The n e w e ng l a n d j o u r na l of m e dic i n e

Clinical Problem-Solving

Caren G. Solomon, M.D., M.P.H., Editor

The Devil Is in the Details

Eli Ben‑Chetrit, M.D., Linda Shavit, M.D., Ariella Tvito, M.D., Maya Korem, M.D.,
and Alon Bnaya, M.D.​​

In this Journal feature, information about a real patient is presented in stages (boldface type) to an expert
clinician, who responds to the information by sharing relevant background and reasoning with the reader
(regular type). The authors’ commentary follows.

A 75-year-old woman was admitted to the hospital with a 4-month history of weight From the Infectious Diseases Unit (E.B.-C.),
loss (total weight loss, 8 kg) and night sweats. She reported no fever, arthralgias, the Adult Nephrology Unit (L.S., A.B.), and
the Department of Hematology (A.T.),
cough, abdominal pain, or diarrhea. Shaare Zedek Medical Center, Hebrew
University–Hadassah School of Medi-
The patient presents with nonspecific yet alarming symptoms. The differential cine, and the Department of Clinical
Microbiology and Infectious Diseases,
­
diagnosis is broad. Weight loss and nights sweats may be associated with a ma- Hadassah–Hebrew University Medical
lignant disorder such as lymphoma, inflammatory conditions such as vasculitis, Center (M.K.) — both in Jerusalem. Ad-
or infections. dress reprint requests to Dr. Ben-Chetrit
at the Infectious Diseases Unit, Shaare
Zedek Medical Center, P.O. Box 3235, Jeru-
The patient was born in Morocco. She was a retired cook and lived alone. She had a salem, Israel, or at ­elibc@​­szmc​.­org​.­il.
4-year history of diabetes mellitus that was complicated by microalbuminuria; N Engl J Med 2019;380:581-6.
glucose levels were well controlled with metformin. She reported that she did not DOI: 10.1056/NEJMcps1808400
smoke, consume alcohol, or use illicit drugs. She had no sick contacts or exposure Copyright © 2019 Massachusetts Medical Society.

to animals. Six years earlier, she had visited Morocco, but she had not traveled
since then.
On physical examination, she appeared well. Her temperature was 36.6°C (97.9°F),
blood pressure 150/74 mm Hg, heart rate 88 beats per minute, and respiratory rate
16 breaths per minute. The oxygen saturation was 98% while she was breathing
ambient air. Funduscopic examination did not reveal signs of retinopathy. There
was no thyromegaly. The heart sounds were normal, apart from a systolic murmur
(grade 2/6) over the apex, and the lungs were clear. The abdomen was soft, with no
organomegaly. There was no lymphadenopathy.

Because the patient was originally from Morocco and had visited that country
6 years earlier, tuberculosis should be considered, even in the absence of respiratory
symptoms. The murmur may suggest infective endocarditis, although no fever was
noted. A malignant disorder or an underlying vasculitis still should be considered.

The hematocrit was 27.8%, the mean corpuscular volume 85 fl, and the red-cell dis-
tribution width 13.5%. The white-cell count was 5700 per cubic millimeter, with
79% segmented neutrophils, 6% monocytes, 11% lymphocytes, and 4% eosinophils.
The platelet count was 180,000 per cubic millimeter. The blood smear was normal.
The blood urea nitrogen level was 27 mg per deciliter (9.6 mmol per liter), and the
creatinine level 1.45 mg per deciliter (130 μmol per liter). Four months earlier, the
blood urea nitrogen level had been 19.6 mg per deciliter (7.0 mmol per liter), and
the creatinine level 0.82 mg per deciliter (70 μmol per liter). The glucose level was

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 The n e w e ng l a n d j o u r na l
160 mg per deciliter (8.9 mmol per liter), sodium
134 mmol per liter, potassium 4.9 mmol per liter,
calcium 9 mg per deciliter (2.25 mmol per liter),
albumin 3.7 g per deciliter, and total protein
8.3 mg per deciliter. Levels of alanine aminotrans-
ferase, aspartate aminotransferase, γ-glutamyl­
transferase, alkaline phosphatase, and bilirubin
were all normal. The glycated hemoglobin level
was 6.9%. The erythrocyte sedimentation rate
was 60 mm per hour. Iron, transferrin, ferritin,
folic acid, and vitamin B12 levels were within the
normal range. Dipstick urinalysis showed +1
blood and +3 protein. Examination of the urine
sediment showed a few red cells but no casts. The
ratio of protein to creatinine in the urine was
6682 mg of protein per gram of creatinine (nor-
mal value, <200), and the ratio of albumin to cre-
atinine in the urine was 2652 mg of albumin per
gram of creatinine (normal range, 0 to 30). Two
sets of blood cultures were sterile. A chest radio-
graph was normal. Abdominal ultrasonography
showed normal-size kidneys and no hydrone-
phrosis. The liver and spleen were not enlarged.
The patient has normocytic anemia, worsening
renal function, and nephrotic-range proteinuria.
Diabetic nephropathy is a leading cause of pro-
teinuria in the elderly, but the relatively acute on-
set of substantial proteinuria, renal insufficiency,
and systemic symptoms in a patient with well-
controlled diabetes suggests a different glomeru-
lar disease. Membranous nephropathy, minimal
change disease, focal segmental glomeruloscle-
rosis, and other glomerulonephritides may be
primary or secondary causes of nephrotic-range
proteinuria in adults. The patient’s weight loss
and night sweats arouse concern for glomerular
disease as a paraneoplastic syndrome. For exam-
ple, membranous nephropathy, a common cause
of nephrotic syndrome in elderly persons, may
be associated with solid tumors, and minimal
change disease may be associated with Hodgkin’s
lymphoma. Computed tomography (CT) of the
chest, abdomen, and pelvis is warranted to de-
termine whether cancer is present. The marked
discrepancy between the urinary protein-to-creat-
inine ratio and albumin-to-creatinine ratio may
indicate the presence of a paraprotein and mono-
clonal gammopathy–related renal disease such
as multiple myeloma. Tubular proteinuria should
also be considered but is unlikely to explain
nephrotic-range proteinuria. The finding of red
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of m e dic i n e
cells in the urine may suggest a nephritic com-
ponent, but this finding is nonspecific, and there
are no casts. Connective-tissue diseases such as
vasculitis associated with antineutrophil cyto-
plasmic antibodies (ANCA) and systemic lupus
erythematosus (SLE) should also be considered.
The normal chest radiograph makes tuberculo-
sis less likely, and the absence of fever and
positive blood cultures argues against infective
endocarditis, although culture-negative endocar-
ditis cannot be ruled out.
CT of the chest, abdomen, and pelvis was per-
formed without the use of contrast material and
showed no masses, lymphadenopathy, or organo-
megaly. A test for antinuclear antibodies was
positive at a titer of 1:200, with a homogeneous
pattern; testing for anti–double-stranded DNA
(dsDNA), anti-Ro, anti-La, anti-Smith, anti-RNP,
and ANCA was negative. Complement levels (C3
and C4) were normal. Tests for cryoglobulins,
rheumatoid factor, and hepatitis B and C viruses
were negative. The IgG level was 2453 mg per
deciliter (normal range, 650 to 1600), IgM 101 mg
per deciliter (normal range, 50 to 300), and IgA
419 mg per deciliter (normal range, 70 to 400).
Serum and urine immunofixation showed a poly-
clonal pattern. The free kappa:lambda ratio was
normal.
The CT does not show evidence of cancer or a
focal infection; however, the fact that contrast
material was not used limits the interpretation.
The low titer of antinuclear antibodies and the
negative test for anti-dsDNA antibodies with
normal complement levels do not support the
diagnosis of SLE, and the negative test for ANCA
does not support a diagnosis of ANCA-associated
vasculitis. The polyclonal gammopathy is incon-
sistent with multiple myeloma and is nonspecific
in lymphoproliferative or infectious conditions.
A renal biopsy was performed, and the patient
was discharged for further follow-up at the ne-
phrology clinic. Three glomeruli were seen on
light microscopy. Proliferation of mesangial cells
— without endocapillary proliferation, crescents,
or fibrinoid necrosis — was noted. An interstitial
infiltrate of lymphocytes, plasma cells, and small
numbers of eosinophils was seen. Immunofluo-
rescence staining was positive for mesangial IgG
(+2 staining), IgM (+2 staining), and C3 (+1 stain-
 Clinical Problem-Solving
ing), as well as lambda and some kappa light
chains. Immunostaining showed no IgA or C1q.
Electron microscopy showed expansion of mesan-
gial regions and mesangial, paramesangial, and
subendothelial electron-dense deposits (Fig. 1).
Podocyte morphologic features were preserved.
Congo red staining identified no amyloid.
In general, evaluation of at least 8 to 10 glomer­
uli is recommended for diagnosis. Given that only
3 glomeruli were sampled, the interpretation of
the kidney biopsy sample is limited. The mesan-
gial deposition of IgM, IgG, and C3 suggests an
immune-complex process. The proliferation of
mesangial cells, along with immune deposition
of IgM and complement, raises the possibility of
IgM nephropathy, but subendothelial electron-
dense deposits are not found in this disorder.
The predominance of lambda free light-chain
deposition might suggest monoclonal gammop-
athy–related renal disease, but monoclonal gam-
mopathy was not detected in blood or urine
samples. The findings on electron microscopy of
mesangial and subendothelial electron-dense de-
posits are consistent with, but not diagnostic of,
membranoproliferative glomerulonephritis, which
may be mediated by the immune complex (as
can be seen in chronic infections, monoclonal
gammopathy, and autoimmune diseases) or, less
commonly, by complement (such as in C3 glo-
merulopathy). The findings on light microscopy
that are typically seen with membranoprolifera-
tive glomerulonephritis — including cellular
proliferation and characteristic changes of the
glomerular basement membrane, such as “split-
ting” or “tram-tracking” — are not reported, but
it is possible that these findings were missed in
the scant biopsy specimen.
At a follow-up appointment 1 month after hospi-
tal discharge, the blood urea nitrogen level had
increased to 50 mg per deciliter (18 mmol per
liter), and the creatinine level had increased to
2.2 mg per deciliter (190 μmol per liter). A 24-
hour urine collection showed 7 g of protein. The
hematocrit was 27.8%, and the white-cell count
was 5300 per cubic millimeter, with 74.5% seg-
mental neutrophils, 7% monocytes, and 15% lym-
phocytes. A regimen of prednisone (60 mg daily)
was started.
Two weeks later, the patient was admitted to
the hospital with fever, chills, and dysuria. The
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blood urea nitrogen level was 67 mg per deciliter
(24 mmol per liter), and the creatinine level was
2.1 mg per deciliter (190 μmol per liter). Salmonella
enteritidis was isolated from urine and blood cul-
tures. The patient noted that she had had two epi-
sodes of diarrhea a week earlier. On questioning,
she reported that she had consumed undercooked
eggs bought directly from a farmer near her
home. Intravenous ceftriaxone was administered
and resulted in rapid clinical improvement. The
prednisone dose was reduced. The fever resolved,
and repeat urine and blood cultures were sterile.
A CT scan obtained without contrast material
showed mild perinephric stranding of the left
kidney and atherosclerotic changes along the aor-
tic arch and descending aorta. After receiving in-
travenous ceftriaxone for 2 weeks, the patient was
discharged with instructions to take oral amoxi-
cillin for 4 weeks.
Consumption of undercooked eggs may pose a
risk for salmonella infection, and treatment with
high-dose glucocorticoids may increase the risk
of invasive disease. The most likely source of
bacteremia is the gastrointestinal tract. The pres-
ence of urinary symptoms, a positive urine cul-
ture for S. enteritidis, and perinephric stranding of
the left kidney may suggest an ascending uri-
nary tract infection, although this route of infec-
tion is rare. Nontyphoidal salmonella bacteremia
in an elderly patient should prompt further im-
*
Figure 1. Renal-Biopsy Specimen.
Electron microscopy shows subendothelial electron-
dense deposits (asterisk). The morphologic features
of podocyte foot processes are preserved (arrows).
583
 The n e w e ng l a n d j o u r na l of m e dic i n e

aging studies to rule out endovascular infection;

noncontrast CT is insensitive for this diagnosis.

Two weeks after discharge, the patient was seen

in the outpatient clinic. She reported that a pru-
ritic rash had developed over the previous 2 weeks.
A diffuse erythematous and violaceous rash with
small plaques, scaling, and desquamation was
seen predominantly on the back, arms, and feet
(Fig. 2). There was no eosinophilia.

Beta-lactam antibiotic agents may cause a rash,

but the rash is usually a maculopapular exan-
them; plaques, scaling, and desquamation are
not typical of an adverse skin reaction to a drug.
In the context of night sweats and weight loss,
vasculitis and cutaneous T-cell lymphoma are
major concerns. Vasculitis is more likely to be
associated with renal insufficiency.

A skin biopsy was performed. Microscopy re-

vealed a mild mononuclear perivascular infiltrate
with clusters of lymphocytes in the upper dermis
(Fig. 3). Polymerase-chain-reaction analysis to de- Figure 2. Photograph of Rash.
tect T-cell receptor gene rearrangement revealed a An erythematous and violaceous rash with small plaques,
monoclonal T-cell peak possibly consistent with scaling, and desquamation developed in the patient,
predominantly on the back (shown), arms, and feet.
cutaneous T-cell lymphoma. A peripheral-blood
smear was normal. A bone marrow biopsy was
performed, and the results showed hypercellular
marrow (40 to 50% cellularity). Reticulin staining Although the hypercellular bone marrow, nor-
showed focal paratrabecular fibrotic aggregates. mocytic anemia, and relative leukopenia may
No atypical or dysplastic cells were seen. Immu- suggest myelodysplastic syndrome, the absence
nohistochemical analysis did not show cutaneous of red-cell and white-cell dysplasia in the periph-
T-cell lymphoma. Immunohistochemical staining eral-blood smear and the absence of increased
blasts, ring sideroblasts, and dysplastic cytologic
of light chains revealed polyclonality. The propor-
tion of cells that stained positive for CD138 (a features on bone marrow biopsy argue against
universal plasma cell marker) was 5%. Congo red this diagnosis. Furthermore, myelodysplastic syn-
staining showed no amyloid. The patient was re- drome would not account for renal dysfunction
ferred to the hematology clinic. or rash. The low percentage of plasma cells and
polyclonality of light chains are inconsistent with
The diagnosis of cutaneous T-cell lymphoma is myeloma. The Congo red staining showing no
challenging because many of its clinical and amyloid argues against amyloidosis.
pathologic features are nonspecific. The discrete
perivascular lymphocytic infiltrate in the upper The patient had recurrent fever and chills and was
dermis (along with clusters of lymphocytes) and readmitted to the hospital before her planned
the monoclonal T-cell peak may suggest mycosis visit to the hematology clinic. Urine and blood
fungoides. However, clonal T-cell receptor gene cultures obtained on admission yielded S. enteriti-
rearrangements may be detected in healthy elderly dis. The patient reported that she had not taken
patients and in patients with benign dermato- oral amoxicillin as recommended and that she
ses. No abnormal cells were seen in a peripher- had continued to eat eggs from the nearby farm.
al-blood smear or in the bone marrow biopsy A transesophageal echocardiogram did not show
specimen. valve vegetations. A positron-emission tomograph-

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 Clinical Problem-Solving

ic scan showed no signs of endovascular or other

infection. Abdominal ultrasonography showed no
gallstones.

The patient’s recurrent salmonella infection may

be explained by her nonadherence to antibiotic
therapy, by repeated exposure to potentially con-
taminated eggs, or by gallbladder colonization
or an endovascular focus of infection. Her older
age and the prolonged glucocorticoid therapy
may also have contributed. Imaging revealed no
gallstones and no endovascular focus of infec-
tion. Recurrent nontyphoidal salmonella bactere-
mia is an acquired immunodeficiency syndrome
(AIDS)–defining condition, and — especially
given the unexplained kidney disease and rash,
which are suggestive of cutaneous T-cell lym-
phoma — human immunodeficiency virus (HIV)
infection should be ruled out.
The white-cell count was 6000 per cubic millime-
ter, with an absolute lymphocyte count of 972 per
cubic millimeter (normal range, 1200 to 3400).
The CD4 count was 110 per cubic millimeter. HIV
type 1 serologic testing was positive, with a viral
load of 156,000 copies per milliliter. Serologic
testing for adult human T-cell leukemia–lym-
phoma virus types 1 and 2 was negative. Antiret-
roviral therapy (ART) with abacavir, lamivudine,
and dolutegravir was started. Sexual history and
risk factors for HIV were addressed in the HIV
clinic after the patient’s discharge from the hospi-
tal. The patient’s husband had died suddenly 10
years earlier; she did not have information on his
medical history. The patient reported that she had
not had sex with other partners and did not recall
ever having received blood products. Six months
after the initiation of ART, the viral load was un-
detectable, the patient felt well, the rash had re-
solved, and renal function had improved (blood
urea nitrogen level, 25 mg per deciliter [8.9 mmol
per liter], and creatinine, 1.6 mg per deciliter
[140 μmol per liter]).
The documentation of HIV infection along with
a low CD4 count and recurrent salmonella infec-
tions is consistent with the diagnosis of AIDS.
Seroconversion had probably occurred several
years before the first admission, as reflected by
the low CD4 count and the presence of compli-
cations that typically manifest late in the course
of HIV infection.
Figure 3. Skin-Biopsy Specimen.
Hematoxylin and eosin staining shows acanthosis and hyperkeratosis in
the epidermis, with foci of basal-cell vacuolization, and a mild mononuclear
perivascular infiltrate with exocytosis of scattered lymphocytes in the upper
dermis. At higher magnification (inset), clusters of lymphocytes (arrow)
can be seen.
C om men ta r y
The primary concern in this 75-year-old woman
who presented with weight loss, night sweats,
and anemia was a malignant disorder, and test-
ing was focused on this suspected diagnosis.
This case illustrates a cognitive bias based on
pattern recognition.1,2 Presumably owing to her
older age, the possibility of AIDS, which may
well have explained all her clinical manifesta-
tions, was considered only late in the course of
illness.
In retrospect, there were many clues to the
diagnosis of HIV infection. The patient’s white-
cell counts showed relative lymphocytopenia,
although treatment with glucocorticoids could
have explained this finding. The nephropathy
was another clue. HIV-associated nephropathy
with nephrotic-range proteinuria is usually a late
manifestation of HIV infection.3 The classic histo-
morphologic finding is collapsing glomerulopa-
thy, a distinctive variant of focal segmental glo-
merulosclerosis with tubulointerstitial disease.4
HIV-associated immune-complex kidney diseases
have been increasingly reported as well.5 Insuf-
ficient glomeruli were sampled in the renal bi-
opsy to determine the cause of renal failure and
proteinuria.

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 Clinical Problem-Solving

Moreover, pruritic rashes are common in pa-
tients with HIV. Paradoxically, cutaneous T-cell
lymphoma, a CD4-positive neoplasm, has been
reported in association with HIV infection.6,7 An
atypical cutaneous lymphoproliferative disorder
— a mainly reactive inflammatory condition that
mimics cutaneous T-cell lymphoma — has also
been described in HIV-infected patients and rarely
progresses to malignant lymphoma.6,8 Distin-
guishing between the two entities may be diffi-
cult. Several weeks after administration of gluco-
corticoids and initiation of ART, the cutaneous
findings resolved. This supports the diagnosis of
an atypical cutaneous lymphoproliferative disor-
der.6,8 Hypercellularity and reticulin fibrosis, as
seen in this patient, are nonspecific but are well
described in bone marrow biopsy specimens from
persons with HIV infection.9 Finally, although re-
currence of nontyphoidal salmonella bacteremia
may have been related to the patient’s nonadher-
ence to antibiotics and possible repeated expo-
sures to a source of salmonella infection, it is an
AIDS-defining condition,10 and in this case it
pointed the physicians to the correct diagnosis.
AIDS was considered in our patient only late
in the course of her illness. The delay in diagno-
sis in this case is probably related, in part, to the
fact that different physicians managed different
problems without considering the whole picture.
Of note was the failure of the treating physicians
to obtain a sexual history or ask about HIV risk
factors until after the diagnosis was made. Fre-
quently, a sexual history is not obtained from
elderly patients; some physicians feel uncom-
fortable addressing this subject.11,12 Among a
national probability sample of 3005 older adults
in the United States, more than half the respon-
dents 65 to 74 years of age and 26% of respon-
dents 75 to 85 years of age reported that they
were sexually active, yet only 38% of men and
22% of women reported that they had had a
discussion with a physician about sexual activity
since the age of 50.11 However, history may not
be revealing; many patients (including elderly
patients) may be reluctant to disclose that they
have risk factors for HIV, and some may be un-
aware of what the risk factors are. The U.S.
Preventive Services Task Force currently recom-
mends routine annual HIV screening in persons
15 to 65 years of age.13
In 2016, almost 5% of the 39,782 patients
who received a new diagnosis of HIV infection
in the United States were 60 years of age or
older.14 This case underscores the need to rou-
tinely consider the possibility of HIV infection,
regardless of the age of the patient.
No potential conflict of interest relevant to this article was
reported.
Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
We thank Prof. Vera Leibovic and Dr. Alexander Maly for their
interpretation of the skin biopsies and Dr. Ana Tobar for her
interpretation of the kidney biopsy.

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