ABSTRACT
ABSTRACT Background. Patients with chronic hepatitis B virus (HBV) are often treated with nucleoside/nucleotide antiviral agents and metabolic bone toxicity is a possible concern. Objective. To determine the relationships between fibroblast growth factor 23 (FGF23), a phosphaturic hormone, bone mineral density (BMD), and bone biochemical abnormalities in these patients. Material and methods. This is a cross-sectional observational study comparing HBV-infected subjects treated for at least one year with tenofovir (TDF), lamuvidine (LVD), entacavir (ETV), or not treated (CON). Patients with abnormalities in either calcium (Ca), phosphate (PO4), intact parathyroid hormone (iPTH) or FGF23 were further evaluated with BMD by DXA. Results. No difference in liver enzymes or renal function seen among groups, but hypophosphatemia was seen in all groups with the highest incidence with TDF treatment (14%). FGF 23 levels were found to be elevated in 11.1% of TDF patients, 2.77% amongst controls. No elevations were found in the LVD or ETV groups. Among a subset of subjects (FGF23, PO4, and/or Ca abnormalities) who underwent further evaluation, 67% had insufficient 25-OH vitamin D, and 30% had elevated 24 h urinary Ca or PO4 excretion. No patients with FGF23 abnormalities had urine abnormalities. 40% had low DXA Z-score (<-2) at spine or hip but there was no difference between control and antiviral treatment groups and the mean FRAX score was 2.33% for major osteoporotic fractures and 0.29% for hip fracture. Conclusion. Abnormalities in bone metabolism, particularly involving vitamin D insufficiency, in HBV-treated subjects were observed with a small increased likelihood in TDF treated patients.
Subject(s)
Humans , Antiviral Agents/therapeutic use , Phosphates/blood , Bone and Bones/drug effects , Calcium/blood , Lamivudine/therapeutic use , Hepatitis B, Chronic/drug therapy , Fibroblast Growth Factors/blood , Tenofovir/therapeutic use , Guanine/analogs & derivatives , Antiviral Agents/adverse effects , Time Factors , Vitamin D Deficiency/chemically induced , Bone and Bones/metabolism , Bone and Bones/diagnostic imaging , Biomarkers/blood , Absorptiometry, Photon , Bone Density/drug effects , Cross-Sectional Studies , Risk Factors , Treatment Outcome , Bone Remodeling/drug effects , Hepatitis B, Chronic/diagnosis , Hepatitis B, Chronic/blood , Fractures, Bone/chemically induced , Tenofovir/adverse effects , Guanine/adverse effects , Guanine/therapeutic useABSTRACT
Entecavir (Baraclude®) is an oral antiviral drug used for the treatment of HBV. Entecavir is a reverse transcriptase inhibitor which prevents the HBV from multiplying. Most common adverse reactions caused by entecavir are headache, fatigue, dizziness, and nausea. Until now, there has been no report of peripheral neuropathy as a side effect associated with entecavir treatment. Herein, we report a case of peripheral neuropathy which probably occurred after treatment with entecavir in a hepatitis B patient. The possibility of the occurrence of this side effect should be carefully taken into consideration when a patient takes a high dose of entecavir for a long period of time or has risk factors for neuropathy at the time of initiating entecavir therapy.
Subject(s)
Humans , Male , Middle Aged , Administration, Oral , Antiviral Agents/adverse effects , Brain/diagnostic imaging , Drug Therapy, Combination , Duloxetine Hydrochloride/therapeutic use , Glucocorticoids/therapeutic use , Guanine/adverse effects , Hepatitis B, Chronic/drug therapy , Polyneuropathies/diagnosis , Prednisolone/therapeutic use , Pregabalin/therapeutic use , Tomography, X-Ray ComputedABSTRACT
BACKGROUND/AIMS: The clinical outcome of patients with a partial virological response (PVR) to entecavir (ETV), in particular nucloes(t)ide analogue (NA)-experienced patients, has not been thoroughly investigated. The aim of the present study was to assess long-term outcomes in NA-naive and NA-experienced chronic hepatitis B patients with a PVR to ETV. METHODS: Chronic hepatitis B patients treated with ETV (0.5 mg/day) for at least 1 year were enrolled retrospectively. PVR was defined as a decrease in hepatitis B virus (HBV) DNA titer of more than 2 log10 IU/mL, yet with residual serum HBV DNA, as determined by real time-polymerase chain reaction, at week 48 of ETV therapy. RESULTS: A total of 202 patients (127 NA-naive and 75 NA-experienced, male 70.8%, antigen positive 53.2%, baseline serum HBV DNA 6.2 +/- 1.5 log10 IU/mL) were analyzed. Twenty-eight patients demonstrated a PVR. The PVR was associated with a high serum HBV DNA titer at baseline and at week 24. Virological response (< 60 IU/mL) was achieved in 46.2%, 61.5%, 77.6%, and 85% of patients with PVR at week 72, 96, 144, and 192, respectively. Resistance to antivirals developed in two NA-experienced patients. Failure of virological response (VR) in patients with PVR was associated with high levels of serum HBV DNA at week 48. CONCLUSIONS: Patients with PVR to ETV had favorable long-term virological outcomes. The low serum level of HBV DNA (< 200 IU/mL) at week 48 was associated with subsequent development of a VR in patients with PVR to ETV.