
Anaphylaclold and Possibly Related Reactions
Presumably because angiotensln·converting enzyme inhibitors affect the metabolism of elcosanoids and polypeptides, inclUding
endogenous bradykinin, patients receiving ACE}nhibitors (including caplopril) may be subject to avariety 01 adverse reactions, some of
them serious.
Headand Neck Angioedema: AngioedemaInvolving the extremities, face, Ij~, mucous membranes, longue, glottis or larynx has been
seen In patients Irealed with ACE inhibitors, Including captopril. If angioedema Involves the tongue, glottis or larynx, airway obstruction
may occur and be falal. Emergencytherapy, including but not necessarily limited 10, sUbculaneous administration of a1:1000 solution of
epinephrine should be prompUyinsUtuted.
Swelling confined to ~_e face, mucous membranes of the mouth, lips and extremities has usually resolved with discontinuatJon of
captopril; some cases required medlcallherapy. (See PRECAUTIONS: Information for Patients and ADVERSE REACTIONS.)
Intestinal Angioedema: Intestinal angioedema has been reported in patients trealed wah ACE lnhibil.ors. These patients presenled
with abdominal pain (with or without naUSeaorvomiting); in somecasesIherewas noprior history of facial angioedemaandC·l esterase
levels were normal. Thf! angioedema Vias diagnosed by procedures Including abdominal CT scan or ultrasound, or at surgery, and
symploms resolved after slopping the ACE inhibitor.lnlestinal angioedema shouldbe Included In the dillerential diagnosis of patlents on
ACEInhibitorspresenting with abdominal pain.
Anaphylactoid reactions during desensitization: Two patienls undergoing desensitizing lreatment wilh hymenoplera venom while
receiving ACE Inhibitors suslained liIe-threatenlng anaphylactoid reactions. In the same patients, these reacUonswere avoided When
ACE inhibilors were temporarity wHhheld, butthey reappeared uponinadvertentrechallenge.
Anaphylactoid reactions during membrane exposure: Anaphylactoid reactions have been reported in pauenls dIalyzed with highflux
membranes and treated concomitantly with an ACE inhibitor. Anaphylactoid reactions have also been reported in patienls
undergoing low-densitylipoproleln apheresls with dextran sulfate absorption.
Neutropenia/Agranulocytosis
Neutropenia «1OOO!mm~ with myeloid hypoplasia has resulted from use of caplopril. About hal( of the neutropenic patients developed
syslemic or oral cavity inlecUons or other features Qf the syndrome of agranUlocytosis.
The risk of neutropeniais dependenton the clinical status of the paUent :
In clinical trials inpatients with hypertension who have normal renat function (serum creatinine less than 1.6 ml}’dL and no collagen
vascular disease), neutropenia hasbeen seenin one patient oul of over 8,600 exposed.
In patienls with some degree of renal failure (serum creatinine at least 1.6 mgldl) but no collagen vascular disease, the risk of
neutropenia in cl!nicallrials was about 1per 500, afrequency over 15 times that for uncomplicated hYpertension. Dally doses of
caplopril were relatively highin these patients, p~rticulartyln view of Ihelrdiminished renal function. In foreign markeling experience
In patients wilh renal fallure, use of allopUrinol concomitantly with caplopril has been assoclaled with neutropenIa but this
association has notappeared in U.S. reports.
In patient& with collagen vascular diseases (e.g’ systemic lupus el)”thematosus, scleroderma) and impaired renal function,·
neutropenia occurred in 3.7 percent oipalients In c1inicat trials.
While f1pne of the over 750 patlents In formal clinlcallrials of heart failure .developed neulropenla, it has occurred during the
subsequent clinical experience. About half of the reported cases had &erurn creatinine ~1.6 mgldL and more than 75 percent were In
patlenls also receiving procainamide.ln heart failure, itappears thatlhe same risk factors for neutropenia are present.
The neutropenia has usually been detected within three months alter caplopril was started. Bone marrow examinations in palienls with
neutropenia consistently showed myeloId hypoplasia, frequently accompanied by erythroid hypoplasia and decreased numbers of
megakaryocytes (e,g’ hypoplasticbone marrowand pancytopenia); anemia and thrombocytopenia were sometimes seen.
In general, neutrophlls returried to normal in about two weeks after captopril was discontinued,·and serious infections Were limned to
clinically complex patients. About 13 percent oIlhe cases of neutropenia have eooed fatally, but afmostall falalitles were In patients with
serious illness, having collagen vascular disease, renalfaHure, heart failure or immunosuppressant therapy, or acombination of these
complicalingfactors.
Evaluation of the hypertensive orheart failure pallent should always Include assessmenl of renal function.
If captoprills used In patients with ImpaIred renal function, white blood cell and differenllal counts shoUld be evalualedpn”orto starting
treatment and at approxlmalely two·weekIntelvels foraboul three monlhs, Ihen periodically.
In patients with collagen vascular disease or Who are exposed to other drugs known to affect the while cells or Immune response.
particularly when there is impaired renal function, captopril should be used only after an assessment of benefit and risk, and then with
caution.
All patients Ireated wilh capt~’” shouldbe told to report any signs of Infection (e.g., sore Ihroat, fever). ‘infection Is susPected, white cell
counts should be performed without delay,
~ince discontinuation of captopril and other drugs has genera/ly led to prompt relurn of the white count to normal, upon confirmation of
neutropenia(neutrophil count<1OOOImm~ Ihe physlcien should wilhdraw captopol and closely follow the patienrs course.
Proteinuria
Total urinary proteins greater than 1gperday were seen in about 0.7 percentaf patients receiving captopril. Aboul90 petcentofaffected
patlents had evidence of prior renal disease or received relatively high doses of captopril (in excess 01150 rng/day), or both. The
nephrotic syndrome occurred In aboul one·fifth of protelnuric patients. In most cases, proteinuria subsided or cleared within six months
whether or not captopril was continued. Parameters of renal function, such as BUN and creatinIne, were s~ldom altered In the patients
with proteinuria.
Hypotension
Excessive hypotension was rarely seen in hypertensive paUenls but is apossible consequence of captopril use in salVvolume depleted
persons (such as those treated vigorously with diurelics), patients with heart faflure or those paUenls undergoing renal dialysis (see
PRECAUTIONS: Drug Interactions.)
In heart failure, where the blood pressure was elther nonnal or low, lranslentdecreases In mean blood pressure greater than 20 percent
were recorded in about half of the patients. This transient hypotension is more likely 10 occur after any of the first several doses and Is
usually welliolerated, producing
either no symptoms or brief mUd IIghUleadedness although,
In rare Instances it has been assoclaled with arrhythmia or conduction defects. Hypotension was the reason for discontinuation of drug in 3.6 patients with heart failure.
BECAUSE OFTHE POTENTIAL FALL IN BLOOD PRESSURE IN THESE PATIENTS, THERAPY SHOULD BE STARTED UNDER
VERY CLOSE MEDlCA~ SUPERVISION.
Astarting dosa of 6.25 or 12.5mg t.i.d. may minimize the hypotensive effect
Pellents should
be followed closely for the first two weeks of treatment and whenever the dose of captopril and/or diurelic Is increased. In patients with
hearffailure, reducing the dose of diuretic, if feasible, mayminimize the fall in blood pressure.
Hypotension is not per se a reason to disconlinue captoprll. Some decrease of systemic blood pressure is acommon and desirable
observation upon initiation of caploprillablets, USP treatment in heart failure. The magnItude of the decrease Is greatesl earty in the
course of treatment; this effect stabHizes within a week or two, and generally relums to prelreatmentlevels, without a decrease in
therapeutic efficacy, wilhlntwomonlhs.
FetallNeonatal MorbiditY and Mortality
ACE inhibitors can cause fetal and neonalal morbidity and death when admlnlslered to pregnant women. Several dozen cases have
been reported In the world literature.WhenpregnancyIs delected,ACE inhibitors should bediscontinuedas soon as possible.
The use of ACE InhIbitors during the second and third trimeslers of pregnancy has been associated with fetal and neonatal injury,
Including hypolension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure. and death. OligohydramnIos has also
been reported, presumably resulling from decreased fetal renal function; oligohydramnios
in this selling has been assoclated with fetal
limb cootraclures, craniofacial defonnalfon, and hypoplastic lung developmenl. Premalunty, Intrauterine growth retardation, and patent
ductus. arteriosus havEl alsobeen reported, althougbJt Is notdear’Yheth.er ~~~e opcurrences were dueto the ACE·inhlbltor exposure.
These adverse effects do notappear to have resulted from Intraulerine ACE·inhibitor exposure that has been limited to the first trimester.
Mothers whose embryos and fetuses are exposed to ACE inhlbilors only during the first trimester should be so Informed Nonetheless,
when patients becomepregnant, physicians shouldmake every effort to discontinue the use 01 captopril as soon a~ possible.
Rarely (probably less often than once In everylhousand pregnancies), no alternative toACE lnhlbll6ts will be found. In these rare cases,
the molhers should be apprised of the potential hazatds to their feluses, and serial ultrasOund examinations should be peJfOlmed to
assess the Intraamnlotlcenvironment.
If oligohydramnios is obselVed, caploprilshould be discon~nued unless it is considered life.saving for lhe mother. Contraction stress
lesting{CST}, a non-stress tosl (NST), or biophysical profiling (BPP) may be approprtate, depending upon the weak 01 pregnency.
Patients and physldans should be aware, however,that oligohydramnios may nol appear unl!! after the fetus has sustained Irreversible
InJury.
Infants with histories of in utero expOsure to ACE inhibitors should be closely observed for hypolension, oliguria, and hyperkalemia. If
oliguria occurs. atlention.should be directed toward support of blood pressure and renal perfusion. Exchangetransfusion or dialysis may
be required as ameans of reversing hypotension and/or sUbsli!utingIor disordered renal fuoction. While captopril maybe removed from
the adult circulation by hemodialysis, there is inadequate data concerning the effectiveness of hemodialysis for removing it from the
clrculalion ofneonates orchildren. Peritoneal dialysis is not effective for removing captopril; there is no Informationconcerning exchange
transfusion for removing captopril from the general circulation. “.
When caplopril was given to rabbits at doses about 0.8 to 70 Urnes (on amglkg basis) the maximum recommended human dose, low
incidences of craniofacial malformations were seen. No teratogenic effects of captopril were seen In studies of pregnant rats and
hamsters. On amg!k:g basts, the doses used were up to 150 times (in hamsters) and 625 times ~n rats} the maximum recommended
humandose.
Hepatic Failure
Rarely, ACE inhibitors have been associated with asyndrome that starts with cholestaUc Jaundice and progresses to fulminant h!3psllc
necrosis and {sometimes} death. The mechanism of this syndrome Is not understood. Patienls receMng ACE inhibitors who develop
Jaundice or marked elevations of hepaticenzymesshould discontinue theACEinhlbllorand receive appropriate medical follOW-Up.
There is currently no manufacturer warning information available for this drug.
Hypertension: Captopril tablets US?are indicated for the Teatment of hypertension.
tn using captopril, conslderallon should be gtven to the risk of neutropenia!agranutocytosls (seeWARNINGS).
Captoprll maybe used as Initial therapy for patientswilh normal renal function, In whomthe rlskls relatively low. In patients with impaired
renal function, particularly those wfth collagen vascular olSeas6, captopril should be reseNed for,hypertenslves who have either
develoPed unacceptable side effecls on otherdrugs, orhave failed to responq satislactorily 10drug cOmbinations.
Captopril is effective alone and in combination with other antihypertensive agents, ~peclally thiazide-type diuretics. The blood pressure
lowering effecls of captoprif and thlazldes are approximalaly a<!dlltva.Heart Failure:Captopril tabletsare indicated in the treatmentof congestive heart failure usually in cornblnatlpn with
diuretics and
di9italls_ The beneficial effect 01 captopril in~eart failure does notrequl.re the presence 01 digllaUs, however, most controlled cliniCal trial
experience with captopril has been in paUentsreceMng digitalis, as well as dluretlctrealmen!. .
Left V~ntrlcular Dysfunction After MYQcar~lal tnlarctlon : Gaplopril tablels are indicated to Improve survival following myocardial
fnfarclion In clinically stable patients with left ventriCUlardysfUnction manlfesled as an ejection fraction ::;40% and 10 reduce the Incidence
01 overt heart failure and subsequenthospitalizations forcongesUve heart failure In these patients.
Diabetic Nephropathy: Captopril lablels are indicated fortha trealment ot diabetic nephropathy (proteinuria> 500 mg/day) in paUents
with type Ilnsulin-dependenl diabetes mellitus and retinopathy. Caplopriltablets decreases the rate of progression of renallns·uffJcienCy
and development of serious adverse clinical outcomes {death or need for renallransplantation or dialysisl.
In considering use of caplopril tablets, it should be noted that In controlled trtals ACE inhibllors have an effect on blogd pressure that is
less in black patients than In nonblacks. In addition, ACE Inhibitors (for which adequate data are available) cause a higher rate of
angioedema in black than In non-black palients {seeWARNINGS: Head and NeckAngloedema and Intestinal AngIQedema}.
Captoprills a specific competitive inhibitor of angio!erlSln I-converting enzyme (ACE), the enzyme responsible for the conversion of
anglolensln Iloanglolensin II.
eaploprills deslgnaled chemically as j-[(2S)-3-mercaplo-2-malhylpropionylj-L-prolina. Moler:ular fonnul. e,H’NO,S [MW 217.29) and
has the follo”NIngstruclural.formula:

Captoprills a white to off-white crystalline powder that may have a slight sulfurous odor; it is soluble in waler (approx. 160 m9fml),
malhanol, and alhanol and sparingly soluQleln chIorolonn and alhyl acelala.
Each scored tablet, for oral administration, contains 12.5 mg, 25 mg, 50 mg or 100 mg of captopril.ln add~ion, each lablet contains the
following inactive ingredients: microcf)”stalline cellulose,comstarch, anhydrous ladose, coHoidalsilicon dioxide, talc andpalmilic acid.