Search PubMed⌕ Search

Biomedical subjects

M S Tanner

Publications and source records attributed to M S Tanner.

At least 91 records · Page 5Linked to original sources

Early introduction of copper-contaminated animal milk feeds as a possible cause of Indian childhood cirrhosis.

Brass and copper household utensils are a possible source of the gross hepatic copper accumulation characteristic of Indian childhood cirrhosis (ICC). In 107 families with a child with ICC, the use of copper or brass for water storage (97%) and of brass for milk storage (90%) or milk boiling (67%) resembled that of neighbouring village control families. However, the feeding history of 132 children with ICC differed from that of 70 children with other hepatic disorders and 311 children in 2 rural control groups. No child with ICC was exclusively breast-fed whereas 10%, 32%, and 25% of the control children were. Duration of breast-feeding was shorter in children with ICC and animal milk was introduced earlier. 57% were started on animal milk before 3 months of age. The age at introduction of animal milk correlated with the age at presentation with ICC. 66 urban Pune children had a feeding history similar to those with ICC, but in these families brass vessels were not used for milk. Experimentally, milk took up copper from utensils more avidly than water did. The copper concentration in milk samples obtained from ICC households, and those obtained experimentally, would supply a copper intake 6 to 20 times greater than that of the breast-fed infant, and similar to that producing copper toxicosis in the lamb. The hypothesis that early introduction of copper contaminated animal milk is of aetiological importance explains many of the epidemiological features of ICC.

Alloys↗

Liver disease in India.

One hundred and twenty-five children with chronic liver disease were seen in Pune in 13 months. Fifty-nine of them, aged 8-39 months, had Indian childhood cirrhosis histologically diagnosed. Their characteristics included an insidious onset of symptoms, a geographical clustering of cases in rural areas north-east of Pune, a high rate of parental consanguinity and affected siblings, and a very high hepatic copper concentration (790-6654 micrograms/g dry weight). Only 8 survived for 6 months, adverse prognostic features being jaundice, ascites, enlargement of the gall bladder, and severe anaemia at presentation. Clinical differentiation from other liver disorders in the same age group was clear in advanced cases but unreliable in earlier cases. Four asymptomatic siblings with hepatomegaly had a benign course. The need for non-invasive methods to diagnose early cases in the community is demonstrated. The other major diagnostic categories were: unresolved hepatitis (12); chronic active hepatitis (7); cryptogenic cirrhosis (6); neonatal hepatitis and biliary atresia (8).

Adolescent↗

Hepatic collagen synthesis in a rat model of cirrhosis, and its modification by colchicine.

Carbon tetrachloride inhalation in phenobarbitone treated rats caused a rapid rise in hepatic prolyl hydroxylase activity which was followed by an increase in hepatic collagen and free proline concentrations. Colchicine in a dose of 5 micrograms/day largely prevented the increase in hepatic collagen. This effect was not mediated by impairment of prolyl hydroxylase activity. Colchicine is of potential therapeutic value in preventing the progression of chronic liver disease to cirrhosis.

Animals↗

Macroamylasaemia and hepatitis in a twelve-year-old boy.

Macroamylasaemia was found in a 12-year-old boy with persistent, severe abdominal pain and mild hepatitis. No abnormality of the pancreatic or bile ducts was demonstrated. Both the symptoms and the biochemical abnormality of macroamylasaemia settled spontaneously over 10 months. Transient, asymptomatic macroamylasaemia was found in the boy's father.

Age Factors↗

Increased hepatic copper concentration in Indian childhood cirrhosis.

19 Indian children with liver disease were studied. 5 in whom a clinical and histological diagnosis of Indian Childhood Cirrhosis was made had massive orcein-staining deposits in liver cells. The hepatic copper content in these 5 cases was strikingly high (1389 microgram/g dry tissue, range 1045--2303) the normal range being 15--55 microgram/g. Of the other 14 cases, only 2 had hepatic copper levels above normal (170 and 262 microgram/g.) This high hepatic copper concentration may be caused by excessive copper ingestion or an abnormality of copper metabolism.

Coloring Agents↗

Orcein-positive liver deposits in Indian childhood cirrhosis.

A striking, previously unreported pattern of orcein-positive deposits attributed to excess copper-binding protein was found in liver-biopsy specimens from twelve cases of Indian childhood cirrhosis. A comparable picture was found only in biopsy specimens from patients with Wilson's disease. Deposits seen in about 20% of the two hundred and seventy-nine cases in various control groups, which were associated with prolonged cholestasis, were slight in comparison. This finding could have important therapeutic and pathogenic implications.

Child↗

Functional intestinal obstruction due to deficiency of argyrophil neurones in the myenteric plexus. Familial syndrome presenting with short small bowel, malrotation, and pyloric hypertrophy.

In 3 infants functional intestinal obstruction, associated with a short small intestine, malrotation, and pyloric hypertrophy, was shown to be due to failure of development of the argyrophil myenteric plexus, with the absence of ongoing peristalsis. 4 infants with similar clinical features have been described previously, and there is evidence for an autosomal recessive mode of inheritance of this syndrome.

Female↗

Hepatic peptidyl prolyl hydroxylase activity and liver fibrosis--a prospective study of 94 infants and children with hepatobiliary disorders.

To assess whether hepatic peptidyl prolyl hydroxylase (PPH) activity could serve as a practical quantitative indicator of hepatic fibrosis or aid in the categorization, diagnosis or prognosis of hepatobiliary disorders in infancy and childhood, the activity of this enzyme has been determined prospectively by a tritium release method in 97 biopsies from 94 infants and children with the following conditions: acute hepatitis of infancy, 10 patients; extrahepatic biliary atresia, 13; previous hepatitis of infancy, 8; alpha-1-antitrypsin deficiency, 6; chronic active hepatitis, 17; chronic persistent hepatitis, 5; glycogen storage disease, 5; and 25 patients with a miscellanea of other liver disorders. PPH activity was considered in relation to diagnosis, biochemical and histological abnormality and subsequent prognosis over a 4-year period. Five liver biopsies which showed no histological abnormality were considered as "controls" having PPH values of 0.72 +/- 0.47 (mean +/- S.D.). PPH activity was significantly elevated in acute hepatitis of infancy, 9 of the 10 infants having PPH greater than 1.66 units (i.e., mean +/- 2 S.D. of the "control" value). Nine infants (70%) with extrahepatic biliary atresia also had PPH activity above this value, as did two with alpha-1-antitrypsin deficiency and 12 patients all in different diagnostic categories. PPH activity did not correlate with hepatic fibrosis as indicated by hepatic hydroxyproline concentration or by histological assessment, or with biochemical tests of liver function within any diagnostic group or in the series as a whole. PPH activity was similar in biopsies with and without histological features of cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Serum type III procollagen and basement membrane proteins as noninvasive markers of hepatic pathology in Indian childhood cirrhosis.

While serum concentrations of antigens of the aminopropeptide of type III procollagen have been considered as indicators of hepatic pathology in adults, the high concentrations normally found in children during growth may preclude their use in pediatric liver disease. To clarify this and to determine the role of other circulating connective tissue-related substances in children, we have measured serum concentrations of antigens related to aminopropeptide of type III procollagen, the 7S domain of type IV collagen and the P1 fragment of laminin in healthy subjects aged 1 month to 4 years and in children with Indian childhood cirrhosis, a particularly aggressive form of liver disease. In healthy subjects, there was a considerable age variation in serum aminopropeptide of type III procollagen but not in 7S collagen or laminin P1. In Indian childhood cirrhosis, all three serum antigens were increased (p less than 0.001) above the upper limit of normal for age. Both the serum 7S collagen and laminin P1 concentrations showed a significant correlation with the degree of intralobular fibrosis and also with the severity of necrosis and cellular infiltration, suggesting that these serum antigens may be a noninvasive means of assessing and monitoring events associated with hepatic fibrosis in Indian childhood cirrhosis. The raised serum aminopropeptide of type III procollagen in Indian childhood cirrhosis did not correlate with any histological parameter assessed. Gel filtration of serum showed that, in healthy subjects, the predominant antigenic form of aminopropeptide of type III procollagen was a degradation peptide smaller than authentic aminopropeptide of type III procollagen; while in Indian childhood cirrhosis the authentic peptide and a larger degradation peptide predominated.(ABSTRACT TRUNCATED AT 250 WORDS)

Basement Membrane↗