Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise defective adult bone mineralisation, distinguish nutritional vitamin-D deficiency from renal or phosphate-wasting causes, interpret the calcium-phosphate-parathyroid pattern, and replace missing substrate safely while treating the underlying disorder.
Bone quantity may be reduced in both osteoporosis and osteomalacia, but osteomalacia leaves osteoid insufficiently mineralised. Ask about diffuse rib, pelvic, hip or foot pain; rising from a chair, stairs, falls and fractures; sunlight, skin pigmentation, clothing, diet and supplements; diarrhoea, bariatric or intestinal surgery; kidney or liver disease; dental history; and anticonvulsant, tenofovir or iron-infusion exposure. Examine gait, proximal power, bone tenderness, deformity and signs of malabsorption or tubular dysfunction.
Interpret tests physiologically rather than treating a vitamin-D number in isolation. Nutritional deficiency commonly lowers 25-hydroxyvitamin D and phosphate while raising ALP and PTH, but calcium may remain in range until advanced disease. In CKD, eGFR, phosphate, PTH and ALP reflect CKD-mineral bone disorder. In isolated hypophosphataemia, urinary handling distinguishes appropriate renal conservation from FGF23-mediated or proximal-tubular loss. A low DXA result is nonspecific and can lead to unsafe antiresorptive treatment if mineralisation failure is missed.
Low sunlight, deeply pigmented skin, covering clothing, limited diet, frailty, obesity and malabsorption reduce vitamin-D availability; liver disease or enzyme-inducing medicines may impair handling.
Advanced chronic kidney disease reduces calcitriol production and phosphate excretion, driving secondary hyperparathyroidism and mixed renal bone disease rather than simple nutritional deficiency.
FGF23-mediated inherited disease or mesenchymal tumours, and proximal tubular disorders such as Fanconi syndrome, cause inappropriate urinary phosphate loss despite hypophosphataemia.
Anticonvulsants, tenofovir, repeated ferric carboxymaltose and aluminium can contribute; hypophosphatasia instead has low alkaline phosphatase and must not be mislabelled.
Osteoblasts produce collagenous osteoid, but inadequate calcium-phosphate product or mineralisation defects prevent hydroxyapatite deposition, leaving mechanically soft bone.
Vitamin-D deficiency reduces intestinal calcium absorption; PTH preserves serum calcium by increasing turnover and renal phosphate loss, so calcium may remain normal while phosphate falls.
Increased osteoblastic effort raises alkaline phosphatase, while newly formed matrix remains inadequately mineralised, producing diffuse pain, microfractures and pseudofractures.
Vitamin-D and phosphate depletion impair proximal muscle performance and postural control, causing difficulty rising or climbing stairs and adding falls to skeletal vulnerability.
Poorly localised rib, pelvic, hip, lumbar or foot pain and bony tenderness are typical, unlike isolated joint-line pain.
Difficulty rising without arm support, climbing stairs or lifting, with waddling gait but preserved sensation, suggests mineral-related muscle dysfunction.
Looser zones are transverse incomplete radiolucent lines with sclerotic margins, often symmetrical at femoral necks, pubic rami, ribs or scapulae.
Housebound status, little skin exposure, dark skin, restrictive diet without supplementation, frailty or malabsorptive surgery increases deficiency probability.
Childhood short stature or deformity suggests inherited disease; adult-onset fractures with severe low phosphate can indicate an FGF23-secreting tumour.
Glycosuria despite normal blood glucose, aminoaciduria, bicarbonate loss, hypokalaemia and low urate accompany generalised proximal tubular phosphate wasting.
Osteoporosis reduces the amount and architecture of normally mineralised bone and usually leaves calcium, phosphate and ALP normal; DXA alone cannot distinguish it.
Polymyalgia, inflammatory myopathy, hypothyroidism and neurological weakness resemble proximal disability; CK, inflammatory markers, thyroid tests and examination localise the process.
Paget disease causes focal high-turnover lesions, while metastasis or myeloma causes destructive pain; imaging distribution and complete biochemical pattern separate them.
Adult hypophosphatasia can cause stress fractures, early tooth loss and pain but has persistently low ALP; bisphosphonates may be harmful if it is mistaken for osteoporosis.
Looser zones and complete fractures occur in ribs, pubic rami, femoral neck, subtrochanteric femur and metatarsals, sometimes bilaterally or at multiple stages.
Proximal weakness, waddling gait and pain impair transfers and balance, leading to falls, deconditioning, dependency and complications of immobility.
Longstanding severe disease may cause kyphosis, pelvic or long-bone deformity and permanent mechanical disability even after mineralisation improves.
Excess calcium or active vitamin D causes hypercalcaemia, hypercalciuria, stones and kidney injury; rapid phosphate therapy can cause hypocalcaemia and ectopic calcification.
Secondary hyperparathyroidism can defend serum calcium at the cost of skeletal mineral and urinary phosphate loss, so normal calcium does not exclude severe disease.
Raised ALP supports active osteomalacia after hepatic disease is excluded; persistently low ALP points away and raises hypophosphatasia.
Low areal density occurs in both deficient mineralisation and osteoporosis; biochemistry and context must be resolved before antiresorptive treatment.
A healthy kidney should conserve phosphate during hypophosphataemia; continued urinary loss identifies a tubular or FGF23-mediated process.
Biochemical substrate improves before skeletal strength and muscle confidence fully recover; rehabilitation and fracture protection remain important during remineralisation.
Do not diagnose osteoporosis from DXA alone when diffuse pain, proximal weakness or abnormal phosphate and ALP suggest a mineralisation disorder.
Do not use serum calcium as a substitute for vitamin D, phosphate, PTH and ALP; compensation can conceal substrate deficiency.
Do not treat persistent hypophosphataemia with vitamin D alone without checking urinary loss, medicines, Fanconi features and FGF23 disease.
Do not prescribe calcitriol as a stronger routine vitamin D; it bypasses regulation and can rapidly cause hypercalcaemia.
Do not begin denosumab or intravenous bisphosphonate while clinically important hypocalcaemia or osteomalacia remains uncorrected.
Do not attribute failure to improve solely to non-adherence; malabsorption, wrong mechanism, fracture or phosphaturic tumour may need detection.
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A housebound adult has diffuse bone pain, proximal weakness, low vitamin D, raised alkaline phosphatase, raised PTH and low phosphate, while adjusted calcium remains normal. What best explains the normal calcium?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Check adjusted calcium and renal function. Use specialist advice in granulomatous disease, lymphoma, hyperparathyroidism, stones, severe CKD, complex pregnancy or malabsorption; avoid duplicated supplements.
Review over-the-counter preparations and calcium intake. Hypercalcaemia or hypercalciuria suggests excess or another mechanism; recommended maintenance is generally compatible with pregnancy.
May cause constipation, stones and hypercalcaemia. Separate from levothyroxine, iron, tetracyclines and quinolones; use monitored exposure in CKD and avoid calcium loading in hypercalcaemia.
Hypercalcaemia and hypercalciuria can develop rapidly; monitor minerals, kidney function and urine calcium, avoid uncoordinated supplements and obtain specialist pregnancy advice.