High prevalence of vitamin D deficiency in patients with HIV

This article is more than 13 years old. Click here for more recent articles on this topic

Almost a third of HIV-positive patients have vitamin D deficiency, Dutch researchers report in the November edition of AIDS Research and Human Retroviruses. Dark skin colour was the most important risk factor for this disorder. Amongst patients with white skin, more patients taking NNRTI-based HIV treatment had vitamin D deficiency than did patients taking antiretroviral therapy based on a protease inhibitor.

Vitamin D is important to good health. It is required for bone health and also plays an important role in the regulation of the immune system. Vitamin D deficiencies have been associated with low CD4 cell counts, an activated immune system and HIV disease progression.

The vitamin can be obtained from diet and is also produced by the skin when exposed to sunlight.



A chemical messenger which stimulates or suppresses cell and tissue activity. Hormones control most bodily functions, from simple basic needs like hunger to complex systems like reproduction, and even the emotions and mood.

immune system

The body's mechanisms for fighting infections and eradicating dysfunctional cells.

multivariate analysis

An extension of multivariable analysis that is used to model two or more outcomes at the same time.

reverse transcriptase

A retroviral enzyme which converts genetic material from RNA into DNA, an essential step in the lifecycle of HIV. Several classes of anti-HIV drugs interfere with this stage of HIV’s life cycle: nucleoside reverse transcriptase inhibitors and nucleotide reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs). 


Clear, non-cellular portion of the blood, containing antibodies and other proteins and chemicals.


Deficiencies in vitamin D can have a number of causes, including ageing, low exposure to sunlight, and poor diet. HIV itself can also affect levels of vitamin D. Furthermore the vitamin is metabolised by the body in the same way as many anti-HIV drugs, using the P450 pathway, and some earlier research had suggested that protease inhibitors can inhibit the body’s ability to metabolise vitamin D.

Blood levels of 25-hydroxyvitamin D are the best measure of vitamin D deficiency.

Dutch investigators therefore designed a cross-sectional (or “snap-shot”) study to examine the prevalence and causes of vitamin deficiency amongst 252 HIV-positive patients who were receiving HIV care between January and August 2006.

Blood levels of the vitamin were measured by analysing levels of 25-hydroxyvitamin D. The investigators also conducted a number of other laboratory tests, measuring levels of parathyroid hormone, serum calcium, CD4 and CD4 cell counts and HIV viral load.

Data were also gathered on the patients’ demographics including race and age, the duration and stage of HIV infection, the use of antiretroviral treatment, medical history, and body mass index.

The patients were also asked to complete a questionnaire providing details of their diet and exposure to sunshine.

Vitamin D deficiency was defined as levels of 25-hydroxyvitamin D below 35nmol/l between April and September and below 25 nmol/l between September and March.

Overall, 29% of patients were assessed as having vitamin D deficiency.

In the investigators' first set of analysis, women were found to have a higher prevalence of vitamin D deficiency than men (58% vs. 25%). This was not an effect of the menopause as the average age of women with or without vitamin D deficiency was the same (approximately 36).

Patients with darker skin colour also had an increased risk of vitamin D deficiency, being present in 19% of white patients, 33% of patients of Mediterranean origin, 44% of Asian patients and 63% of black patients. This finding was supported by data showing that median levels of 25-hydroxyvitamin D were significantly higher in white patients (60 nmol/l) than black patients (27 nmol/l, p < 0.001).

Of the patients not taking antiretroviral therapy, 25% had vitamin D deficiency compared to 30% of individuals taking anti-HIV drugs.

Amongst the patients taking HIV treatment, there was a higher prevalence of vitamin D deficiency amongst those taking a non nucleoside reverse transcriptase inhibitor than seen in those taking a protease inhibitor (37% vs. 23%).

When the investigators stratified their results by skin colour, they found that white patients taking a protease inhibitor had significantly higher levels of 25-hydroxyvitamin D than either white patients taking an NNRTI or no HIV treatment (p = 0.007). However, amongst patients with black skin colour, the type of HIV treatment (or no treatment) did not significantly affect levels of 25-hydroxyvitamin D.

There were no significant differences in diet or exposure to sunlight between the patients with or without vitamin D deficiency.

In multivariate analysis, the only factor that was shown to be significantly associated with an increased risk of vitamin D deficiency was skin colour (adjusted odds ratio = 5.4, 95% CI 2.3-12,2, p < 0.001).

Patients taking both protease inhibitors and NNRTIs had levels of parathyroid hormone that were significantly higher than those observed in patients who were not taking HIV treatment (both comparisons, p < 0.001).

However, the investigators found that rates of CD4 cell count recovery were similar in patients with or without vitamin D deficiency.

The researchers conclude, “an adequate vitamin D status is necessary for the maintenance of good bone mineral density. Therefore the vitamin D status of HIV-infected patients, especially those having a dark skin colour or receiving NNRTI- protease inhibitor-containing [antiretroviral therapy], should be evaluated” by measuring both 25-hydroxyvitamin D and levels of parathyroid hormone. “By doing so vitamin D deficiency could be detected early and treated.”


Van den Bout-Van Den Beukel, C. et al. Vitamin D deficiency among HIV type 1-infected individuals in the Netherlands: effects of antiretroviral therapy. AIDS Research and Human Retroviruses 24: 1375-82, 2008.