Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2821_Библиотеки_им_академика_М_И_Перельмана
.pdf
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
Theevaluationofpatientswithapresumedtendinopathyofthelowerextremitymustbegin
with a completehistory andphysicalexamination. Admittedly, physical findingsmayfailto
distinguishanoverusetendinopathyfromthatcausedbyasystemicprocess.However,patients
maypresentwithapreviousdiagnosisofasystemicdisease.Andinotherpatients,thehistory
mayaidpractitionersindiagnosis,ascomplaintssuchasmorningstiffnessorinvolvementof
multipleanatomiclocationsareoftenindicativeofanunderlyingsystemicprocess.
Althoughtherapeuticinterventionsforlowerextremitytendinopathiesaremostdependent
on the tendon involved and patients’ prior treatments, those individuals with tendinopathy
manifesting due to a systemic disease may benefit from additional treatments targeting the
underlyingprocess. Theseinterventions,suchasoral hypoglycemicmedicationsfor patients
withdiabetes,playacriticalrolenotonlyinminimizingthemusculoskeletalmanifestationsbut
alsoincontrollingthesequelaeofthediseaseprocessthroughoutthebody.Assuch,wecannot
overstatethepivotalroleofmusculoskeletalcliniciansinthediagnosisandtreatmentoffoot
andankletendinopathies,particularlywhenduetosystemicdisease.
REFERENCES
AstromM,RausingA.ChronicAchillestendinopathy:asurveyofsurgicalandhistopathologicfindings.ClinOrthopRelat
Res.1995;316:151–164.
HashimotoT,NobuharaK,HamadaT.Pathologicevidenceofdegenerationasaprimarycauseofrotatorcufftear.Clin
OrthopRelatRes.2003;415:111–120.
Kannus P, Jozsa L. Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891
patients.JBoneJointSurgAm.1991;73:1507–1525.
KhanKM,MaffulliN,ColemanBD,etal.Patellatendinopathy:someaspectsofbasicscienceandclinicalmanagement.
BrJSportsMed.1998;32:346–355.
MovinT,GadA,ReinholtFP, etal. Tendonpathologyinlong-standing achillodynia. Biopsyfindingsin 40 patients. Acta
OrthopScand.1997;68:170–175.
Potter HG, Hannafin JA, Morwessel RM, et al. Lateral epicondylitis: correlation of MR imaging, surgical, and
histopathologicfindings.Radiology.1995;196(1):43–46.
AbateM,SilbernagelKG,SiljeholmC,etal.Pathogenesisoftendinopathies:inflammationordegeneration?ArthritisRes
Ther.2009;11:235.
JamesSL,BatesBT,OsternigLR.Injuriestorunners.AmJSportsMed.1978;6:40–50.
RolfC,MovinT.Etiology,histopathologyandoutcomeofsurgeryinachillodynia.FootAnkleInt.1997;18:565–569.
MarrCM,McMillanI, Boyd JS,etal. Ultrasonographic andhistopathologicalfindingsinequinesuperficialdigital flexor
tendoninjury.EquineVetJ.1993;25:23–29.
Williams IF,McCullaghKG,Goodship AE,etal. Studies onthe pathogenesisofequinetendonitis following collagenase
injury.ResVetSci.1984;36:326–338.
WilliamsLN,ElderSH,BouvardJL,etal.Theanisotropiccompressivemechanicalpropertiesoftherabbitpatellartendon.
Biorheology.2008;45:577–586.
Yamamoto E,Hayashi K,Yamamoto N. Mechanical properties ofcollagen fascicles from the rabbit patellar tendon. J
BiomechEng.1999;121:124–131.
AlfredsonA,ThorsenK,LorentzonR.Insitumicrodialysisintendontissue:highlevelsofglutamate,butnotprostaglandin
E2inchronicAchillestendonpain.KneeSurgSportsTraumatolArthrosc.1999;7:378–381.
MaffulliN,WongJ,AlmekindersLC.Typesandepidemiologyoftendinopathy.ClinSportsMed.2003;22:675–692.
KaderD,SaxenaA,MovinT,etal.Achillestendinopathy:someaspectsofbasicscienceandclinicalmanagement.BrJ
SportsMed.2002;36:239–249.
GissenK,AlfredsonH.Neovascularizationandpaininjumper’sknee:aprospectiveclinicalandsonographicstudyinelite
juniorvolleyballplayers.BrJSportsMed.2005;39:423–428.
Ohberg L,LorentzonR, Alfredson H. Neovascularizationin Achilles tendons withpainful tendinosisbutnotinnormal
tendons:anultrasonographicinvestigation.KneeSurgSportsTraumatolArthrosc.2001;9(4):233–238.
Knobloch K, Kraemer R, Lichtenberg A, et al. Achilles tendon and paratendon microcirculation in midportion and
https://t.me/medicina_free
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
insertionaltendinopathyinathletes.AmJSportsMed.2006;34:92–97.
JarvinenM, JozsaL,KannusP, etal.Histopathologicalfindingsinchronic tendondisorders.Scand J Med Sci Sports.
1997;7:86–95.
CurwinSL.Theaetiologyandtreatmentoftendinitis.In:HarriesM,WilliamsC,StanishWD,etal.,eds.OxfordTextbook
ofSportsMedicine.2nded.Oxford,UK:OxfordUniversityPress;1998:610–632.
KrikendallDT,GarrettWE.Functionandbiomechanicsoftendons.ScandJMedSciSports.1997;7:62–66.
MagnussonSP,HansenP,AagaardP,etal.Differentialstrainpatternsofthehumangastrocnemiusaponeurosisandfree
tendon,invivo.ActaPhysiolScnad.2003;177:185–195.
McGoughRL,Debski RE,Taskiran E, etal. Mechanical properties ofthelong headof the bicepstendon. Knee Surg
SportsTraumatolArthosc.1996;3:226–229.
MuramatsuT,MuraokaT,TakeshitaD,etal.Mechanicalpropertiesoftendonandaponeurosisofhumangastrocnemius
muscleinvivo.JApplPhysiol.2001;90:1671–1678.
Sheehan FT, Drace JE. Human patellar tendon strain. A non-invasive, in vivo study. Clin Orthop Relat Res.
2000;370:201–207.
BarnesGRG,PinderDN.Invivotendontensionandbonestrainmeasurementandcorrelation.JBiomech.1974;7:35–42.
Mosler E, Folkhard W, Knorzer E, et al. Stress-induced molecular re-arrangement in tendon collagen. J Mol Biol.
1985;182:589–596.
WrenTA,LindseyDP,BeaupreGS,etal.Effectsofcreepandcyclicloadingonthemechanicalpropertiesandfailureof
humanAchillestendons.AnnBiomedEng.2003;31:710–717.
AhmedIM,LagopoulosM,McConnellP,etal.BloodsupplyoftheAchillestendon.JOrthopRes.1998;16:591–596.
FreyC,ShereffM,GreenidgeN.Vascularityoftheposteriortibialtendon.JBoneJointSurgAm.1990;72:884–888.
Astrom M, WestlinN. Bloodflow in thehuman Achilles tendonassessedbylaser Doppler flowmetry. J Orthop Res.
1994;12:246–252.
GarrettNE,MappPI,CruwysSC,etal.RoleofsubstanceP ininflammatoryarthritis.AnnRheumDis. 1992;51:1014–
1018.
Hart DA, Frank CB,Bray RC. Inflammatory processes in repetitive motion andoveruse syndromes; potential role of
neurogenicmechanismsintendonsandligaments.In:GordonSL,BlairSJ,FineLJ,eds.RepetitiveMotionDisordersof
theUpperExtremity.Rosemont,IL:AmericanAcademyofOrthopaedicSurgeons;1995:247–262.
GotohM,HamadaK,YamakawaH,etal.IncreasedsubstancePinsubacromialbursaandshoulderpain inrotatorcuff
diseases.JOrthopRes.1998;16:618–621.
MaffulliN,IrwinAS,KenwardMG,etal.Achillestendonruptureandsciatica:apossiblecorrelation.BrJ SportsMed.
1998;32:174–177.
MagraM,MaffulliN.Geneticaspectsoftendinopathy.JSciMedSport.2008;11:243–247.
AbateM,SchiavoneC,PelottiP,etal.Limitedjointmobilityindiabetesandageing:recentadvances inpathogenesisand
therapy.IntJImmunopatholPharmacol.2010;23:997–1003.
BeasonDP,AbboudJA,KuntzAF,etal.Cumulativeeffectsofhypercholesterolemiaontendonbiomechanicsinamouse
model.JOrthopRes.2011;29:380–383.
OzgurtasT,YildizC,SerdarM,etal.IshighconcentrationofserumlipidsariskfactorforAchillestendonrupture?Clin
ChimActa.2003;331:25–28.
JunyentM,GilabertR,ZambónD,etal.TheuseofAchillestendonsonographytodistinguishfamilialhypercholesterolemia
fromothergeneticdyslipidemias.ArteriosclerThrombVascBiol.2005;25:2203–2208.
ChoiHK,MountDB,ReginatoAM.Pathogenesisofgout.AnnInternMed.2005;143:499–516.
SchlesingerN,ThieleRG.Thepathogenesisofboneerosionsingoutyarthritis.AnnRheumDis.2010;69:1907–1912.
GaidaJE,CookJL,BassSL.Adiposityandtendinopathy.DisabilRehabil.2008;30:1555–1562.
GaidaJE,AlfredsonL,KissZS,etal.DyslipidemiainAchillestendinopathyischaracteristicofinsulinresistance.MedSci
SportsExerc.2009;41:1194–1197.
CondeJ,GomezR,BiancoG, etal. Expanding the adipokinenetworkincartilage:identificationand regulation of novel
factorsinhumanandmurinechondrocytes.AnnRheumDis.2011;70:551–559.
Cilli F, Khan M, Fu F, et al. Prostaglandin E2 affects proliferation and collagen synthesis by human patellar tendon
fibroblasts.ClinJSportMed.2004;14:232–236.
GaidaJE,AlfredsonH,KissZS,etal.AsymptomaticAchillestendonpathologyisassociatedwithacentralfatdistribution
inmenandaperipheralfatdistributioninwomen:acrosssectionalstudyof298individuals.BMCMusculosk eletDisord.
2010;11:41.
BatistaF,NeryC,PinzurM,etal.Achillestendinopathyindiabetesmellitus.FootAnkleInt.2008;29(5):498–501.
PopelkaS,HromadkaR,VavrikP,etal.Isolatedtalonaviculararthrodesisinpatientswithrheumatoidarthritisofthefoot
andtibialisposteriortendondysfunction.BMCMusculosk eletDisord.2010;11:38.
https://t.me/medicina_free
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
AmericanDiabetesAssociation.Diagnosisandclassificationofdiabetes mellitus.DiabetesCare.2012;35(Suppl1):S64–
S71.
JohnsonKA.Tibialisposteriortendonrupture.ClinOrthopRelatRes.1983;177:140–147.
KarjalainenPT, SoilaK, Aronen HJ,et al.MR imagingof overuse injuriesof theAchilles tendon. AmJ Roentgenol.
2000;175(1):251–260.
Rockett MS, Waitches G, Sudakoff G, et al. Use of ultrasonography versus magnetic resonance imaging for tendon
abnormalitiesaroundtheankle.FootAnk leInt.1998;19:604–612.
Grant TH, KelikianAS, Jereb SE,et al.Ultrasounddiagnosisof peronealtendontears. Asurgicalcorrelation.J Bone
JointSurgAm.2005;87(8):1788–1794.
Leung JLY, Griffith JF. Sonography of chronic Achilles tendinopathy: a case-control study. J Clin Ultrasound.
2008;36(1):27–32.
BeeharryD,CoupeB,BenbowEW,etal.FamilialhypercholesterolaemiacommonlypresentswithAchillestenosynovitis.
AnnRheumDis.2006;65:312–315.
PinedaC,Amezcua-GuerraLM,SolanoC,etal.Jointandtendonsubclinicalinvolvementsuggestiveofgoutyarthritisin
asymptomatichyperuricemia:anultrasoundcontrolledstudy.ArthritisResTher.2011;13:R4.
ScottAT,LeIL,EasleyME.Surgicalstrategies:noninsertionalAchillestendinopathy.FootAnkleInt.2008;29(7):759–771.
Mafulli N, Longo UG, Petrillo S, et al. Management of tendinopathies of the foot and ankle. Orthop Trauma.
2012;26(4):259–264.
Ohberg L, LorentzonR,Alfredson H. Eccentric traininginpatientswithchronic Achilles tendinosis: normalizedtendon
structureanddecreasedthicknessatfollow-up.BrJSportsMed.2004;38(8):8–11.
BasfordJR.Lowintensitylasertherapy:stillnotanestablishedclinicaltool.LasersSurgMed.1995;16:331–342.
HamiltonB,PurdamC.Patellatendinosisasanadaptiveprocess:anewhypothesis.BrJSportsMed.2004;38:758–761.
RobertsonVJ,BakerKG.Areviewoftherapeuticultrasound;effectivenessstudies.PhysTher.2001;81:1339–1350.
Al-AbbadH, Simon JV. The effectiveness of extracorporeal shock wave therapy on chronic Achilles tendinopathy: a
systematicreview.FootAnkleInt.2013;34(1):33–41.
RasmussenS,ChristensenM,MathiesenI,etal. Shockwave therapyfor chronic Achilles tendinopathy: a double-blind,
randomizedclinicaltrialofefficacy.ActaOrthop.2008;79(2):249–256.
Rompe JD, Furia J, Maffulli N. Eccentric loading versus eccentric loading plus shock-wave treatment formidportion
Achillestendinopathy:arandomizedcontrolledtrial.AmJSportsMed.2009;37(3):463–470.
NotarnicolaA,MorettiB.Thebiologicaleffectsofextracorporealshockwavetherapy(eswt)ontendontissue.Muscles
LigamentsTendonsJ.2012;2(1):33–37.
Mani-Babu S, Morrissey D, Waugh C, et al. The effectiveness of extracorporeal shock wave therapy in lower limb
tendinopathy:asystematicreview.AmJSportsMed.2015;43(3):752–761.
EppleyB,WoodellJE,HigginsJ.Plateletquantificationandgrowthfactoranalysisfromplatelet-richplasma:implications
forwoundhealing.PlastReconstrSurg.2004;114:1502–1508.
Woodell-MayJE,RiddermanDN,SwiftMJ,etal.Producingaccurateplateletcountsforplateletrichplasma:validationof
ahematologyanalyzerandpreparationtechniquesforcounting.JCraniofacSurg.2005;16(5):749–756.
MontoRR.PlateletrichplasmatreatmentforchronicAchillestendinosis.FootAnk leInt.2012;33(5):379–385.
Licht H, Murray M, Vassaur J, et al. The relationship of obesity to increasing health-care burden in the setting of
orthopaedicpolytrauma.JBoneJointSurgAm.2015;97(18):e73.
NarayanKM,BoyleJP,GeissLS,etal.Impactofrecentincrease inincidenceonfuturediabetes burden: U.S.,2005–
2050.DiabetesCare.2006;29(9):2114–2116.
https://t.me/medicina_free
H
umanimmunodeficiencyvirus(HIV)hasnowspreadtoeverycountryintheworld,witha
totalof33.3millionaffectedasperthe2009UNAIDSglobalreport;189,165casesof
HIVandacquiredimmunodeficiency syndrome (AIDS)havebeendiagnosedandreportedin
NewYorkCitysincethebeginningoftheepidemic.Tremendousresearchhasbeenachieved
onHIVoverthepastdecadetoimprovehealthoutcomesofpeoplelivingwithHIV.However,
therehasbeenverylittlewrittenevaluatingtheprevalenceofpedalcomplicationsofpatients
withHIV.ThepurposeofthisstudywastoinvestigatepedalcomplicationsofHIVpatientsin
anEastHarlemfootclinic.
Aretrospectivechartreviewwasperformedforthetreatmentofpedalcomplicationwith
theconcurrenceoftheInternationalClassificationofDiseases,NinthRevision(ICD-9)code
042.00;153HIV-infectedadultpatients’medicalrecords fittheinclusion–exclusioncriteria.
Therewere88femalesand65malesinthe40-to74-yearagegroup,theaverageagebeing
55.1years.Themostcommonpedalcomplaintswere onychomycosisin107patients(70%),
neuropathy in 101 patients (66%), tyloma in 62 patients (41%), tinea pedis in 60 patients
(39%),xerosisin59patients(39%),andlongitudinalmelanonychiain10patients(7%).The
mostco-commonmorbiditywasdiabetesin37patients(24%).Ofthosewithneuropathy,only
18%werediagnosedwithdiabetes,showingthatneuropathyisasignificantfindinginHIV+
patientsonitsown.
Our retrospective review sheds some light on the pedal complications in this patient
population,whichhasnotbeenextensivelystudiedinthepast.Furtherresearchiswarrantedto
examine the complications more closelyin a larger pool, with specific comparisons to be
madebetweenHIVneuropathyanddiabeticneuropathy.
ThisisaliteraturereviewofPubMedandMedlinewiththepurposeofthestudytolook
forsomeofthemostcommonpedalcomplicationsandtheprevalenceofeachinHIV-infected
personstoestablishtheprevalenceandcomparethemtotheresultsofourstudyperformedat
FootClinicofNewYork.Thedataoftheirprevalenceamongsuchhigh-riskgrouparelacking,
andthereisnoonestudythatdiscussestheproblemcollectively.
Verylittlehasbeenwritteninregardtothepedal complicationintheHIVpopulation.A
widespectrumofpedalcomplicationsareassociatedwithHIVinfection,butitisimportantto
remember that not all are related to the infection itself and the same complications could
happeninnormalimmune-competentpersons.HIVinfectioncanaltertheclinicalpresentation
https://t.me/medicina_free
andcourse of any condition, and many conditions may be more severe in an HIV-infected
person.Infectionshouldalwaysbeconsideredinanypresentationinvolvingthefeet.
Depending on the stage of a patient’s disease, opportunistic infections (OIs) may be
responsibleforthepedalcomplications.IftheCD4countis>300cellsperµL,thenanOIis
lesslikely.
HISTORICALPERSPECTIVE
AIDSwasfirstdescribedintheUnitedStatesin1981.Itiscausedbyalentivirus(subfamily
ofretroviruses),theLatinword“lentus”meaningslow,denotingthelonglatentphasebetween
infection and clinical presentation. Retroviruses use the enzyme reverse transcriptase to
generateproviralDNAfromRNA(reverseoftheusualdirectionofgenetictranscription).The
termHIVwasacceptedin1986andtherearetwotypes.HIV-1isarapidlymutatingvirusthat
is morevirulent and rapidlyprogressive than HIV-2, whichis predominantlyfound inWest
Africa.HIV-1isdividedintothreegroupsofM(maingroup),whichisfurthersubdividedinto
atleast11 subtypesorclades, O (outlier group) andN(newgroup).HIV-2 is divided into
groupsAtoG.ThemostcommongroupworldwideisHIV-1typeM.
1
AdecadeafterthefirstdescriptionofAIDS,theepidemichasbecomeaworldwidepublic
healthproblem. Initially, HIV transmissionoccurred predominantlyamong homosexuals and
intravenous drug users in developed countries, and among heterosexuals in developing
countries.
Subsequently, HIV transmission among heterosexuals increased also in developed
countries.Currently, HIV seroprevalenceamong heterosexualsvaries from 0.1% to 1.4% in
Europeand0.3%to0.6%inNorthAmericatoashighas39%insomeregionsofsub-Saharan
Africa.2The majorityofthe 40millionpeoplelivingwithHIV/AIDS(ofwhom70%arein
sub-SaharanAfrica)areyoungadults,butabout3millionare50yearsoldorolder.Sincethe
introductionofhighlyactiveantiretroviraltherapy(HAART)inthemid-1990s,HIV-infected
patients live longer, and the proportion of deaths due to diseases of aging has increased.
3
Althoughmenwhohavesexwithmenremainthegroup athighest riskinthe United States,
thereisanincreasingburdenofthediseaseamongAfrican-Americans,heterosexualmenand
women,andyoungpeople.
4
FIGURE23-1.NewHIVDiagnosesintheUnitedStatesfortheMost-AffectedSubpopulations,2015.(CDC.
https://t.me/medicina_free
DiagnosesofHIVinfectionintheUnitedStatesanddependentareas,2015.HIVSurveillanceReport2016;27.
Subpopulationsrepresenting2%orlessofHIVdiagnosesarenotreflectedinthischart.Abbreviation:MSM,men
whohavesexwithmen.)
Attheendof2013,anestimated1.2millionpersonsaged13andolderwerelivingwith
HIV infection in the United States, including an estimated 161,200 (13%) persons whose
infectionshadnotbeendiagnosed.
5
TheCentersforDiseaseControlandPrevention(CDC)reportsin2015that39,513people
werediagnosedwithHIVinfectionintheUnitedStatesandestimates265,330newinfections
couldoccurinthenextfiveyears,ifcurrenttesting,treatment, andpre-exposureprophylaxis
(PrEP)trendsremainthesame(Fig.23-1).
To remedy this situation, the CDC currently recommends voluntary “opt-out” HIV
screeningathealthcarecenters,whichmeansthatHIVtestingisperformedunlessthepatient
declines.
7
ETIOLOGYANDPATHOGENESIS
HIV is an RNA virus (retrovirus) that binds to the CD4 antigen, mainly expressed on the
surfaceofhelperTlymphocytesanddendriticcells,includingLangerhanscells.Coreceptors
for HIV are the chemokine receptors CCR5 and CXCR4. Viral RNA undergoes reverse
transcriptiontoDNA,whichis incorporated into the hostDNA.Viral replicationoccursby
transcriptionofproviralDNAintoviralmRNA,whichisassociatedwithadeclineintheCD4
cellcountandconsequentlyimpairedcellularimmunity.Afterinitialexposure,HIVreplicates
withindendriticcellsoftheskinandmucosabeforespreadingthroughlymphaticvesselsand
developingintoasystemicinfection.Thisleaves a windowofopportunityfor postexposure
prophylaxis(PEP)usingantiretroviraldrugstoblockreplicationofHIV.
8
HIVistransmittedthroughblood,semen,vaginalsecretions,andbreastmilk.Thevirushas
also been isolated from saliva, tears, urine, amniotic fluid, and cerebrospinal fluid.
7,9
The
routes of HIV transmission are sexual intercourse, sharing infected needles or syringes,
transfusionofbloodorbloodproducts,frommothertobabyduringbirthorbreast-feeding,and
occupational exposure of health care professionals. The approximate risks of infection are
listedinTable23-1.
In comparison to the risks shown in the table, the average transmission risk after
percutaneousexposureofahealthcareprofessionalis6%to30%forhepatitisBvirus(HBV)
and 2% for hepatitis C virus (HCV). To minimize the risk of blood-borne pathogen
transmissionfrompatients,allhealthcareprofessionalsshouldadheretostandardprecautions,
includinghandwashing,protectivebarriers,andcareintheuseanddisposal ofneedlesand
sharp instruments.10 Semen represents the main vector for HIV dissemination. HIV-1
replication may occur in macrophages in the testis and/or prostate, which may constitute
pharmacologic sanctuaries protectingthe virusagainst HAART.Persistenceofvirusrelease
into the semen may occur despite an undetectable blood viral load (BVL).11 Vertical
transmissionof HIV from mothertobaby is increased with CD4counts<500cellsper µL,
intrapartumuseofinvasiveprocedures,ruptureofmembranes>6hours,andlabor>5hours.
https://t.me/medicina_free
Table23-1.
1.
2.
3.
4.
HAART reducestheriskofmothertobabytransmissionfromabout18% toless than1%.
12
HIVinfectionisusuallydiagnosedbydetectingantibodiesinaserumsample.Thereisadelay
(window period) betweeninfectionand a positive HIV antibody test, varying from 2 to 6
weeksandupto3months.Duringthistime,thepersonisoftenveryinfectiouswithahighviral
load,butantibodytestsmaybefalse-negative.Therefore,plasmashouldbetestedforHIVp24
antigenandRNAbyatechniquesuchaspolymerasechainreaction.
1
ApproximateHIVTransmissionRiskFollowingaSingle
ExposuretoHIVInfection
%Risk
Vaginaloranalinsertiveintercourse 0.03–0.09
Vaginaloranalreceptiveintercourse 0.1–3
Oral(fellatio) 0.04
Occupational:
Mucousmembranecontact 0.1
Needle-stickinjury 0.3
Transfusionof1unitofblood 90–100
(DatafromPattmanR,SnowM,HandyP,etal.OxfordHandbookofGenitourinaryMedicine,HIV,andAIDS.
Oxford,UK:OxfordUniversityPress;2008:345–548.)
WhentheCD4countsare<200cellsperµLcertainAIDSdefiningillnesses,suchasOTs,
candevelop(Appendix1)(seeTable23-2).
Apartfrom theseOIs,otherAIDSdefiningconditionsincludeCD4count<200cells per
mm3, non-Hodgkinlymphoma (NHL), Kaposi sarcoma (KS), invasive cervical cancer,HIV
encephalopathy,andwastingsyndromeduetoHIV.Ifuntreated,theaveragetimebetweenHIV
infectionandAIDSisabout10years.BVLpredictsthelikelyrateofdiseaseprogressionand
indicates responsetotherapy. BVL <5,000 copies per mL generallysuggests a low rate of
progression in the next 5 years and >55,000 copies per mL is associated with increased
progression.HIV-associatedOIscan affectvirtuallyany organ or system,andarecausedby
organismsthosearerarelypathogenicifthecellularimmunesystemisintact.
APPENDIX1:
OrganismsCausingOpportunisticInfectionsinHIV+Patients
Bacteria:Salmonella,Mycobacteria(M.tuberculosis,M.kansasii,M.avium-intracellularecomplex,M.
genavense,M.simiae,M.celatum),Bartonellahenselae,andB.quintana
Viruses:Herpessimplex,Cytomegalovirus,Varicellazostervirus,Humanpapillomavirus,Epstein–Barrvirus,
HepatitisB,HepatitisC,Polyomavirus,Poxvirus,Parvovirus,Adenovirus,ErythrovirusB19
Fungi:Candida,Pneumocystisjiroveci(carinii),Cryptococcusneoformans,Histoplasmacapsulatum,
Aspergillusspecies,Coccidioidesimmitis,Penicilliummarneffei,Blastomyces
Protozoa/Parasites:Cryptosporidiosis,Microsporidiosis,Isosporabelli,Strongyloidesstercoralis,Toxoplasma
gondii,Leishmaniasis
https://t.me/medicina_free
Table23-2.
Infection
SincetheintroductionofHAARTinthemid-1990s,therehasbeenadramaticdecreaseinthe
incidence of OIs in HIV-infected subjects.13 This decrease is due to restoration of cell-
mediatedimmunityinducedbyHAART,whereasproteaseinhibitorsusedduringHAARTmay
haveadirecteffectagainsttheproteasesofparasites.16However,patientsremainvulnerable
to OIs for approximately 2 months after starting HAART. Sometimes OIs occur despite
increased CD4countsbecauseofimpaired functioningofCD4effectormemoryT cells and
deregulationofBcellsthatmaypersistdespitechangesintheCD4count.
17
CD4+CountandOpportunisticConditionsinHIVInfection
CD4+Count
(cells/mm3) InfectiousComplications NoninfectiousComplications
>500 Acuteretroviralsyndrome
Candidalvaginitis
Persistentgeneralized
lymphadenopathy
Guillain–Barrésyndrome
Myopathy
Asepticmeningitis
200–500 Pneumococcalandotherbacterialpneumonias
Pulmonarytuberculosis
Herpeszoster
Oropharyngealcandidiasis
Kaposisarcoma
Oralhairyleukoplakia
Cervicalneoplasiaandcancer
B-celllymphoma
Anemia
Mononeuropathymultiplex
Idiopathicthrombocytopenicpurpura
Hodgkinlymphoma
Lymphocyticinterstitialpneumonia
<200 Pneumocystispneumonia
Disseminatedhistoplasmosisand
coccidioidomycosis
Miliaryandextrapulmonarytuberculosis
Progressivemultifocalleukoencephalopathy
Wasting
Peripheralneuropathy
HIV-associateddementia
Cardiomyopathy
Vacuolarmyelopathy
Progressivepolyradiculopathy
Non-Hodgkinlymphoma
<100 Disseminatedherpessimplex
Toxoplasmosis
Cryptococcosis
Cryptosporidiosis,chronic
Microsporidiosis
Candidalesophagitis
<50 Disseminatedcytomegalovirus
DisseminatedMycobacteriumaviumcomplex
(DatafromRefs.8,12–15.)
The resurgence of tuberculosis (TB) in the United States is largely linked to the HIV
epidemic. Multidrug-resistant (MDR)-TBandextensive drug-resistant TB have emerged as
threatstoTBcontrol. HIVinfectionmaybe associated withprimaryMDR-TB, possiblyby
causing malabsorption of anti-TB drugs and acquired rifamycin resistance. HIV-infected
patientswithMDR-TBhaveincreasedmortality.
18
ProphylaxisagainstdisseminatedMycobacteriumavium-intracellularecomplexinfection
https://t.me/medicina_free
with azithromycin or clarithromycin is recommended for all patients withCD4 counts <50
cellsperµL.
Malignancy
HIV-1maycontributetothedevelopmentofmalignancythroughseveralmechanisms,including
infectionbyoncogenicviruses,impairedimmunesurveillance,orimbalancebetweencellular
proliferationanddifferentiation.
14
Theincidenceofcertainmalignanciesis increased with impairedcellular immunity.The
AIDSdefiningcancers (ADCs)areKS,NHL,andcervicalcarcinoma,whichareassociated
with DNA viruses, namely KS-associated herpes virus, Epstein–Barr virus, and human
papillomavirus(HPV),respectively.
19
Inthepre-HAARTera,approximately10%ofHIV-infectedpersonshadcancer.HAART
hasdramaticallyreducedtheincidenceandmortalityofKSandNHL,buthasnotsignificantly
decreasedtheincidenceofcervicaloranalcancer.Althoughreduced,theincidenceofKSand
NHLremainshigherinHIV-infectedthannoninfectedpatients.
12,19,20
Sincetheintroductionof HAART,rates ofnon-ADCs haveincreased andthey currently
compriseabout70%ofcancersinHIV-infectedpeople.21Non-ADCsincludecarcinomaofthe
anus, lung, breast, skin, conjunctiva, head and neck, liver, testis and prostate, Hodgkin
lymphoma, plasma-cell neoplasia, multiple myeloma, leukemia, melanoma, and
leiomyosarcoma.
22,23
The risk of HPV-associated cancers of the anus, cervix, oropharynx,
penis, vagina, and vulva is increased among HIV-infected persons. Therisk increases with
advancing immunosuppression, reflecting gradual loss of control over HPV-infected
keratinocytes.InfectionwithoncogenicHPVmayfacilitateHIVacquisition.
24,25
Currently, malignancies are the most frequent cause of death (around a third) of HIVinfected patients. Non-ADC accounts for more morbidity and mortality than ADC in the
HAARTera.ThereasonsincludethedecreasedoccurrenceofOIsandADCs,longersurvival
ofHIV-infectedpatients,andthepossibleoncogenicroleofHIVitself.TheuseofHAARTis
associatedwithlowerratesofnon-ADCs.
26
TreatingcancerinHIV-infectedpatientsremainsachallengebecauseoflatepresentation,
immunosuppression, drug interactions, compounded side effects, and the potential effect of
chemotherapyonCD4count3andHIV-1viralload.17Nonetheless,HIV-infectedpatientswith
cancershouldreceivethesametreatmentasHIV-uninfectedpatients.
27
CURRENTTHERAPY
Since the approval of zidovudine as the first anti-HIV drug two decades ago, remarkable
advancesintheunderstandingofHIV/AIDSpathogenesisanddrugdevelopmenthaveledtothe
currentavailabilityofmorethan30drugsandfixeddosecombinationstotreatHIVinfection
(Appendices2and3).
ThemediansurvivalafterAIDSdiagnosishasincreasedsignificantlyduringtheHAART
era,whichhastransformedHIVfromanalmostuniformlyfatalconditiontoachronicdisease.
https://t.me/medicina_free
1.
a.
b.
2.
3.
1.
2.
3.
OtherbenefitsofHAARTincludepotentialreductionofHIVtransmissionamong adultsand
decreaseofmothertochildtransmission.
However,incountrieswhereearlyaccesstoHAARTisnotreadilyavailable,deathisstill
mostoftenduetoAIDS-relateddisorderssuchasOIsandadvancedAIDSstatus.
28
HIVdrugresistancemaybeintrinsicoracquiredasaresultofmutationsinviralproteins.
The overall prevalence of baseline genotypic resistance is about 30%. Resistance is
disseminatedby transmissionofresistantmutationsselectedduring therapy.To minimizethe
development of drug resistance, a combination of at least three drugs from at least two
differentclassesshouldbeused(Appendices4and5)(seeTable23-3).
7
ThebenefitsofbeginningHAARTatCD4counts<200cellsperµLarewelldocumented.
Recent studies have suggested that 350 cells per µL should be the minimum threshold for
initiationofHAART.
28,29
APPENDIX2:
ClassificationofAntiretroviralDrugs
Reversetranscriptaseinhibitors:impairconversionofviralRNAtoproviralDNA
NRTIs
NNRTIs
Proteaseinhibitors:preventproteaseprocessingofviralsubunitsleadingtoassemblyofinfectivevirions
Fusioninhibitors:preventbindingofHIVtoCD4orchemokinereceptors(CCR5orCXCR4)
APPENDIX3:
AntiretroviralDrugs
1
NRTIs NNRTIs PIs FIs
Abacavir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Tenofovir
Zalcitabine
Zidovudine
Delavirdine
Efavirenz
Etravirine
Amprenavir
Atazanavir
Fosamprenavir
Indinavir
Lopinavir
Nelfinavir
Ritonavir
Saquinavir
Enfuvirtide
Maraviroc
Raltegravir
APPENDIX4:
StandardRegimensforHAART
2NRTIsplus1NNRTItenofovir/emtricitabineorabacavir/lamivudine
2NRTIsplus1PI(usuallyboostedwithlow-doseritonavir)
Triplenucleosideanalogcombinations
ThereiscontroversyabouttheguidelinesforinitiatingHAART,especiallytheCD4cellcountatwhichHAART
shouldbestarted(Appendix5).
APPENDIX5:
https://t.me/medicina_free
Соседние файлы в папке Библиотека им академика М.И. Перельмана