Hansen, J.D.L.

Roberts, B.

Truswell, A.S.

Wannenburg, P.

Watson, C.E.

Wittmann, W.

English

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A. S. TRUSWELL, J. D. L. HA SEN, W. WITfMA 'N, P. WAN E BURG. B. ROBERTS A '0 C. E. WATSON, Deparrmellrs utMedicine, Child Healrh alld Parhology, Ulliversiry of Cape TOIVIlSERUM LIPOPROTEINS AND PHOSPHOLIPIDS IN RELATION TO FATTY LIVERIN KWASmORKOR*S.A. TYDSKRIF VIR GENEESKUNDE 887REFERENCESL Robinson. D. S. and Seakins, A. (1962): Biochim. biophys. Acta(Amst.). 62, 163.2. Farber. E. (1966): Gastroenterology, 50, 137.3. Lewis. B.. Hansen. J. D. L.o Wittmann. W., Krut. L. H. and Stewart,F. (1964): Amer. J. Clin. Nutr., IS, 16L4. Craviow, J.. De la Pena. C. L. and Burgos, G. (1959): Metabolism,8. 722.5. Chatterjee. K. and Chaudhuri. J. N. (1961): Indian J. Pedia!.. 28, 195.6. Anderson. J. T .. Keys, A., Fidanza. F .. Keys. M. H., Bronte-Stewart.B.. Kupcs. P. and Werner. L. (1956): Clin. Chem., 2, 145.7. Lees. R. S. and Hatch. F. T. (1963): J. Lab. CIin. Med .. 61, 518.8. Parker. F. and Petersen, N. F. (1965): J. Lipid Res., 6. 455.Seven of the patients' liver biopsies showed 3+ fatty change,(the 'severe fatty liver' group); the other 7 had lesser gradesof fatty change from 0 to 2 +. The severe fally liver grouphad significantly lower serum albumin concentration (P <·00 ). This appeared to give a better indication of severe fattyliver than clinical palpation of the liver.All but one of the 14 cases had normal serum a-lipoproteincholesterol concentrations before treatment. The mean valueswere 39 mg. on admission, 41 mg. on day 9 and 39 mg. per100 m!. at recovery on day 18. The one child whose initialserum a-lipoprotein cholesterol was subnormal had the lowestadmission serum albumin of all the cases. Double a-lipopro-tein bands were seen in the first sera from some cases.By contrast, the serum j3-lipoprotein cholesterol averaged60 mg. before treatment, rose to a peak value of 148 mg. atday 9 and settled at 116 mg. per 100 m\. on recovery. All 14cases showed low initial values and a peak during treatmentcompared with their final j3-lipoprotein cholesterol values.During treatment, j3-lipoprotein cholesterol showed a signifi-cantly lower peak in the cases with severe fatty liver. Withthe Lees and Hatch electrophoresis method, distinct pre-j3lipoprotein bands were seen to appear during treatment.Serum total phospholipids followed the same pattern asj3-lipoprotein cholesterol: 136 mg. on admission, 220 mg. onday 9 and 187 mg. /100 m!. at recovery. On day I, lecithinmade up 59°~ of the phospholipids-a. percentage indistin-guishable from 60% in 10 normal adults. During treatment thepercentage of lecithin remained approximately constant andit was 58 0 0 at recovery. The absolute concentration of lecithinand the total phospholipids reached a higher peak (on day 9)in the group with severe fatty liver.Our results are compatible with the decreased lipoproteinprotein synthesis hypothesis if we postulate that j3-lipoproteinsare much more sensitive to dietary protein deficiency thana-lipoprotein. It is suggested Ibat the maintenance of thepercentage of lecithin in serum phospholipids is a pointagainst the lipotropic factor deficiency hypothesis.We should like to thank Dr. G. Barbezat for painstakinghelp with the clinical work. This work was supported by theSouth African Council for Scientific and Industrial Research,and US Public Health Service grant AM-03995.R Oktober 1966The present studies were intended to test two hypotheses thatmight explain fatty liver in kwashiorkor:I. Decreased synthesis of the protein part of lipoproteinsresulting from dietary protein deficiency could impede trans-port of lipids from the liver. In experimental animals, agentswhich inhibit protein synthesis, like ethionine and puromycin,cause a fatty liver with low serum lipids. J " The same combina-tion is seen in kwashiorkor before treatment.' The onlypublished reports on serum lipoproteins in kwashiorkor bothdescribe a relative and absolute decrease of a-lipoproteins.'·5The method used was scanning of paper electrophoretic strips,which is not very reliable. If this can be confirmed it would beof interest because a-lipoproteins contain more protein thanj3-lipoproteins.2. Lipotropic factor deficiency. Combined dietary deficiencyof choline and methionine could impair synthesis of lecithin(phosphatidyl choline) which is the main transport phospho-lipid in serum. The use in medicine of preparations containinglipotropic factors is based on very little human evidence. Iffatty liver ever results from dietary deficiency of lipotropicfactors in man, it might be expected in kwashiorkor.Fourteen children with kwashiorkor were admitted to themetabolic ward. (Cases requiring plasma or blood transfusionwere not included.) They were rehydrated and given vitaminK•. Percutaneous liver biopsy was done the day after admis-sion, provided the plasma prothrombin was satisfactory. Thepatients were treated with fat-free, high-protein diets, vitamins(excluding lipotropic factors), minerals, penicillin and sulpha-diazine, and other treatments where necessary. Venous bloodwas taken after an 8-hour fast the morning after admissionand every 4th (or 5th) morning thereafter for 3 weeks. All thechildren recovered.The liver biopsy specimens were graded independently byone of us (C.E.W.) 0 to 4 + according to the degree of fatlychange present histologically. Serum lipoproteins were sepa-rated by horizontal paper electrophoresis, following themethod of Anderson er al.,' but with I % human albuminincluded in the buffer. The a- and j3-lipoprotein bands werecut out, extracted, and cholesterol measured by the Abell-Kendall method" In addition, lipoproteins were separated asdescribed by Lees and Hatch.' The stained strips wereexamined for pre-j3 lipoprotein bands.Serum was extracted with chloroform-methanol, 2: 1. Phos-pholipids were fractionated by thin-layer chromatography onsilica gel G in the solvent system chloroform-methanol-aceticacid-water, 80: 30: 8 :4. Individual phospholipids were visua-lized with iodine vapour. Lecithin and sphingomyelin bandswere scraped off. Phosphorus was determined by the methodof Parker and Petersen.'"'Abstract of a paper read at Research Forum, University of Cape Town,20 July 1966.U.S. FOOD AND DRUG ADMINISTRATIONDEFECTIVE PACKAGI G MATERIAL IN STERILE SURGICAL KITSThe United States Food and Drug Administration advises thatthe Sterilon Corporation, 500 Northland Avenue, Buffalo, NewYork, is recalling its sterile surgical aids (catheters, intravenousfeeding sets, and disposable scalpels) which were packagedbefore December 1965. The packaging material used up tothat time has been found to be defective after prolongedstorage, and the possible contamination of the contents wouldbe a serious health hazard.The Sterilon Corporation sent recall letters to all of itscustomers who may have received any of the suspect lots,including foreign consignees. Because of the serious hazard tohealth which could develop if defective package seals lead tocontamination of the contents with pathogenic bacteria, theUnited States Food and Drug Administration has requestedthat it be made known that the following shipments of thesuspect materials were made to a South African firm-Glaxo-Allenburys (SA) (Pty) Ltd.:On 22 July 1965, 3 dozen each of 117-14 catheters, lot no.18002, and 117-18 catheters, lot no. 18695. On 9 March 1965,2 dozen each of 155-18, 155-20 and 155-22 catheters, lot no.18517.

Serum lipoproteins and phospholipids in relation to fatty liver in kwashiorkor

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Serum lipoproteins and phospholipids in relation to fatty liver in kwashiorkor

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