We report a 7-year old white girl who was admitted because of acute severe hepatic failure. Her complete blood count revealed pancytopenia and a bone marrow aspiration was consistent with acute lymphoblastic leukemia (ALL). Blasts cells were positive for cytoplasmic CD3 and cell surface T-associated markers. Viral, metabolic, immune and toxic causes for hepatic failure were ruled out. Treatment pre-phase with prednisone was started and liver function tests clearly improved after one-week therapy. However, due to her hepatic insufficiency, daily etoposide was administered orally during 15 days. On day 33 complete remission was achieved and hepatic function was normal, except for an increase in the bilirubin level which normalized on day 72. She received our current treatment for intermediate risk ALL and is still receiving continuation phase therapy, currently, with normal liver function and good tolerance to chemotherapy + 8 months after achieving complete remission.

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In a previous work we pointed out the hlgh correlation among the presence of antithyroid antibodies (AB), thyrold function alteration and clinical symptans in children with insulin dependent diabetes mellitus (DMID). In the actual study, the chronic lymphocitic thyrolditis (CLT), antithyroid AC and alteration function in patients wlth DMID was evaluated. From a total of 228 pts,in 78 (age 11.6 + 4.31, basal TSH and/or post TRH, T4, T3 by RIE and microscmal antifraction (MiAE) antithyroid AC and antlthyrcqlobulin (A'lg) haemoglutlnation was done. CLT presence (Fisher's criteria) was determined in 20 pts (25%): 16 girls, 4 toys; 11,6 years + 3. 43, 90% (18/20) of which presented thyroid functlon alteration with high basal TSH -X 7.39 + 3.49 u W (p-x 0.001) and or frank hyper response to TRH (>of 25 uLknl). 85% of the patients presented cllnical symptans; goiter was detected in 65%. CLT prevalence was significatively greater in the first four years of the diabetes evolution. The frequency of MiAF positive titles was 15.4% of the diabetlc and 50% of CLT patients. m e to the high prevalence, 258, we conclude that thyroid function study, AC dosage and clinical exam must be lncluded In all the children with DMID, specially in the flrst four years after the onset of the dlsease. In all patlents during the first year of life(range:O-10 months,X:3 nonths).Seven died before one year of age,and two when they were 3 years old(range:O-36 months,X:1,7 years).source of infection was: blood transfusion in 3(2 nothers and 1 child),tatm in both parents in 1,drug adlctlon in parents in 4,durg adiction and prctrusculty in 1.Autopsles were performed and processed routinely.5/9 had hepathomegaly;3/9 splenomegaly;2/9 cardimqa1y;and 1 child had lntraventrlcular bleedlnq.Lwphoid depletion in nodes was observed In 5/9 while heperplasia in lj9~Thymic involution was observed In 1/9 while 4/9 had lymphold depletion in their thymuses. In 1/9 the thymus was normal. Hepatic steatosis was observed in 7/9 and non speclflc hepatitis ln 6/9.Dlffuse alveolar damage was recorded in 4/9,PHL/LIP In 2/9 and lung angimtosis in 2/9.Acute myocarditls was found in 2/9 and myocardial lnfarctlon in 1/9. Sepsis by CMV was found in 3/9, and South Pmerican trypanosmiasis, histoplasmosis,congenital syphllls and pneumxystis carinii,one case each.We did not see neoplastic diseases,proMly becuase of the early age of death of our cases. Abut 80-90% of post-transfusional hepatitis and 50% of sporadlc hepatltis,so called non A non B Hepatitis, are produced by HVC. The prevalence of Anti-HVC is about 0.4-2.28 in blccd donors.AEter an acuteHVC infection,50-60%of patlentswill progress to a chronic state,and 20% of then wlll have an hepatic cirrhosis.The objetive of this study was to evaluate the anti HVC prevalence in different high risk groups.subjects and Methcds:131 patients considered as high risk groups were selected:a)69 wlth hepatic disease (fD,34 boys,r:lm -18y);b)23 wlth hemato-oncolqic disease (H-0,13 boys,r:2.5-16y);c) 39 with chronic renal failure (CRF,19 b...

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