Buffalo Hump is commonly reported in adults with HIV-associated lipodystrophy. Accumulation of fat over the dorso-cervical spine is reported in 2% to 13% of HIV infected patients with a higher prevalence (6 to 13%) in those showing any other feature of the lipodystrophy syndrome [
4]. The pathogenesis underlying this aspect of lipodystrophic syndrome is poorly understood. Guallar
et al. reported that Buffalo Hump adipose tissue shows specific disturbances in gene expression with respect to subcutaneous fat from HIV-1-infected/HAART-treated patients [
5]. Some reports indicate that Buffalo Hump is associated with other physical features of the lipodystrophy phenotype and suggest that hyperinsulinemia, insulin resistance, obesity, and hypercortisolism, are important components of this phenotype [
6‐
9]. The close relationship between Buffalo Hump and glycaemic parameters suggests patients with Buffalo Hump are at higher risk for diabetes and metabolic syndrome. In fact, biochemically, patients with Buffalo Hump tend to have or develop signs or symptoms of metabolic syndrome. Mallon
et al. reported that patients with Buffalo Hump had higher BMI and more total limb and abdominal fat than patients without Buffalo Hump. Current data indicate that a possible contributing cause, but not the main one, could be exposure to antiretroviral drugs: risk factors for Buffalo Hump are longer duration of use of protease inhibitors and longer duration of use of zidovudine [
10]. Palacios
et al. showed that Buffalo Hump was associated with treatment with saquinavir, indinavir, efavirenz, tenofovir and stavudine. Moreover, time of exposure to stavudine and fat loss, one of stavudine's major side-effects, were associated with Buffalo Hump [
11]. Previous reports, however, indicated that the appearance of buffalo hump could not be associated with any specific component of HAART regimes and that it is associated with specific disturbances in gene expression of adipose tissue [
4,
5].
We report the development of the Buffalo Hump cannot be attributed to hypercortisolism; insulin resistance, diabetes, dyslipidemia, hyperlactatemia and metabolic syndrome were not present. Moreover, there were no significant changes noted in our patient's diet, body weight and BMI. Her lifestyle was normal and she followed a regular exercise program.
At the moment she is not in therapy with antiretroviral drugs that are described as the cause of Buffalo Hump; on the other hand she developed this side effect three months after the switch of the antiretroviral therapy to RAL plus unboosted ATV. A caveat of this report is that she had a history of exposure to antiretroviral drugs (Zidovudine, Stavudine, Indinavir) associated with the development of Buffalo Hump. This condition may have predisposed the patient to develop the disorder and could constitute a background that contributes to the final appearance of buffalo hump after raltegravir plus atazanavir treatment. Current data indicate that the etiology of HIV-associated Buffalo Hump remains elusive but is likely multifactorial and includes, metabolic disorders, genetic factors, receipt of ART and HIV infection itself [
12].