Case Reports in Medicine vomiting, and diarrhoea. Anorexia may also result from anxiety and depression, which are both common psychiatric complications of HIV infection [15]. Other recognised causes of inadequate nutrient intake include dysphagia and odynophagia, which may be due to infections of the oral cavity, posterior pharynx, or oesophagus. Both micronutrient and macronutrient malabsorption have been observed in the wasting syndrome, and nutrient malabsorption may occur with or without diarrhoea [10, 16]. Chronic diarrhoea leading to malabsorption may either be due to the HIV virus itself (i.e., AIDS enteropathy) or due to occult opportunistic infections (e.g., Cytomegalovirus, Clostridium diﬃcile, and Mycobacterium avium intracellular bacteria, among others) [17]. In AIDS enteropathy, no speciﬁc pathogen can be isolated from the gut, and the chronic diarrhoea, motility disturbances, and mucosal atro- phy accompanying this condition have been attributed to the direct eﬀects of HIV, especially as viral proteins have been found in the gut mucosa [18]. AIDS enteropathy is a diagnosis of exclusion; however, complete exclusion of all opportunistic causes of diarrhoea in HIV-infected patients is a challenging task sometimes requiring invasive techniques [17, 19]. Consequently, the WHO recommends the use of empiric antimicrobials and constipating drugs such as loperamide, for treatment of chronic HIV-related diarrhoea in resource poor settings [20]. By leading to malabsorption and/or changes in pharma- cokinetics of the ART medications, chronic diarrhoea may also contribute to HAART treatment failure. In a clinical study by Brantley et al. [21], AIDS-related diarrhoea and weight loss were associated with both subtherapeutic plasma levels of antiretroviral medications and protozoan pathogens in stool. Hence, in patients receiving HAART, prompt and eﬀective treatment of chronic diarrhoea is essential to prevent both weight loss and HAART treatment failure. Various metabolic abnormalities leading to weight loss have been described in HIV-infected patients, and these abnormalities have been attributed to several etiologies including the HIV virus itself, concomitant opportunistic infections, cytokine dysregulation, and hormonal imbalances accompanying HIV infection, as well as ART medications [10, 11]. A failing HAART regimen leads to persistent viral replication and progressive immunosuppression as reﬂected in the CD4 cell count. Correlations have been established between high HIV viral load, low CD4 cell counts, and weight loss [4, 22, 23]. In HAART experienced patients with suppressed plasma viral load, weight loss has been attributed to the persistence of HIV in peripheral blood monocytes and macrophages [24]. The persistence of HIV leads to excessive cytokine activation and dysregulation, and this in turn triggers various metabolic abnormalities that lead to weight loss such as increase in resting energy expenditure, proteolysis, and hypercatabolism. Cytokines may also inhibit anabolism by causing growth hormone resistance and by reducing hepatic production of insulin-like growth factor-1, a messenger of growth hormone [25]. The increase in resting energy expenditure and cytokine dysregulation in HIV infection may be intensiﬁed by concomitant opportunistic 3 infections [10]. Various cytokines, such tumour necrosis factor α, interleukins-1 (IL-1), IL-6, and interferon gamma, have been implicated in these metabolic perturbations [11]. By interfering with lipid metabolism in muscle, elevated levels of proinﬂammatory cytokines such as TNF-α also lead to muscle weakness and muscle atrophy [26]; both are characteristics features of the wasting syndrome. The use of HAART has also been independently associ- ated with an increase in resting energy expenditure, and this has been suggested as one of the factors perpetuating weight loss in the HAART era [4, 10]. Although sometimes challeng- ing to distinguish, even with appropriate body composition measurements, HAART-induced weight loss often leads to loss of fat loss and/or fat redistribution (Lipodystrophy) with little or no loss of lean body mass [10]. Conversely, the wasting syndrome is characterised by a complex interplay of lean body and fat loss depending on baseline body weight and other factors such as gender [10, 27]. With progressive HIV infection, women lose a higher amount of body fat relative lean body mass while men lose more LBM than fat [27]. These gender diﬀerences in weight loss have been attributed greater premorbid fat stores in women than men, as well as due biological and hormonal factors [27]. Hypogonadism, represented by low levels androgen such as testosterone, may accompany HIV infection in men [28], and it may be as a result of the suppressive eﬀects of cytokines on testicular steroidogenesis, as well as due to functional disorder of the hypothalamus and/or primary testicular failure [29]. Androgen deﬁciency inhibits protein synthesis and this may favour a greater loss of muscle mass relative to fat mass in men. In women, testosterone levels are normally low and although androgen deﬁciency has been reported in some women with weight loss, their contribution to weight loss in women is less understood [30]. Intensive nutritional rehabilitation to prevent or reverse weight loss remains the cornerstone of management of the wasting syndrome [10, 12]. The aims are to improve appetite and nutrient absorption by addressing all immediate causes of anorexia and malabsorption, such as oral sores and diarrhoea, to improve intake of adequate calories made up of high-protein and low-fat meals in addition to micronutrients supplementation, and to correct psychosocial issues that aﬀect nutrient intake such as poverty and depression, by providing social and psychological support. In view of the principal role of HIV in the pathogenesis of the wasting syndrome, eﬀective HAART aimed at reducing viral load to undetectable levels and sustaining immune restoration as reﬂected in improving CD4 cell count is indispensable [12]. In combination with adequate caloric intake, ﬁtness training by progressive resistance exercises (e.g., lift of light weights and body building exercises) increases muscle function and strength, as well as lean body mass and weight [31]. Conversely, aerobic exercises (e.g., walking, jogging, and running) may result in little or no increase in body mass or weight. Pharmacological treatments are usually reserved for patients who fail nutritional therapy. Appetite stimulants (e.g., Megestrol acetate), recombinant human growth hor- mone (Serostim), and androgenic steroids (e.g., testosterone)