Hi all.
One of the things I try to do for patients is “condition-specific” research, which is admittedly informal but nonetheless focused on their needs. I try to search through a wide range of authoritative publications; I even go to libraries (ya know, the places with all the books).
I had an interesting but unsettling conversation tonight with a patient that is considering ADR, but learned of some system bone density issues he is facing. I did some research on his behalf, but was reminded of past conversations with other patients with similar symptoms and metabolic (bone) disorders. Some of these articles are below.
So my question – where the heck are all the research dollars that could be answering the questions that these studies seem to raise? Do the answers that research
might reveal matter to patients within this community?
I can't help but to notice the international "flavor" of the few citations I found on this subject...
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Bone Mineral Density Loss in HCV
Reported by Jules Levin
DECREASED BONE MINERAL DENSITY IN NONCIRRHOTIC PATIENTS WITH CHRONIC HEPATITIS B OR C
Ingolf Schiefke 1 , Gudrun Borte 2 , Manfred Wiese 3 , Eva Schenker 1 , A. Fach 1 Department of Gastroenterology, University of Leipzig; 2 Department of Radiology, University of Leipzig; 3 Muncipal Hospital `St. Georg', Teaching Hospital of the University of Leipzig, Germany
Background/Aims: Several previous studies suggest that loss of bone mineral density is common among patients with chronic liver diseases. We studied bone mineral metabolism and density in patients with chronic hepatitis B or C without cirrhosis.
Methods: Biochemical markers of bone turnover and bone mineral density were measured in 42 consecutive patients. They are suffering from viral hepatitis B (n = 13) and hepatitis C (n = 29). Bone mineral density was measured by dual x-ray absorptiometry in the lumbar spine and femoral neck. The values were expressed as the T and Z score. Bone metabolism markers and hormone profiles were measured.
Results: Bone mineral density was lowered in 29 (69%) of our investigated 42 patients with chronic hepatitis B or C (femoral neck: 0.711 ± 0.129 g/cm*cm; lumbar spine: 0.951 ± 0.126 g/cm*cm). 8 of the 29 osteopenic patients (28%) have osteoporosis. T-score value in chronic Hepatitis C patients was more decreased (femoral neck T: •1.59 ± 0.98; lumbar spine T: •1.10 ± 1.09) compared with patients with chronic hepatitis B (femoral neck T: •1.31 ± 1.00; lumbar spine T: •0.79 ± 1.29). Serum and urine biochemical markers were within the normal limits in both groups.
Conclusion: Chronic hepatitis B or C in noncirrhotic patients may induce bone loss. In view of our results and according to previous studies this secondary effect of chronic hepatitis should be further investigated in following studies with larger number of included patients. Markers of bonemetabolism and bone mineral density might be used in monitoring these patients to reduced their risk of developing osteoporosis.
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Painful postoperative neuritis is common after lumbar decompression in patients with hepatitis B and C. The Spine Journal, Volume 4, Issue 5, Pages S69-S70 N. Ahn, U. Ahn, J. Datta, B. Ipsen, H. Basran, Z. Post, T. Salsbury, W. Reed, Jr., A. Bailey, W. Hopkins
Reduced bone mineral density and altered bone turnover markers in patients with non-cirrhotic chronic hepatitis B or C infection.
Schiefke I, Fach A, Wiedmann M, Aretin AV, Schenker E, Borte G, Wiese M, Moessner J.
Department of Medicine II, University of Leipzig, Philipp-Rosenthal Str. 27, 04103 Leipzig, Germany.
schi@medizin.uni-leipzig.de
AIM: Previous studies suggest that loss of bone mineral density (BMD) frequently occurs in patients with chronic viral liver disease, presenting with histologically proven liver cirrhosis. However, little is known about the occurrence of bone disease in non-cirrhotic patients with chronic hepatitis B or C. Therefore, it was the aim of this study to evaluate this particular population for BMD and bone turnover markers. METHODS: Biochemical markers of bone turnover and BMD were measured in 43 consecutive patients with HCV (n = 30) or HBV (n = 13) infection without histological evidence for liver cirrhosis. Mean age was 49 years (range 26-77 years). BMD was measured by dual X-ray absorptiometry in the femoral neck (FN) and the lumbar spine (LS) region. In addition, bone metabolism markers were measured. RESULTS: BMD was lowered in 25 (58%) of the patients with chronic hepatitis B or C (FN: 0.76 (0.53-0.99); LS: 0.96 (0.62-1.23) g/cm(2)). Eight (32%) osteopenic patients were diagnosed with osteoporosis. Bone-specific alkaline phosphatase (P = 0.005) and intact parathyroid hormone (iPTH) (P = 0.001) were significantly elevated in the more advanced stages of fibrosis. Mean T-score value was lower in patients with chronic hepatitis C as compared to patients suffering from chronic hepatitis B; however, the difference was not statistically significant (P = 0.09). CONCLUSION: There was a significantly reduced BMD in non-cirrhotic patients with chronic hepatitis B or C infection. Alterations of bone metabolism already occurred in advanced liver fibrosis without cirrhosis. According to our results, these secondary effects of chronic viral hepatitis should be further investigated.
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Multiple sclerosis after hepatitis B vaccination in a 16-year-old patient
Daniella Terney, Sándor Beniczky, Péter Barsi, István Kondákor, József Perényi, Béla Faludi, Magdolna Szapper, László Vécsei
Daniella Terney Department of Neurology, Albert Szent-Gy?rgyi Medical and Pharmaceutical Centre, University of Szeged, P.O. Box 427, H-6701 Szeged, Hungary; Sándor Beniczky Department of Neurology, Albert Szent-Gy?rgyi Medical and Pharmaceutical Centre, University of Szeged, P.O. Box 427, H-6701 Szeged, Hungary; Péter Barsi Department of Radiology, OPNI, H?v?sv?lgyi út 116, H-1021 Budapest, Hungary; István Kondákor Department of Neurology, University of Pécs, Rét u. 2, H-7623 Pécs, Hungary; József Perényi Department of Neurology, OPNI, H?v?sv?lgyi út 116, H-1021 Budapest, Hungary; Béla Faludi Department of Neurology, University of Pécs, Rét u. 2, H-7623 Pécs, Hungary; Magdolna Szapper Department of Neurology, OPNI, H?v?sv?lgyi út 116, H-1021 Budapest, Hungary; László Vécsei Department of Neurology, Albert Szent-Gy?rgyi Medical and Pharmaceutical Centre, University of Szeged, P.O. Box 427, H-6701 Szeged, Hungary
Correspondence to: László Vécsei Department of Neurology, University of Szeged , Semmelweis u. 6 , H-6725 Szeged, Hungary (Tel:36-62-545351 Fax:36-62-545597 Email:vecsei@nepsy.szote.u-szeged.hu )
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