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References
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1. Baker JP, Detsky AS, Wesson DE, etal. Nutritional assessment: a comparison of clinical judgment and
objective measurements. N Engl J Med. 1982;306(16):969–972.
2. Detsky AS, McLaughlin JR, Baker JP, etal. What is subjective global assessment of nutritional status?
JPEN J Parenter Enter Nutr. 1987;11(1):8–13.
3. Frisancho AR. New norms of upper limb fat and muscle areas for assessment of nutritional status. Am J
Clin Nutr. 1981;34(11):2540–2545.
4. Klidjian AM, Foster KJ, Kammerling RM, Cooper A, Karran SJ. Relation of anthropometric and dyna-
mometric variables to serious postoperative complications. Br Med J. 1980;281(6245):899–901.
5. Webb AR, Newman LA, Taylor M, Keogh JB. Hand grip dynamometry as a predictor of postop-
erative complications reappraisal using age standardized grip strengths. JPEN J Parenter Enter Nutr.
1989;13(1):30–33.
6. Hamilton GF, McDonald C, Chenier TC. Measurement of grip strength: validity and reliability of the
sphygmomanometer and jamar grip dynamometer. J Orthop Sports Phys er. 1992;16(5):215–219.
7. Windsor JA, Hill GL. Weight loss with physiologic impairment. A basic indicator of surgical risk. Ann
Surg. 1988;207(3):290–296.
8. Klidjian AM, Archer TJ, Foster KJ, Karran SJ. Detection of dangerous malnutrition. JPEN J Parenter
Enter Nutr. 1982;6(2):119–122.
9. Hunt DR, Rowlands BJ, Johnston D. Hand grip strength—a simple prognostic indicator in surgical
patients. JPEN J Parenter Enter Nutr. 1985;9(6):701–704.
10. Katelaris PH, Bennett GB, Smith RC. Prediction of postoperative complications by clinical and nutri-
tional assessment. Aust N Z J Surg. 1986;56(10):743–747.
11. Hickman DM, Miller RA, Rombeau JL, Twomey PL, Frey CF. Serum albumin and body weight as
predictors of postoperative course in colorectal cancer. JPEN J Parenter Enter Nutr. 1980;4(3):314–316.
12. Davies CWT, Jones DM, Shearer JR. Hand grip—a simple test for morbidity after fracture of the neck
of femur. J R Soc Med. 1984;77(10):833–836.
13. Mahalakshmi VN, Ananthakrishnan N, Kate V, Sahai A, Trakroo M. Handgrip strength and endurance
as a predictor of postoperative morbidity in surgical patients: can it serve as a simple bedside test? Int
Surg. 2004;89(2):115–121.
14. Kalfarentzos F, Spiliotis J, Velimezis G, Dougenis D, Androulakis J. Comparison of forearm muscle
dynamometry with nutritional prognostic index, as a preoperative indicator in cancer patients. JPEN J
Parenter Enter Nutr. 1989;13(1):34–36.
15. Guo CB, Zhang W, Ma DQ, Zhang KH, Huang JQ. Hand grip strength: an indicator of nutritional
state and the mix of postoperative complications in patients with oral and maxillofacial cancers. Br J Oral
Maxillofac Surg. 1996;34(4):325–327.
16. Chen CH, Ho C, Huang YZ, Hung TT. Hand-grip strength is a simple and effective outcome predictor
in esophageal cancer following esophagectomy with reconstruction: a prospective study. J Cardiothorac
Surg. 2011;6:98.
17. Rabinovitz M, Pitlik SD, Leifer M, Garty M, Rosenfeld JB. Unintentional weight loss. A retrospective
analysis of 154 cases. Arch Intern Med. 1986;146(1):186–187.
18. Marton KI, Sox HC, Krupp JR. Involuntary weight loss: diagnostic and prognostic significance. Ann
Intern Med. 1981;95(5):568–574.
19. Lankisch PG, Gerzmann M, Gerzmann JF, L ehnick D. Unintentional weight loss: diagnosis and prog nosis.
e first prospective follow-up study from a secondary referral centre. J Intern Med. 2001;249(1):41–46.
20. ompson MP, Morris LK. Unexplained weight loss in the ambulatory elderly. J Am Geriatr Soc.
1991;39(5):497–500.
21. Metalidis C, Knockaert DC, Bobbaers H, Vanderschueren S. Involuntary weight loss. Does a negative
baseline evaluation provide adequate reassurance? Eur J Intern Med. 2008;19(5):345–349.
22. Bilbao-Garay J, Barba R, Losa-Garcia JE, et al. Assessing clinical probability of organic disease in
patients with involuntary weight loss: a simple score. Eur J Intern Med. 2002;13(4):240–245.
23. Ramboer C, Verhamme M, Vermeire L. Patients’ perception of involuntary weight loss: implications of
underestimation and overestimation. Br Med J (Clin Res Ed). 1985;291(6502):1091.
84.e1
CHAPTER
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13
Obesity
KEY TEACHING POINTS
• Obesity increases the risk of diabetes, cardiovascular disease, and overall mortality.
• The best measures of obesity are body mass index (BMI) and waist circumference.
Thresholds predicting increased mortality are BMI > 25 kg/m2 and waist circumference
>102 cm (>40 inches) in men and >88 cm (>35 inches) in women.
• Abdominal obesity (elevated waist-to-hip ratio [WHR]) indicates a worse prognosis that
gluteal-femoral obesity (reduced WHR).
I. Introduction
Obesity increases the risk of coronary artery disease, diabetes, hypertension, osteoarthritis, cholelithiasis, certain cancers, and overall mortality.1 Clinicians have recognized the hazards of obesity
for thousands of years (according to one Hippocratic aphorism, “Sudden death is more common
in those who are naturally fat than in the lean”).2 Two-thirds of U.S. adults are overweight or
3
obese.
II. The Findings and Their Significance
Several different anthropometric parameters have been used to identify those patients at greatest risk for the medical complications of obesity. e most important ones are body-mass index
(BMI), skinfold thickness, waist-to-hip ratio (WHR), waist circumference, and abdominal sagittal diameter.
A. BODY MASS INDEX (BMI)
1. The Finding
BMI (or the Quetelet index) is the patient’s weight in kilograms divided by the square of his
height in meters (kg/m2). If pounds and inches are used, the quotient should be multiplied by
703.5 to convert the units to kg/m2. An individual is overweight if the BMI exceeds 25 kg/m2, and
obese if the BMI exceeds 30 kg/m2.
BMI was derived by a 17th century Belgian mathematician and astronomer, Lambert-AdolpheJacques Quetelet, who discovered that this ratio best expressed the natural relationship between
weight and height.
4
3
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3—GENERAL APPEARANCE OF THE PATIENT
2. Clinical Significance
BMI is an easy and reliable measurement that correlates well with precise measures of total body
fat (r = 0.70 to 0.96), much better that other formulas of weight (W ) and height (H) (e.g., W/H,
W/H3, W/H
sure, incidence of coronary events, and overall mortality.
0.3).5,6
BMI also correlates significantly with a patient’s cholesterol level, blood pres-
7,8
e arbitrary cutoff of 25 kg/m2 was chosen in part because it reflects the level at which there
is a significant increase in mortality. Many studies of BMI and mortality revealed a J-shaped
relationship (i.e., both lean and overweight patients have increased mortality), but the increased
risk of lean individuals is likely explained by cigarette use, short duration of follow-up, and illnessrelated weight loss.
7,8
B. SKINFOLD THICKNESS
Another measure of obesity is total skinfold thickness, which is estimated by adding together the
skinfold thickness (measured with calipers) of multiple sites (mid-biceps, mid-triceps, subscapular,
and supra-iliac area). ese sums are then converted by formulae into estimates of total body fat,
which correlate well with more traditional measures (r = 0.7 to 0.8).5 Measurements of skinfold
thickness are rarely used today, in part because of their complexity, but mostly because relatively
few studies show the parameter is clinically significant.
C. WAIST-TO-HIP RATIO
1. The Finding
WHR is the circumference of the waist divided by that of the hips. It is based on the premise that
the most important characteristic of obesity is its distribution, not its quantity. Abdominal obesity
(also called android, upper body, or apple-shaped obesity; Fig. 13.1) has a much worse prognosis
than gluteal-femoral obesity (also called gynoid, lower body, or pear-shaped obesity).
Most authorities measure the waist circumference at the midpoint between the lower costal
margin and the iliac crest and the hip circumference at the widest part of the gluteal region.
Adverse health outcomes increase significantly when the WHR exceeds 1 in men and 0.85 in
women, values that are close to the top quintiles in epidemiologic studies.
9
e French diabetologist Jean Vague is usually credited with making the observation in the
1940s that abdominal obesity, more common in men, is associated with worse health outcomes
than obesity over the hips and thighs, more common in women (even so, American life insurance
companies made the same observation in the late 1800s).10 Vague’s original index of masculine dif-
ferentiation, a complicated index based on skinfolds and limb circumferences,11 is no longer used,
having been replaced in the 1980s by the much simpler WHR.
2. Clinical Significance
Even after controlling for the effects of BMI, WHR correlates significantly with blood pressure,
cholesterol level, incidence of diabetes mellitus, stroke, coronary events, and overall mortality.
3. Pathogenesis
e main contributor to abdominal obesity is visceral fat (i.e., omental, mesenteric, and retroperitoneal fat), not subcutaneous fat. Visceral fat is metabolically active, constantly releasing free fatty
acids into the portal circulation, which probably contributes to hyperlipidemia, atherogenesis, and
hyperinsulinemia.15 Gluteal-femoral fat, on the other hand, is metabolically inactive except during
pregnancy and the postpartum period, which has led some to suggest that the role of lower body
12–14
13—OBESITY
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Abdominal obesity
Gluteal-femoral obesity
Fig. 13.1 Comparison of abdominal and gluteal-femoral obesity. Abdominal obesity is depicted in the
top row; gluteal-femoral obesity in the bottom row. The drawings in this figure are adapted from photographs
published by Jean Vague,11 who is credited with first associating adverse health outcomes with abdominal
obesity.
fat is to help guarantee the survival of the species, by providing a constant source of energy to the
lactating female even when external nutrients are unavailable.
D.
WAIST CIRCUMFERENCE
Waist circumference is simply the numerator of the WHR calculation. It has the advantages of
being simpler to measure and of avoiding attention to the hips, which, because they encompass
bone and skeletal muscle as well as fat, should have no biologically plausible relationship to diabetes, hypertension, and atherosclerosis. Recommended cutoffs for increased health risk are a waist
circumference >102 cm (>40 inches) for men and >88 cm (>35 inches) for women.
Waist circumference is strongly associated with risk of death, independent of BMI.
circumference is also a criterion for the metabolic syndrome (defined as the presence of three or
more of the following five variables: large waist circumference, hypertension, elevated triglycerides, reduced high-density lipoprotein cholesterol, and elevated fasting glucose).
16
13,17
Waist
18
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3—GENERAL APPEARANCE OF THE PATIENT
E. SAGITTAL DIAMETER
Because waist circumference encompasses both subcutaneous and visceral fat, investigators have
looked for better anthropometric measures of just visceral fat. One proposed measure is the sagittal diameter, which is the total anterior-posterior distance between the anterior abdominal wall
of the supine patient and the surface of the examining table. eoretically, visceral fat maintains
the abdominal depth in the supine patient, whereas subcutaneous fat allows the abdominal depth
to partially collapse from the force of gravity.19 Even so, there are few studies of this measure and
most correlate it with variables of uncertain clinical significance such as cardiovascular risk factors
or the amount of visceral fat visualized on body imaging.
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
15
References
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1. Brown WV, Fujioka K, Wilson PWF, Woodworth KA. Obesity: why be concerned? Am J Med. 2009;122
(4 suppl 1):S4–S11.
2. Lloyd GER, ed. Hippocratic Writings. Penguin Books; 1978.
3. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United
States, 2011–2012. JAMA. 2014;311(8):806–814.
4. Jelliffe DB, Jelliffe EF. Underappreciated pioneers. Quételet: man and index. Am J Clin Nutr.
1979;32(12):2519–2521.
5. Womersley J. A comparison of the skinfold method with extent of ‘overweight’ and various weight-
height relationships in the assessment of obesity. Br J Nutr. 1977;38(2):271–284.
6. Barreira TV, Staiano AE, Harringto DM, etal. Anthropometric correlates of total body fat, abdominal
adiposity, and cardiovascular disease risk factors in a biracial sample of men and women. Mayo Clin Proc.
2012;87(5):452–460.
7. de Gonzalez AB, Hartge P, Cerhan JR, etal. Body-mass index and mortality among 1.46 million white
adults. N Engl J Med. 2010;363:2211–2219.
8. Prospective Studies Collaboration Whitlock G, Lewington S, etal. Body-mass index and cause-specific
mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet. 2009;373(9669):
1083–1096.
9. Björntorp P. Obesity. Lancet. 1997;350(9075):423–426.
10. Kahn HS, Williamson DF. Abdominal obesity and mortality risk among men in nineteenth-century
North America. Int J Obes Relat Metab Disord. 1994;18(10):686–691.
11. Vague J. e degree of masculine differentiation of obesities: a factor determining predisposition to dia-
betes, atherosclerosis, gout, and uric calculous disease. Am J Clin Nutr. 1956;4(1):20–34.
12. Egger G. e case for using waist to hip ratio measurements in routine medical checks. Med J Aust.
1992;156(4):280–285.
13. Pischon T, Boeing H, Hoffmann K, etal. General and abdominal adiposity and risk of death in Europe.
N Engl J Med. 2008;359(20):2105–2120.
14. Sahakyan KR, Somers VK, Rodriguez-Escudero JP, etal. Normal-weight central obesity: implications
for total and cardiovascular mortality. Ann Intern Med. 2015;163(11):827–835.
15. Snijder MB, van Dam RM, Visser M, Seidell JC. What aspects of body fat are particularly hazardous and
how do we measure them? Int J Epidemiol. 2006;35(1):83–92.
16. Tsai AG, Wadden TA. In the clinic: obesity. Ann Intern Med. 2013;159(5):ITC3-1–ITC3-15. quiz
ITC3-16.
17. Cerhan JR, Moore SC, Jacobs EJ, etal. A pooled analysis of waist circumference and mortality in 650,000
adults. Mayo Clin Proc. 2014;89(3):335–345.
18. Alberti KG, Eckel RH, Grundy SM, etal. Harmonizing the metabolic syndrome; a joint interim state-
ment of the International Diabetes Federation Task Force on Epidemiology and Prevention; National
Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International
Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16):
1640–1645.
19. van der Kooy K, Seidell JC. Techniques for the measurement of visceral fat: a practical guide. Int J Obes
Relat Metab Disord. 1993;17(4):187–196.
88.e1
CHAPTER
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14
Cushing Syndrome
KEY TEACHING POINTS
• The most common cause of Cushing syndrome is exogenous administration
of corticosteroid hormones. Endogenous causes are Cushing disease (excess
adrenocorticotropic hormone [ACTH] production from a pituitary tumor), ectopic
production of ACTH, and adrenal tumors.
• In patients with suspected disease, the following findings increase probability of Cushing
syndrome: thin skin, ecchymoses, proximal muscle weakness, truncal obesity, and
osteoporosis.
• In patients with suspected disease, the following findings decrease probability of Cushing
syndrome: generalized obesity, normal skin thickness, and absence of moon facies.
• In patients with ACTH-dependent Cushing syndrome, the presence of significant weight
loss or rapid onset of symptoms increases the probability of ectopic ACTH syndrome.
• Additional patients without hypothalamic-pituitary-adrenal disorders may develop some
of the findings of Cushing syndrome, including those with chronic alcoholism or human
immunodeficiency virus (HIV)-infection taking antiretroviral agents.
I. Introduction
Cushing syndrome refers to those clinical findings induced by excess circulating glucocorticoids, such as hypertension, central obesity, weakness, hirsutism (in women), depression, skin
striae, and bruises. e most common cause is exogenous administration of corticosteroid
hormones.1 Endogenous Cushing syndrome results from pituitary tumors producing adrenocorticotropic hormone (ACTH) (i.e., Cushing disease, 60% to 70% of all endogenous cases),
ectopic production of ACTH (usually by small cell carcinoma of the lung or carcinoid tumors
of the lung or mediastinum, 5% to 10% of cases), adrenal adenomas (10% to 20% of cases), or
adrenal carcinoma (5% to 7% of cases).
are referred to as ACTH-dependent disease, because the elevated cortisol levels are accompanied by inappropriately increased ACTH levels. Adrenal tumors are ACTH-independent
disease.
e bedside findings of Cushing syndrome were originally described by Harvey Cushing
in 1932.3 Corticosteroid hormones were first used as therapeutic agents to treat patients with
rheumatoid arthritis in 1949; within 2 years, clear descriptions of exogenous Cushing syndrome
appeared.
4
1,2
Cushing disease and the ectopic ACTH syndrome
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3—GENERAL APPEARANCE OF THE PATIENT
II. The Findings and Their Pathogenesis
Table 14.1 presents the physical signs of more than 1500 patients with Cushing syndrome.
A. BODY HABITUS
Patient with Cushing syndrome develop central obesity (also known as truncal obesity or centripetal
obesity), a term describing accumulation of fat centrally on the neck, chest, and abdomen, which con-
trasts conspicuously with the muscle atrophy affecting the extremities. ere are three definitions of
central obesity: (1) obesity sparing the extremities (a subjective definition and also the most common
5,6
one);
(2) the central obesity index, a complicated ratio of the sum of 3 truncal circumferences (neck,
chest, and abdomen) divided by the sum of 6 limb circumferences (bilateral arms, thighs, and lower
legs), in which a value greater than 1 is abnormal;7 (3) obesity as defined by an abnormal waist-to-hip
circumference ratio (i.e., >1 in men and >0.85 in women; see Chapter 13).8 e abnormal waistto-hip circumference is not recommended because there are many false positives (i.e., for Cushing
syndrome).
Other characteristic features of the Cushing body habitus are accumulation of fat in the bitem-
poral region (moon facies),9 between the scapulae and behind the neck (buffalo hump or dorsal
cervical fat pad), in the supraclavicular region (producing a “collar” around the base of the neck),8
and in front of the sternum (dewlap, named after its resemblance to the hanging fold of skin at
the base of the bovine neck, see Fig. 14.1).10 Morbid obesity is rare in Cushing syndrome.
11
TABLE 14.1 ■ Cushing Syndrome – Frequency of Individual Findings
Physical Finding
Vital signs
Hypertension 64–88
Body habitus
Moon facies 67–92
Central obesity 44–97
Buffalo hump 34–75
Skin findings
Thin skin 27
Plethora 28–94
Hirsutism, women 48–81
Ecchymoses 23–75
Red or purple striae 46–68
Acne 21–52
Extremity findings
Proximal muscle weakness 39–68
Edema 15–66
Other
Significant depression 12–40
*Information is based on 1522 patients from references.
enrolled >50 patients with disease.
†
Diagnostic standard: for Cushing syndrome, elevated daily cortisol or
corticosteroid metabolites, or both, with loss of circadian rhythm and with
abnormal dexamethasone suppression tests.
‡
Results are overall mean frequency or, if statistically heterogenous, the range of
values.
†
5,31,34,35,40–44
Frequency (%)
Each study
*
‡
14—CUSHING SYNDROME
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Temporal
Supraclavicular
Dorsal scapular
Episternal
Fig. 14.1 Distribution of adipose tissue in Cushing syndrome. Rounding of cheeks and prominent bitem-
poral fat produces the characteristic moon facies. Fat also may accumulate bilaterally above the clavicles
(supraclavicular collar), in front of the sternum (episternal area, or dewlap), and over the back of the neck
(dorsal cervical fat pad, or buffalo hump). .In these drawings, the dotted line depicts normal contours of
patients without Cushing syndrome
e truncal obesity of Cushing syndrome reflects increased intraabdominal visceral fat, not
subcutaneous fat,
12
probably from glucocorticoid-induced reduction in lipolytic activity and acti-
91
vation of lipoprotein lipase, which allows tissues to accumulate triglyceride.
B.
HYPERTENSION
Hypertension is present in three of four patients with Cushing syndrome. e pathogenesis of
hypertension in Cushing syndrome is complex and incompletely understood. Proposed mechanisms include changes in the renin-angiotensin system, mineralocorticoid activity, sympathetic
system reactivity, and vasoactive substances.
13,14
C.
SKIN FINDINGS
e characteristic skin findings are thin skin, striae, plethora, hirsutism (in women), acne, and
ecchymoses.
Significant thinning of the skin probably arises from corticosteroid-induced inhibition of epi
dermal cell division and dermal collagen synthesis.
recommend using calipers (either skinfold calipers or electrocardiograph calipers) on the back of
the patient’s hand, an area lacking significant subcutaneous fat and thus representing just epidermis and dermis.
15,16
In women of reproductive age, this skinfold should be thicker than 1.8
Precise cutoffs have not been established for men, whose skin is normally thicker than women’s, or
for elderly patients, whose skin is normally thinner than younger patients.
e striae in patients presenting with Cushing syndrome are wide (
deep
red or purple, in contrast to the thinner, paler pink or white striae that occur nor
mally during rapid weight gain from other causes.
abdomen, but may occur on the buttocks, hips, lower back, upper thighs and arms. In one
of Cushing original patients, wide striae extended f rom the lower abdomen to the axillae.
Pathologically, striae are dermal scars, with collagen fibers all aligned in the direction of stress,
covered by an abnormally thin epidermis.
they may result from rupture of the weakened connective tissue of the skin, under tension
from central obesity, which leaves a thin translucent window to the red and purple colored
dermal blood vessels. Striae are more common in younger patients with Cushing syndrome
than older patients.
17,20
8,14
To measure skin thickness, many experts
16
>1
cm) and colored
5,17,18
Striae are usually found on the lower
19
e pathogenesis of striae is not understood, but
mm.
-
15
-
3
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3—GENERAL APPEARANCE OF THE PATIENT
Plethora is an abnormal diffuse purple or reddish color of the face.5 Hirsutism and acne occur
because of increased adrenal androgens.
8,17
Ecchymoses probably appear because the blood vessels,
lacking connective tissue support and protection, are more easily traumatized.
e severity of striae, acne, and hirsutism correlate poorly with cortisol levels, indicating that
other factors—temporal, biochemical, or genetic—play a role in these physical signs.
17
D. PROXIMAL WEAKNESS
Painless proximal weakness of the legs is common and prominent in Cushing syndrome,
especially in elderly patients.20 Because the weakness is a true myopathy, patients lack
fasciculations, sensory changes, or reflex abnormalities. Chapter 61 discusses how to assess
proximal muscle strength.
E. DEPRESSION
Patients with Cushing syndrome may have crying episodes, insomnia, impaired concentration,
difficulty with memory, and suicide attempts.
cortisol level,21 and unless the depression antedates the endocrine symptoms by years, it usually
improves dramatically after treatment.
21,22
e severity of depression correlates with the
22
F. PSEUDO-CUSHING SYNDROME
Several disorders, including chronic alcoholism, depression, and HIV infection, may mimic the
physical or biochemical findings of Cushing syndrome. Patients with chronic alcoholism may
develop the physical findings or the biochemical abnormalities associated with Cushing syndrome, or both, most likely due to the overproduction of ACTH by the hypothalamic-pituitary
axis, an abnormality that resolves after several weeks of abstinence.
have the biochemical abnormalities of Cushing syndrome, but they usually lack the physical findings.25 Patients with HIV infection, particularly if they are receiving protease inhibitors, may
develop some of the physical findings (especially the buffalo hump and truncal obesity) but rarely
the biochemical abnormalities.
26–29*
23,24
Depressed patients may
III. Clinical Significance
A. DIAGNOSTIC ACCURACY OF FINDINGS
EBM Box 14.1 presents the diagnostic accuracy of individual physical signs for Cushing
syndrome, as applied to over 650 patients with suspected disease. e findings that significantly
increase the probability of Cushing syndrome are thin skinfold (likelihood ratio [LR] = 115.6),
ecchymoses (LR = 4.5), proximal muscle weakness (LR = 3.8), central obesity (LR = 3), and
plethora (LR = 2.7). (e astronomical LR for thin skinfold thickness [LR = 115.6] derives
from young women presenting with hirsutism and menstrual irregularity and thus applies only to
similar patients.) e findings that decrease the probability of Cushing syndrome are generalized
obesity (LR = 0.1), absence of moon facies (LR = 0.1), absence of central obesity (LR = 0.2), and
normal skinfold thickness (LR = 0.2).
*e term “pseudo-Cushing syndrome” is usually applied to patients with both clinical and biochemical
evidence of hypercortisolism. erefore, the term does not usually include HIV-infected patients with
buffalo humps or truncal obesity, because these patients usually lack biochemical abnormalities.
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