Osteomalacia due to Fanconi’s syndrome and renal failure caused by long-term low-dose adefovir dipivoxil

Shimohata, Homare; Sakai, Shinsuke; Ogawa, Yujiro; Hirayama, Kouichi; Kobayashi, Masaki

doi:10.1007/s10157-012-0762-8

Cited by 16 publications

(13 citation statements)

References 2 publications

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“…Respect to other papers [8][9][10][11][12][13][14][15][16][17] that reported the association between adefovir and renal-toxicity, in the present case, using HPLC, we documented low plasma levels of vitamin D responsible of femoral fractures after an accidental fall related to muscle cramps.…”

supporting

confidence: 54%

Adefovir dipivoxil-induced development of osteomalacia and Fanconi syndrome during the treatment of hepatitis B virus (HBV)-related cirrhosis

Staltari¹,

Caroleo

Michniewicz

et al. 2014

CMI

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A 55-year-old man (height = 175 cm, weight = 68 kg, Body Mass Index = 22.2 kg/ m 2 ) came to our observation in December 2012 due to the onset of bone pain, muscle cramps, and asthenia. Past history revealed that about 24 years before (1988) a chronic hepatitis B (anti-HBe positive) infection was diagnosed and 15 years later (2003) liver biopsy and endoscopy documented the presence of cirrhosis (Child 5A) with esophageal varices, respectively.On 2005, a treatment with pegylated interferon (180 µg/week subcutaneously) was started (HBV-DNA = 10,000,000 IU/ml), but 18 months later (February 2007) for the persistence of high HBV-DNA levels (HBV-DNA = 352,000 IU/ml), pegylat- Why we describe this caseNotwithstanding adefovir is considered safe at the dosage of 10 mg/day, renal function must be carefully evaluated in order to prevent systemic disease and bone fracture. This case report could be useful in order to perform an appropriate prescription in HBV patients treated with adefovir and a risk of kidney or bone disease (e.g. patients taking non steroidal antinflammatory drugs, aminoglycosides, corticosteroids or menopausal women) ed-interferon was stopped and lamivudine (100 mg/day) was administered. During the follow-up, three months later ( Rate before adefovir = 78.26 ml/min/1.73 m 2 ; during adefovir treatment = 57.38 ml/min/1.73 m 2 ) Abstract Adefovir dipivoxil is a nucleotide analog reverse transcriptase inhibitor used to treat adult patients affected by HBeAg-positive and HBeAg-negative chronic hepatitis B and with clinical evidence of lamivudine-resistant hepatitis B virus (HBV). Adefovir administered at a dosage of 10 mg/day is generally well tolerated, even if renal toxicity, type Fanconi syndrome, was reported during long-term treatments. We report a case of osteomalacia with Fanconi syndrome and pathologic fracture of the femur related to long-time (67 months) adefovir treatment (10 mg/day) in a patient with compensated hepatitis B virus (HBV) cirrhosis (Child 5A) and with a previous normal renal function (estimated Glomerular Filtration . The patient was switched to entecavir at a dose of 1 mg/day, with both suppression of viremia and improvement of osteomalacia and Fanconi syndrome; the patient's follow-up is still ongoing after 22 months. Sviluppo di osteomalacia e di sindrome di Fanconi durante il trattamento con adefovir in un paziente affetto da cirrosi epatica HBV-correlataCMI 2014; 8(4): 109-114 http://dx.doi.org/10.7175/cmi.v8i4.969 1 Rete Regionale di informazione sul farmaco,

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supporting

confidence: 54%

Adefovir dipivoxil-induced development of osteomalacia and Fanconi syndrome during the treatment of hepatitis B virus (HBV)-related cirrhosis

Staltari¹,

Caroleo

Michniewicz

et al. 2014

CMI

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“…The adefovir is the nucleotide analogue and excreted by the active transportation through the translocator from the renal tubule, as well as the glomerular filtration. [20] The adefovir causes the nephrotoxicity due to the cell necrosis by inhibiting the mytocondria DNA synthesis and the nephrotoxicity increases more due to improper excretion by directly affeting the translocator. [24] A total of 13 patients stop using the adefovir as the treatment and 6 of them change the medicine to the entecavir.…”

Section: Discussionmentioning

confidence: 99%

Two Cases of Hypophosphatemic Osteomalacia After Long-term Low Dose Adefovir Therapy in Chronic Hepatitis B and Literature Review

Jeong

Lee

et al. 2014

J Bone Metab

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Adefovir dipivoxil (ADV) is a nucleotide used as long-term therapy of chronic hepatitis B. Many published reports have shown that long-term high-dose therapy with adefovir can be associated with proximal renal tubular dysfunction resulting in significant hypophosphatemia, renal insufficiency and osteomalacia. We have encountered two patients who developed evidence of hypophosphatemic osteomalacia while on long-term low-dose adefovir therapy for chronic hepatitis B. We report on its clinical features and its potential resolution with cessation of the drug and supplementation with phosphate. We also reviewed the other published cases associated with hypophosphatemic osteomalacia after low-dose adefovir therapy. The symptoms and the hypophosphatemia improved after cessation of the drug and supplementation with phosphate in most cases. Patients taking adefovir long-term should receive regular investigation of the phosphate level and renal function.

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“…In these disorders, phosphatonins (phosphaturic hormones) inhibit renal tubular reabsorption of phosphate and reduce serum 1, 25-dihydroxyvitamin D level by mediating the several enzymes associated with vitamin D metabolism. [5–8] In clinical practice, this disorder cannot be only induced by phosphaturic mesenchymal tumor, [9,10] but also secondary to SS [4,11,12] or hyperparathyroidism, [13] even related to the adefovir therapy. [2,14] Although the clinical symptoms of HO are unspecific or noncharacteristic, it is very important and valuable to reveal etiological cause of this disorder to provide appropriate therapy.…”

Section: Discussionmentioning

confidence: 99%

Adult-onset hypophosphatemic osteomalacia associated with Sjogren syndrome

Shen

Zhang²,

Hu³

et al. 2017

Medicine

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Rationale:Hypophosphatemic osteomalacia (HO) is a metabolic bone disease, exhibiting different etiologies such as genetic mutation, tumor induction, dysimmunity, or renal disease. Sjogren's syndrome (SS) is a connective tissue disorder commonly involving exocrine glands; however kidney involvement is also encountered, leading to abnormal phosphorus metabolism, even HO.Patient concerns:A 47-year-old female patient presented progressively worsening pain in the chest wall, back and bilateral lower extremities as well as muscle weakness was referred to our department.Diagnoses, interventions and outcomes:Due to the laboratory test results, radiographic findings and pathologic results, she was diagnosed with adult-onset HO associated with SS. She was then treated with alkalinization, steroids, neutral phosphate, calcium supplements together with activated vitamin D. So far, she recovered uneventfully with relieved pain and increased serum phosphorus level.Lessons:HO may be secondary to renal tubular acidosis of SS patients, and it might be a diagnostic challenge when the kidney involvement in SS is latent and precede the typical sicca symptoms.

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Osteomalacia due to Fanconi’s syndrome and renal failure caused by long-term low-dose adefovir dipivoxil

Cited by 16 publications

References 2 publications

Adefovir dipivoxil-induced development of osteomalacia and Fanconi syndrome during the treatment of hepatitis B virus (HBV)-related cirrhosis

Adefovir dipivoxil-induced development of osteomalacia and Fanconi syndrome during the treatment of hepatitis B virus (HBV)-related cirrhosis

Two Cases of Hypophosphatemic Osteomalacia After Long-term Low Dose Adefovir Therapy in Chronic Hepatitis B and Literature Review

Adult-onset hypophosphatemic osteomalacia associated with Sjogren syndrome

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