Q.765. What is the prognosis of PTLD? How to improve?

 KIDNEY TRANSPLANT

 

Q.765. What is the prognosis of PTLD? How to improve?

A. Prognosis is poor, but can be improved by:

(1) Technique of monitoring EBV viral  load, to detect risk ptn.                                                        

(2) New therapies: Adoptive immunotherapy, 👈 using EBV-sp.  C.T.L.s. (cytotoxic “T” lymphocytes)

.. So, thorough pre-Tx. evaluation, avoid excessive im/m.+ standard Iry & IIry preventive strategies: ⮞  

v Cessation of smoking.  🚭

v Uterine cervix smear.

v If cancer occur ] Reduce im/m. greatly.

Q.766. What is meant by “Adoptive immunotherapy”?        👓

 

A.The exquisite specificity of cytotoxic T lymphocytes (CTLs) has led investigators to attempt to isolate cells é significant antitumor activity; infusion of these cells is referred to as ⮚adoptive immunotherapy. It has a possible role in refractory Hodgkin lymphoma, based upon the ability to generate clones of cytotoxic T-lymphocytes that’re sp. for Ep.-Barr virus latent Ags [LMP1& LMP2 or Reed-Sternberg cells]. Expanded clones of these cells may have a therapeutic role in Hodgkin lymphoma whose Reed-Sternberg cells express Ep.-Barr viral Ag.

Q.767. What else?     😉

A. I.X. Infectious complications(See also, Q.679), it depends on:

v Intensity of exposure é hospital & community. 

v Overall state of immunosuppression.                                                                                    

    Fishman & Rubin divided it periodically to : 0-1 m.  1-6  m   &  🠉6 m.

Q.768. Which factors can affect the net state of immunosuppression?

A. Net state of immunosuppression could be affected by:

1)   Im/m. dose, duration & type.

2)   Co-morbid dis.:  e.g. [D.M. – U.T.I.]

3)   Integrity of mucocutanous barriers.

4)   Infection with virus affecting the immune system.

Q.769. What is the “spectrum” of PTLD?

A. Spectrum of PTLD:      I. 😃  II. 😑  III. 😌

 I. Early (50 %)➤ [Infectious mononucleosis–like illness, Pth.: Preserved  architec-ture-“Polyclonal”. * ttt: (Reduce im/m. dose+acyclovir), Prognosis is good]. 😃

II. Polymorphic PTLD (30%)➤[infectious mononucleosis –like illness (+/-)- Wt. loss- Localized Sm.-Pth.: intermediate polyclonal- * ttt.: [Reduce dose of im/m.- + acyclovir-If poor response ➤ttt. like III.] 😑

III. Monoclonal PTLD (20%): [fever- Wt. loss- Localized Sm.– Monoclonal] Pth.: High grade lymphoma + marked atypia - poor prognosis.* ttt. [🠋im/m. to low dose steroid only + Combin. of : Surgery-Chemo./Radiothpy+ Rituximab.]  😌 

Q.770. When can a female recipient allowed to be pregnant?    

A. Certain criteria to be fulfilled:   ✋            

ΠGood general health 18 m. before conception.

 Stable allograft fuction, i.e. Pl. cr. £ 0.2 mg/dl.

Ž Minimal “H.T.” & minimal “proteinuria”.

 Immunization at maintenance dose.

 No pelvi-calyceal dilatation at a recent U/S.

N.B.:

-    👆  [H.T., pre-eclampsia, prematurity, low birth wt.] are more common in pregnant recipient.

-      In labor, take care of the ureter, kid. function, to avoid HUS & Ac. Rj.

-      MMF. ] Teratogenic. 👆

-      Aza, CNI & Steroids ] SAFE in Utero.     😃

                             

Q.771. What Lipid abnormalities can be seen after renal transplantation?

A. Abn. lipid profile is a common complication of R.Tx., but a causal association of dyslip. & CVS risk has not been proven. However, due to high incid. of athrsc. dis. events in R.Tx., we consider R.Tx. a coronary heart dis. equivalent risk. So, assessment & ttt of dyslipidemia in R.Tx. ptn. shd be part of routine post-R.Tx. care. Im/m. drugs, esp.👉steroids, CNI & rapamycin, frequently ➤2^nd ry dyslip. Regimens shd be individualized to decrease competing risks of Rj. & CVS dis.. Dyslip. shd be assessed upon presentation for T.x. and quarterly thereafter.

Lifestyle modification, e.g. abstinence fr. alcohol, ttt of hyperglycemia, physical activity, wt reduction & low-fat diets requires a specified R.Tx. dietician. If TrG. > 500 mg/dL (>5.65 mmol/L)➤lifestyle modific. + correc. of 2^ndry causes/3m, If failed ➤ ezetimibe  alone, if costy ➤ nicotinic a. alone. Do NOT use👆fibrates . If LDL ≥100 mg/dL (≥2.6 mmol/L) ➤life style modific. + statin . Use👉atorvastatin, 10 mg/d (of choice.), to a goal <70 mg/dL (1.8 mmol/L). We can increase ator. to max. of 80 mg/d. or rarely>40 mg/d. é Csp or tcrol., if failed to 🠟 LDL, ezetimi-be can be added , if myopathy or drug interactions occur, try fluvastatin or prava-statin (little or no msc. toxicity & not metb. by CYP3A4) . Some start é fluvastatin/pravastatin, if not tolerated ➤ ezetimibe (Zetia 10 mg) alone.

If LDL<100 mg/dL (<2.6 mmol/L),TrG.>200 mg/dL (>2.26 mmol/L) & non-HDL cholesterol >130 mg/dL (>3.36 mmol/L) ➤life style modific.+ statin to 🠟non-HDL chol. < 130 mg/dL (3.36 mmol/L). We sugg.: ator. 10 mg/d., (of choice). Increase ator. to  max. of 80 mg/d. or rarely >40 mg/d. é Csp. or tacro. Use ezetimibe  as additional ag. if goals are not met é statin alone. If not tolerated ➤ ezetimibe alone.  Isolated low HDL<40 mg/dL (<1.03 mmol/L)➤lifestyle modifications. Our goals to 🠉HDL > 45 mg/dL in ♂ & > 55 mg/dL in ♀ & to 🠟non-HDL cholesterol < 130 mg/dL (3.36 mmol/L). If failed to achieve these goals➤ator. 10 mg/d. (of choice), incr. to max. 80 mg/d. or rarely > 40 mg/d. é Csp. or tcrol. Drug interactions & S.E. é combination of lipid-lowering ag. & im/m.➤ [signif. myopathy & rhabdomyolysis]. Safety of comb. (fibrates + statins) has not bn well-studied & better 👆avoided .

 

Q.772. Discuss hyperuricemia and gout in renal transplant recipients?

A. Dcrease uric a. excretion can occur after R.Tx., esp. é of Csp. to prevent graft Rj.. Impaired urate excretion⮚hyperuricemia & not uncommonly to gouty arthritis,  which’s often difficult to ttt due to CKD & interaction of gout medications (e.g. colchicine, NSAIDs, allopurinol) & Tx. medication (e.g. Csp, Aza., diuretics). A.Smtic hyperuricemia shd not be ttt.ed in organ Tx. recipient. Colchicine & Csp both inhibit p-glycoprotein action, so for Ac. gout flare ttt in Tx. recipient receiving Csp or another p-glycoprotein inhibitor, colch. shd be limited to a single oral dose of 0.6 mg & not repeated for at least 3 d.. For gout flare prox: a colchicine dose of 0.3 mg/d. or E.O.D. (according to R. func.) cn be given. In either case, careful monitoring for colchicine-induced myoneuropathy & blood cytopenias shd be under-taken to mitigate sequale of excessive colchicine levels. Alternative approaches: short-term NSAID & supplementation of the baseline corticosteroid dose most Tx. recipients receive. Slow (10-14 d.) rather thn rapid tapering of steroids to baseline dose is recomm. to avoid rebound gout flares. Long-term s. urate-lowering in Tx. recipient needs to be undertaken é special care. 

XOI. (allopurinol & febuxostat) shd be avoided in ptn.s treated é Aza., because Aza metabolism involves conversion of 6-mercaptopurine to 6-thiouric acid in a reaction catalyzed by xanthine oxidase. Accumulation of 6-mercaptopurine can ➤severe bone marrow toxicity é setting of co-administration of Aza. & XOI. Replacement of Aza é MMF (doesn’t affect xanthine oxidase activity) for graft protection presents a suitable option if gout ttt needs use of a XOI.  Allopurinol titration is strongly recommended, esp. é R.I. & diuretic use in Tx. reciepient If recommendations é allopurinol restriction acc. to cr. cl. are followed, goal: (<6.0 mg/dL) s. urate is often not achieved or maintained, and use of ⮚febuxostat (no dose adj. is needed if cr.cl. >30 mL/min) should be considered. In Tx. recip. é N. or near normal R. func. use of a uricosuric ag. may be considered, esp. where benzbromarone is available. Losartan 👉is the only uricosuric ARB & may serve as a useful adjunctive agent in gouty recipient.

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