Intended for healthcare professionals

Education And Debate

Lesson of the Week: Hypovitaminosis D in immigrant women: slow to be diagnosed

BMJ 1996; 312 doi: https://doi.org/10.1136/bmj.312.7030.570 (Published 02 March 1996) Cite this as: BMJ 1996;312:570
  1. Jeannine F J B Nellen, registrara,
  2. Yvo M Smulders, registrara,
  3. P H Jos Frissen, consultanta,
  4. Ed H Slaats, clinical chemista,
  5. Joseph Silberbusch, consultanta
  1. a Department of Internal Medicine, Onze Lieve Vrouwe Gasthuis, 1e Oosterparkstraat 279, PO Box 95500, 1090 HM Amsterdam, Netherlands
  1. Correspondence to: Dr Nellen.
  • Accepted 17 November 1995

Vitamin D deficiency in adults eventually leads to the osteomalacia syndrome, with its characteristic clinical features of bone pain, muscle weakness, and difficulty in walking. Even in moderate deficiency there is both biochemical and histological evidence of secondary hyperparathyroidism and increased bone remodelling. At this stage the characteristic symptoms of classic osteomalacia may still be absent, although irreversible cortical bone loss has already occurred. This is referred to as hypovitaminosis D osteopathy stage I.1

Hypovitaminosis D osteopathy should be considered in immigrant women with musculoskeletal pain

Hypovitaminosis D is common in western Europeans, especially in patients with malabsorption and in elderly people eating a deficient diet. An increased incidence of hypovitaminosis D osteopathy among immigrant women could be expected because of their low intake of calcium and vitamin D, minimal exposure to sunlight, skin pigmentation, and high parity.2 We report symptomatic hypovitaminosis D in six immigrant women, focusing on the time between the first consultation with a doctor and the establishment of the correct diagnosis.

Patients, methods and results

We diagnosed hypovitaminosis D osteopathy as musculoskeletal pain in the presence of an increased intact parathyroid hormone concentration, a decreased concentration of 25-hydroxycholecalciferol, and a favourable clinical response to vitamin D replacement. We analysed the general practitioner's and hospital notes of all patients with this disorder who had been referred to this department from January 1990 to December 1992. From the notes we recorded (a) the time taken to refer the patient to this department, where the hypovitaminosis D osteopathy was eventually diagnosed; (b) the symptoms reported by the patients (localised or diffuse bone pain, difficulty in walking with or without muscle weakness, neurological complaints such as paraesthesia or muscle spasms, and non-specific complaints such as fatigue and malaise); and (c) referrals to other specialties, undue diagnostic procedures, and unsuccessful therapeutic interventions.

Table 1 shows the demographic and clinical data of six patients who satisfied the above criteria. The duration of complaints before diagnosis varied from 7 to 103 months (mean 59.2 (SD 36.2)). In retrospect, the symptoms the patients complained of were typical of hypovitaminosis D osteopathy from the beginning. Symptoms were at first unrecognised or misinterpreted. Previous referrals were mostly to orthopaedic surgeons and for many x ray examinations and blood tests. All patients had been prescribed non-steroidal anti-inflammatory drugs, and four had undergone intensive physiotherapy.

Table 1

Demographic and clinical data on six immigrant female patients with hypovitaminosis D

View this table:

In three cases misinterpretations had serious therapeutic consequences. One patient (case 2) was treated with prednisone for suspected polymyalgia rheumatica, one woman (case 1) received oestrogen because osteoporosis was suspected, and one woman (case 6) underwent cholecystectomy because of subcostal and back pains combined with a solitary gall stone. In all three cases the initial treatment was ineffective.

Relevant laboratory results are shown in figure 1. All patients had a creatinine concentration within the normal range. The concentration of 25-hydroxycholecalciferol was normal in one patient (case 5), who later admitted treating herself with vitamin D shortly before.

Fig 1
Fig 1

Biochemical results in the six patients at time of diagnosis. Horizontal lines show normal reference values and numbers are case numbers of patients

Treatment with vitamin D and calcium was started in all patients. They all became free of symptoms within three months, and alkaline phosphatase activity and intact parathyroid hormone concentration became normal within one to two years.

Discussion

The most striking finding of this survey was the long time it took to establish a correct diagnosis of vitamin D osteopathy. Complaints were taken seriously by doctors, as shown by the amount of diagnostic procedures, therapeutic interventions, and referrals—mostly directed at disclosing orthopaedic and rheumatic diseases.

The delay in diagnosis may have been due to unfamiliarity with the clinical picture of hypovitaminosis D osteopathy and, possibly, a language barrier. Peach et al found that history taking with special attention to change in gait, place of birth, vegetarian diet, and whether arms were usually covered outdoors was more effective than biochemical tests in screening patients.3 The bone pain of hypovitaminosis D is usually dull and poorly localised, often beginning in the lower back and later spreading to the pelvis and hips, upper thighs, upper back, and ribs. Characteristically, the pain is symmetrical, is not felt below the knee and shoulder, and is felt in the bones rather than in the joints. On questioning, patients often complain of muscle weakness and difficulty in walking.

The biochemical results in our patients corresponded to published data on moderate vitamin D deficiency.4 Calcium concentration is often normal, and phosphate concentration can be low, normal, or raised. Alkaline phosphatase activity has a low specificity and a wide range of normal values. Concentrations of 25-hydroxycholecalciferol may be within the normal range because of seasonal variation or, occasionally, self treatment.5 Secondary hyperparathyroidism is the first stage of hypovitaminosis D osteopathy, and intact parathyroid hormone concentrations do not return rapidly to the normal range after treatment has been started.6 Whether intact parathyroid hormone concentrations can be used as an index of disease activity deserves further study. In the absence of a totally sensitive and specific biochemical marker for this disorder, the typical combination of biochemical test results provides strong support for the diagnosis of hypovitaminosis D osteopathy. An alternative approach in clinically suspected disease would be to store serum samples and to evaluate clinical improvement after a test dose of 10000 IU of vitamin D plus extra calcium. Apart from being cheaper and more practical, this approach may even prove to be the best treatment.

We conclude that hypovitaminosis D osteopathy in immigrant women may remain undiagnosed for an unacceptably long time. A higher degree of suspicion in this patient group should shorten the delay and may reduce the number of undue investigations.

References

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