of inflammatory and noninflammatory myopathies and suggest that the test is not helpful in the routine diagnostic workup of muscle complaints, even after a priori selection of patients for CK plus CRP abnormalities.

Adolescent↗
PubMed2006

Analgesic and disease modifying effects of interferential current in psoriatic arthritis.

Interferential current (IFC) was suggested to improve the skin manifestations of psoriasis vulgaris, possibly by enhancing the intracellular concentration of cyclic AMP. We assessed the efficacy of IFC on psoriatic arthritis (PsA). Nine consecutive patients were analyzed at baseline and after 16 weeks of IFC therapy. Bipolar IFC was applied twice daily to hands, feet plus all affected joints. IFC improved SF-36 assessed body pain, but not other SF-36 subscales. Morning stiffness, tender joint counts, and physician assessed disease activity improved. In contrast, visual analogue scale assessed pain, CRP and ESR measurements were unchanged. MRI of the most affected hand or foot documented a tendency towards worsened tendinitis, soft tissue swelling, and new joint space narrowing and erosions. Bone scintigraphy showed a trend towards deterioration. New joints became inflamed within treated sites. Thus IFC has analgesic effects in PsA, but does not have a satisfactory disease modifying effect.

Adult↗
PubMed2005

Mitochondrial DNA depletion in liver tissue of patients infected with hepatitis C virus: contributing effect of HIV infection?

OBJECTIVES: It has been suggested that chronic hepatitis C virus (HCV) infection depletes mitochondrial DNA (mtDNA) in the liver. Because decreased mtDNA levels were also found in humans infected with HIV, we investigated whether HIV may have aggravated hepatic mtDNA depletion in individuals with HCV infection. METHODS: In this cross-sectional study, liver biopsies were performed in a total of 40 individuals prior to any antiviral therapy. The individuals were recruited from the Hospital Clinic, Barcelona and the HIV Centre, Dusseldorf. Seventeen patients were negative for HIV and HCV and were biopsied for liver enzyme elevation of unknown cause (controls), 14 individuals had chronic HCV but no HIV infection, and nine subjects were coinfected with both viruses. mtDNA and liver histology were centrally assessed. RESULTS: The groups did not differ with respect to age, gender, liver function tests and HCV viral load, where applicable. mtDNA levels were decreased by 19% in the HCV-monoinfected group (P=0.03) and by 27% in the HIV/HCV-coinfected subjects (P=0.02) compared to controls. The mtDNA content, however, did not differ between individuals with HCV monoinfection and HCV/HIV coinfection (P=0.75). The degrees of liver fibrosis, inflammatory activity or steatosis did not correlate with mtDNA content. CONCLUSIONS: Liver mtDNA content is reduced in both HCV-monoinfected and HIV/HCV-coinfected patients. Under the limitations of our study, we could demonstrate only a slight trend towards more pronounced mtDNA depletion in HIV/HCV-coinfected subjects.

Adult↗
PubMed2005

Immunosuppressive treatment of chronic periaortitis: a retrospective study of 20 patients with chronic periaortitis and a review of the literature.

BACKGROUND: Retroperitoneal fibrosis (RPF) and inflammatory aneurysm of the abdominal aorta (IAAA) are regarded as two manifestations of the same disease, termed "chronic periaortitis". OBJECTIVE: To determine the optimal therapeutic and diagnostic approaches to IAAA. METHODS: The outcome of medical immunosuppressive and surgical treatment of 20 patients was examined. Measurements of the C reactive protein (CRP) were compared with contrast enhanced imaging studies in the follow up of the patients. RESULTS: The diameter of the periaortic mantle and its contrast enhancement improved in 13/15 (87%) patients given immunosuppressive treatment for a period of more than 6 months. Strong contrast enhancement was associated with a substantial rise in CRP, but no correlation between the CRP value and thickness of the fibrotic mass was found, even at intraindividual follow up. CONCLUSIONS: Immunosuppressive treatment should be included in the first line treatment of patients with RPF and should be maintained long term. Imaging studies are better than CRP measurements in the evaluation of response to treatment.

Adult↗
PubMed2004

[Lactic acidosis in HIV-patients--diagnosis and treatment].

Lactic acidosis is a life-threatening complication of antiretroviral therapy with an incidence of about 1% per year. Its clinical onset is often abrupt, with uncharacteristic muscular, cardiac or hepatic symptoms. Lactic acidosis is caused by nucleoside analogue reverse transcriptase inhibitors (mainly didanosine, stavudine and zalcitabine), which are relatively strong inhibitors of gamma polymerase, the enzyme responsible for the replication of mitochondrial DNA. Zidovudine is also a mitochondrial toxin, but its toxicity probably reflects several mechanisms unrelated to mtDNA-depletion. When lactic acidosis is diagnosed, nucleoside analogues and other mitochondrial toxins, such as valproic acid and acetylsalicylic acid, must be discontinued immediately. Uridine should be supplemented, a cocktail consisting of vitamins, L-carnitine and coenzyme Q10, may be given.

Acid-Base Equilibrium↗
PubMed2004

Liquid chromatographic method for the determination of uridine in human serum.

To evaluate uridine levels in humans we developed a very sensitive and specific high-performance liquid chromatographic method for the determination of uridine in serum. We use techniques which are available in a standard analytical laboratory. Chromatographic analysis was carried out on a Phenomenex Aqua C18 5 micro 125A column protected by a guard cartridge system. Potassium dihydrogen phosphate buffer-acetonitrile was used as an eluent and oxypurinol as the internal standard. All sample preparation steps were done at 4 degrees C and the autosampler was cooled down to 4 degrees C. The calibration curve was linear throughout the calibration range from 0.25 to 100 micromol/l. This method was primarily established to evaluate uridine serum levels in patients with HIV infection since patients on highly active antiretroviral therapy (HAART) might develop metabolic disturbances that could lead to severe and fatal lactic acidosis due to mitochondrial toxicity. It is suggested that a limited or inadequate uridine supply is at least in part responsible for the onset of such deterioration.

Calibration↗
PubMed2002

[Inherited and acquired disorders of mitochondrial DNA].

Human mitochondrial DNA (mtDNA) resides in thousands of copies in each cell and encodes for 13 structural proteins which are subunits of the respiratory chain. Point mutations, deletions, and decreased copy-number (mtDNA-depletion) are now functionally and genetically linked to human disease. Although mtDNA is inherited maternally, some mutations may arise spontaneously and others are inherited in a mendelian fashion, which is attributed to defective nuclear genes. MtDNA-mutations are also associated with aging and with tumors but in these conditions probably not of functional significance. Mutations of mtDNA may be acquired by exposure to toxic substances (such as alcohol or doxorubicin). An acquired copy number defect (mtDNA-depletion) is dose-limiting for some antiviral nucleosides and nucleotide analogues. The internist encounters predominantly myopathies, cardiomyopathies, lactic acidosis or diabetes mellitus but mtDNA-changes also lead to neurological, hematological and renal symptoms. A syndrome of fat redistribution, termed lipodystrophy, is now observed with long-term therapy of HIV-patients and has been associated with mtDNA-depletion. Therapy with vitamins, radical scavengers and L-carnitine is recommended, but of limited success.

Adolescent↗
PubMed2001

["Catastrophic systemic lupus erythematosus" with Rosai-Dorfman sinus histiocytosis. Successful treatment with anti-CD20/rutuximab].

HISTORY AND ADMISSION FINDINGS: A 59-year old woman was admitted with a four-month history of polyarthritis, myalgias and photosensitivity insufficiently responsive to methotrexate, corticosteroids and azathioprin. On physical examination she presented with symmetric ankle edema, polyserositis, petechial bleeding and swelling of cervical, axillary and inguinal lymph nodes. INVESTIGATIONS: Laboratory analysis revealed a trilinear cytopenia without signs of hemolysis. Acute phase proteins were elevated. Furthermore antinuclear antibodies, anti-phospholipid IgM antibodies, hypocomplementemia, a spurious IgGkappa paraprotein were noted. CT scans confirmed lymphadenopathy and revealed a pleural and pericardial effusion. Bone marrow biopsy showed marked hypercellularity and polyclonal plasmocytosis. Based on these findings systemic lupus erythematosus was initially suspected. However when abdominal MRI showed a retroperitoneal mass, an extensive histological workup, which also included lymph nodes and spleen, revealed numerous plasma cells and histiocytes in dilated sinuses, diagnostic of Rosai-Dorfman sinus histiocytosis. TREATMENT AND COURSE: High dose corticosteroids, intravenous gamma-globulin and repeated courses of cyclophosphamide failed to improve the pancytopenia, as did splenectomy. The patient was given the anti-CD20 monoclonal antibody Rituximab and all signs and symptoms improved dramatically. 18 months after the last treatment, the patient is in complete clinical and hematological remission. CONCLUSIONS: Sinus histiocytosis of Rosai/Dorfman can be associated with or mimic severe SLE. Rituximab, an anti-CD20 monoclonal antibody, may improve the antibody-mediated pathogenetic mechanism underlying both entities.

Acute-Phase Proteins↗
PubMed2000

[Mitochondrial medicine for internists].

Human mitochondrial DNA (mtDNA) is a small, circular molecule, encoding for the translational machinery of the mitochondrion, as well as for 13 structural proteins that are all subunits of the respiratory chain. Point mutations, deletions, and copy-number variations are now functionally and genetically linked to human disease. Despite the fact that mtDNA is solely transmitted from the mother to the offspring, e.g. is maternally inherited, some mutations may occur spontaneously or may be acquired due to defects in nuclear DNA, e.g. are inherited in a mendelian fashion. The internist encounters predominantly myopathies, cardiomyopathies, lactic acidosis or diabetes mellitus but mtDNA-changes are also present with neurologic, hematologic and renal symptoms. Acquired mtDNA alterations are responsible for important drug side effects, such as ifosfamide, carboplatin, doxorubicin or nucleoside-analog reverse-transcriptase inhibitors. A specific mtDNA point-mutation predisposes to aminoglycoside-induced sensorineural deafness.

DNA Mutational Analysis↗