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lndian l. Pathol, Miuobiol 4l. Q): 169-171, 1998

Systemic Amyloidosis in Hodgkin's Disease

DsnNesswan N LerulewaR, SuonrR R Recsuwa*rn,, Drrnrl Gunra,PaRrsn Jarru, ARvuto G Valeruo

Departntent of Pathotogy; Grant Medical Coltege €tSir l.l. Group of Hospitals Bonfiay

ABSTRACT

Secondary amyloidosis as a complication of Hodgkin's disease hai been describedas being unusual to rare in occurence. We report a case in which the clinicat picturewas that of a renal failure, etiology of which could not be determined but which provedto be amyloidosis secondary to clinically unrecognised Hodgkin,s disease.

Key words : Amyloidosis, Hodgkin's disease. r

CASE REPORT Laboratory investigations revealed aHaemoglobin of 4.1 gm1o, a total WBC

. count of 13,000/cu mm and a

- A 1'7 year'old man was admitted in differential count'of Neutrophils 70"/,,January 1991 with complaints of ,, Lymphocytes zg7o, Eosinopirils l% stdiarrhoea, breathlessness, cough with Monoc-ytes 17,. ESR was gbmm at thdexpectoration and loss of appetite since end oi t hour. Uriie examination10 days. In January 1,990 he was showed moderate proteninuria. BUNhos-pitalized for generalized weakness was '312mg%. S. ireatinine was 5.5and fatigue and,was treated as a case mgo/". An irterial blood gas analysisof anaemia witli'2 units of blood and revealed metabolic acidos-is. Patient,soral hematiniis. In November 1990 he subsequent clinical course was markedsuffered from fever with edema feet. by twi episodes of generalized tonicExamination had revealed cionic convulsions ind respiratoryhepatosplenomegaly and enlarged . arrest which led to his death on 4thc.ervical

- lymph nodes. He was day of hospitalisation.

diagnosed as a case of anaemia withhypoproteinemia. Lymph node biopsy Autopsy findingsat tnat tlme was reported by privateconsuftant as 'atypical lymphadenitis'. External Examination revealedrnls ibroPsy was not available to us for pallor, bilateral cervical lymphadeno-review.

-Physical Examination revealed pathy and pitting edema or r+t.that patient was emaciated and drowsy, l t

I:iFh"9 3.2 Kg, there was pallor, Gross pathologybilateral pitting oedema of feet and

i,lTE"9l;mobile, nontender cervical Examination of individual organslymPh nodes measuring 0.5 - 1 cm in revealed :diameter. Lymph nodei at other sites

::1: T:lpalpable. B.P. was 60 mm Hg Lyntph nodes : cervical, mediastinallcystottc). spleen was palpable 3-4 cm, and paraaortic group of lymph nodessoft and nontender, 'Liver

was lusi were enlarged and measured 1-a chr inflf!':. Respiratory system ,"rruilud diameter. Eut section of these lymph:;:1::^:t""pitations

at the base of both nodes showed homogeno", -g.'r;irn

r"s rurrE,s. white appearance.

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170 Lanjezoar et al

Spleen : was enlarged and weighed600 grams. Capsular surface and cutsurface of spleen revealed grayish whitenodular tumor deposits of 0.2-1 cmdiameter (figure 1).

Liver : was enlarged and it's cutsurface showed waxy appearance.

Fig, 7 : Gross photograph of cut surfaceof the spleen showing dffitsely distributedgrayish zohite tumor deposits.

Kidneys: Both kidneys were enlargedand pale. Cut surface of both kidneysrevealed widening of cortex.

Examination of lungs did not revealevidence of tuberculosis. Examinationof heart, brain and gastrointestinal tractshowed normal anatomical features.

Light Microscopy findings

Lymph Node : Architectiire oflymph node was effaced and wasreplaced by diffuse cellular infiltrate ofplemorphic variant of R-S giant cells,histiocytes plasma cells andlymphocytes along with presence ofhomogenous eosinophilic interstitialdeposits which I showed greenishbirefringence by polarising microscopeon congo red stained slide. Spleen :

Microscopic examination showedpresence of R-S giant cells along with

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Indian l. Pathol. Microbiol. April 1998

histiocytes, lymphocytes and plasmacells (figure 2). Nodular deposits ofhomogenous_pink amyloid material wasalso demonstrated in histologicalsections of spleen (figureJ),_Amyloidwas also demonstrated in liver, kidneys& adrenals. There was no evidence oftuberculosis or other chronicinflammatory lesion in any of theorgans. Microscopic examination ofbrain did not reveal any pathology.

Fig, 2 : Photonicrogrnph of tl.te spleensltowing lymphocytes, ltistocytes and R-Sgiant cells haaing' binucleate andmultinucleateforms (H A E x 500).

Fig. 3 : Pltotorticrograph of tlrc syleensl:ozrling large, nodular massess of anyloiddeposits (H €t E x 500).

DISCUSSION

The signif icance of coexistingamyloidosis with Hodgkin's disease

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Indian J. Pathol, Microbiol. April 1998 171

was for the first time reported byWallace et alr and till today about50 cases have been reported2-*6. All thereported cases, including ours, aretypical of the secondary type ofamyloidosis that is involving liver,spleen, kidneys and adrenals.There seems to be no associationbetween amyloidosis and any.specificform of Hodgkin's diseaser. In majorityof the cases amyloidosis developedafter the diagnosis of Hodgkin'sdisease, however, occasionallyamyloidosis and Hodgkin's diseasewere diagnosed simultaneously{. In ourcase, the picture liresented was that ofa progressive renal failure secondaryto massive renal amyloidosis and thediagnosis 'of amyloidosis withHodgkins disease was established afterdeath. In a case of Hodgkin's disease,development of proteinuria and edemashould make one suspect of secondaryamyloidosis.

REFERENCES

1. Wallace SL, Feldman DJ, Berlin I, Har-ris C, Glass IA : Amyloidosis inHodgkin's Disease. AM I Med 8 ;

552-567, t950.

2. Gledhill RC, Shillitoe A) : Purpura andAmyloidosis in Hodgkin's Disease. BMl1 : 1335-1337,7952.

3. Sherman'M|, Morales JB, Bayrd EDSchierman WD: Amyloid nephrosissecondary to Hodgkin's Disease. Arclr

. lrtt. Med 95 : 618-621, 1955.

4.'' Winaver SJ, Feldman SM : Amyloidnephrosis in Hodgkin's Disease.A.M.A. Arclt Int Med 104 : 793-796,1959.

5. Azzopardi lG, Lehner T : Systemicamyloidosis and malignant disease :

I Clin Path 19 : 539-548, 1966.

" 6. Tuzuner N, Avanoglu. Y, Aktuglu G,Dogusoy G, Muftuoglu A: AmlyoidosiCin Hodgkin's disease : Am I Med 92 :

446-448, 7992.

(( Reprint Request : Dr. D.N. Lanjewar,Associate Professor,

Grant Medical College, Bombay - 400 008Received - 4-1-96 Accepted - 18-B-9G

lndian ]ournal of Pathology andshould be read as Seema-bhiraj

ERRATA

Microbiolog y 4O(3), 1997,|ain, P. Bhalla and SNA

Page 433 authorsRizvi.