Acquired hypophosphatemic osteomalacia is easily misdiagnosed or neglected by rheumatologists: A report of 9 cases

Abstract

The aim of the present study was to assist rheumatologists in differentiating hypophosphatemic osteomalacia (HO) from mimic rheumatology diseases. Clinical data was obtained from 9 patients with acquired HO, initially misdiagnosed as mimic rheumatologic diseases. The data were retrospectively analyzed and a literature review was performed. The etiology of the cases was as follows: Adefovir dipivoxil-induced Fanconi syndrome was present in 6 of the cases, 2 were tumors and 1 case was chronic nephropathy. The chief complaint was thoracic or back pain and arthralgia, followed by progressive muscle weakness and dramatic movement limitation. All patients were transferred to 3-6 hospitals for extended periods due to misdiagnosis with conditions such as ankylosing spondylitis, chronic arthritis, lumbar disc disease, osteoporosis and somatoform disorder. Hypophosphatemia was observed in the patients and bone scans revealed diffusely decreased tracer uptake, with multiple hot spots of fractured sites and involved joints. Furthermore, patients' bone density was markedly low compared with the normal range for their age and sex. In the present study, 6 of the patients recovered when adefovir dipivoxil was stopped. In 1 case, hypophosphatemia was ameliorated following tumor resection. The remaining patients, 1 with sub-skull tumor and 1 with chronic kidney disease, had poor prognoses due to incurable diseases. In conclusion, diagnosing HO is challenging for rheumatologists and physicians. Basic examinations of electrolyte balance and bone mineral density should be performed, as should tumor screening and a careful collection of patient medical history and drugs in young patients with unexplained thoracic or back pain and muscle weakness. Removing any secondary etiology, such as drugs may dramatically improve the patients clinical manifestations and result in an improved prognosis.

Hypophosphatemic osteomalacia in neck femur fracture: Case series

“…Endocal Forte OD, Protocol Supplement 2tsp with milk BD Adophos Sachet in ½ glass of Water QID, Tab. Rocaltrol (2.5) QID, average Patient were walking without support in an average 2 weeks, Pain decreased and also there is improvement of haematological parameter , X-ray shows signs of healing fracture These findings are similar to LING LI [14] et al they found Clinical data was obtained from 9 patients with acquired HO, initially misdiagnosed as mimic rheumatologic diseases. The data were retrospectively analyzed and a literature review was performed.…”

“…Typically, HO is either inherited [9] , a result of tumor-induced osteomalacia (TIO) [11] , druginduced [10] or a symptom of chronic kidney disease [12] . Patients with inherited or TIO have been widely reported on by endocrinology or oncology specialists, however HO is often misdiagnosed in clinical practice as ankylosing spondylitis (AS), chronic arthritis, lumbar disc disease, osteoporosis and somatoform disorder, as it typically presents with the same signs and symptoms of these rheumatologic diseases, including bone pains, thoracic or back pain, muscle weakness, proximal myopathy and arthralgia [14] . Diagnosis of HO remains a challenge to rheumatologists and physicians due to its low prevalence and nonspecific manifestations.…”

Fanconi syndrome induced by adefovir dipivoxil: a case report and clinical review

“…The main characteristics of 32 patients with ADV-induced FS, including eight patients in our institution and 24 published cases, are summarized in Table 4 . 5 , 18 , 22 , 23 , 36 – 43 …”

“…Moreover, a study using a 6‐month follow‐up period found that patients with chronic kidney disease and tubule acidosis have a poor prognosis. 22 …”

“…Some descriptive studies identified male sex, decreased eGFR at the start of ADV treatment, hypertension, diabetes, cirrhosis, East Asian ethnicity, low body mass index, treatment with ADV for more than 24 months, residence in rural areas, and prior use of nephrotoxic drugs as risk factors for ADV-induced FS. 7,18,22,23 A study that focused on kidney tubular dysfunction induced by ADV identified a long treatment duration and older age at treatment initiation as risk factors via logistic regression analysis. 24 However, the number of cases was not sufficient, and further research and analysis are required.…”