Optimal nutrition is an important part of human immunodeficiency virus (HIV) care; to support the immune system, limit HIV-associated complications as well as maintain better quality of life and survival. The presentation and nature of malnutrition in patients with HIV has changed dramatically over the past 30 years from predominantly a wasting syndrome to lipodystrophy and, now, frailty. Nevertheless, we continue to see all 3 presentations in patient care today. The pathogenesis of poor nutrition in HIV-infected patients depends on caloric intake, intestinal nutrient absorption/translocation, and resting energy expenditure, which are features seen in all chronic diseases.

Keywords

AIDS wasting syndrome

Malnutrition

Lipodystrophy

Frailty

HAART

Key points

Introduction

An adage popular in the early part of the nineteenth century stated, if you understand syphilis, you understand all of medicine. In the latter part of nineteenth century the adage evolved to state, if you understand tuberculosis you understand all of medicine. In the current era, it can be said that if you understand human immunodeficiency virus (HIV)/AIDS, you understand all of medicine. These all are multifaceted diseases affecting multiple organ systems, and the implications span multiple levels within the health care system.

The history of HIV infection in the developed world can be divided into 2 eras, one preceding (1981–1996) and the other following (1996) the availability of highly active antiretroviral therapy (HAART). Much of the developing world remains in the pre-HAART era, although the number of treated patients has increased progressively over the past 10 years. In contrast, untreated patients, either through the lack of diagnosis or unwillingness to adhere to treatment, continue to be seen in the developed world, including severely malnourished patients, similar to those seen in the pre-HAART era.

Nutritional consequences in HIV infection have been recognized since early in the epidemic. Protein-calorie malnutrition (wasting) with depletion of lean mass, fat, and micronutrients was the most common problem in the pre-HAART era and led to shortened survival and diminished quality of life.1 The pathogenesis of wasting is multifactorial and related mainly to altered caloric intake, intestinal injury with nutrient malabsorption, and/or increased metabolic demands from the active infections.2 Although the specific disease complications are limited to patients with AIDS or other immune deficiency states, the clinical-pathological correlations of malnutrition are the same as in nonimmune deficiency–mediated conditions. Also, as in non-AIDS patients, wasting exacerbates the immune deficits, promotes debility and dependency, and shortens the lifespan.3 The success of HAART in reconstituting immune function and reducing morbidity ultimately allows HIV-infected individuals in North America to live as long as the general population.4

The widespread use of HAART has markedly improved clinical outcomes and decreased the prevalence of wasting. However, many treated patients develop a cluster of other nutritional alterations, including changes in body fat distribution, as well as dyslipidemia and insulin resistance, without wasting of muscle or other lean tissues.5,6 The lipodystrophy syndrome, as it has come to be called, has attracted considerable clinical and experimental attention.7,8 The causes are multifactorial, which led to a wide-ranging discussion about cause and effect and the relative roles of host, disease, and treatment in its pathogenesis.

The initial responders to the AIDS epidemic were in a unique situation in that they faced a brand new disease, with no evidence base for evaluation and management to help or hinder them. It soon became clear that the clinical manifestations represented disease complications and that the underlying disease and its causes had to be distinguished from the clinical complications of immune deficiency. For example, there was an initial reluctance by some surgeons to perform major surgery on patients with HIV/AIDS because of reports of poor clinical outcomes, whereas later observations showed that the poor results were related to protein calorie malnutrition and not to HIV/AIDS per se. The perceptions that progressive wasting is a universal phenomenon and that everyone with immune deficiency has intestinal dysfunction were subjected to clinical investigation and were shown not to be true.9,10 In fact, the approach to nutrition in HIV/AIDS fits the classic clinical conundrum: How is what we are seeing the same as in other diseases, and how is it different?

Initially, there was little to go on other than the classic teachings of medicine. The situation fostered inductive reasoning as well as the performance of clinical trials to develop an evidence base. The response to HIV/AIDS was the first clinical condition in which nonmedical activists came to play an important role in the design and implementation of clinical trials, and they also played a crucial role in promoting acceptance and participation by HIV-infected people worldwide.

In this article, the authors describe the current knowledge on nutrition in the setting of HIV/AIDS, both in the presence and absence of antiretroviral therapy. The authors provide clinical descriptions and discuss pathogenic mechanisms, evaluation, and management of wasting and of lipodystrophy. The authors also briefly discuss the topic of nutritional assessment. The discussion of many topics, such as diabetes mellitus, cardiovascular disease, fat distribution, and so forth, is limited, as they are covered in greater detail elsewhere in this issue.

Methods to assess nutrition

Although the high prevalence of weight loss and protein-calorie malnutrition was obvious from the earliest description of patients with AIDS, the only literature to guide the early clinicians was a subjective diagnosis of slim disease in a report from Africa. HIV/AIDS was one of the first diseases to be studied nutritionally using quantitative measures of body composition other than body weight.

Initial clinical studies, performed mainly on inpatients, demonstrated the weakness of using weight-based measures to estimate nutritional status.1 Because of the wide ranges of premorbid body weights or body mass index (BMI) values as well as normal values, it may be difficult to detect wasting from a single measurement. The assessment of body weight provides no information about body composition: It cannot distinguish fat from muscle; it cannot distinguish lean mass from excess fluid, and it cannot detect micronutrient deficiencies at all. Body weight measurements were frequently difficult to interpret in patients with AIDS, especially hospitalized patients in whom wide swings in body weight resulted from diarrheal illnesses and from intravenous fluid administration. Quantitative measures of body composition had been developed more than 30 years before but had few clinical applications other than in examining the changes that occur during critical illness, aging, and obesity.

Wang and colleagues11 organized body composition analysis by categorizing the measurements by level: atomic, molecular, cellular, tissue/organ, and whole body (Table 1). For example, the measurement of total body nitrogen by neutron activation analysis is part of the atomic level of measurement, whereas the measurement of total body water by isotope dilution is part of the molecular level of measurement and so forth. The 2 major rules of this organization are that the sum of all of the components within any...