Glyoxalase I activity in erythrocytes from severely malnourished children

The enzyme glycoxalase I (glyox I) is involved in metabolic detoxification, and requires glutathione (GSH) as a cofactor. Given the low concentration of whole blood GSH in children with oedematous malnutrition, it is possible that the function of this pathway may be compromised in these children. Glyox I activity was therfore assayed in erythocytes taken from 133 severely malnourished children and 21 age-matched controls. The mean values (ñSEM) for the marasmic group (marasmus: 105 ñ 4/u/gm Hb) and the group with kwashiorkor (Kwash: 103 ñ 4/u/gm Hb) were not significantly different from controls (cont: 104 ñ 2u/gm HB)>. In the group with marasmic-kwashiorkor (M-K: 88 ñ 4u/g Hb) Glyox I activity was significantly lower in controls (p < 0.005), as well as in children with marasmus (p < 0.005), and kwashiorkor (p < 0.05). Enzyme activity was lower than normal in 45 per cent of the MK group. Seven children died subsequent to admission; in five cases Glyox I activities were exceedingly low. There was a weak positive correlation between Glyox I activity and whole blood levels of GSH (r=0.215). We conclude that Glyox I activity is relatively unaffected in malnutrition, except in those with M-K and especially those who do not survive the acutely malnourished state

Pathology of the lungs in childhood malnutrition in Jamaica: light and electron microscopy

The autopsy records of 115 children with severe protein-energy malnutrition were reviewed. Sections of the lung histology showed evidence of bacterial pneumonia in 49 per cent of cases. An additional 18 per cent showed bronchitis, bronchiolitis or interstitial pneumonitis. Aspiration of gastric contents was evident in 10 per cent of cases; 6 per cent showed pulmonary oedema and congestion. In the remaining cases, no lung pathology was identified (17 per cent ). In 8 cases, rapid autopsy examination permitted fixation of lung tissue for electron microscopy. These included 4 cases of bronchopneumonia, one of which was associated with viral pneumonia. Another interstitial pneumonitis, probably of viral aetiology, was also studied. Both these virus-associated cases showed loss of type I pneumocytes and hyperplasia of type II pneumocytes. Another patient with herpes simplex hepatitis showed necrotic emboli in pulmonary capillaries with virions, as well as colonies of interstitial bacteria. One patient with acute pulmonary oedema displayed severe endothelial cell swelling on electron microscopy. In one case, there was no evidence of respiratory changes, apart from desquamation of type I pnuemocytes. Useful information can be obtained on the fine structure of the lung, using samples taken soon after death.

Peroxisomes and the hepatic pathology of childhood malnutrition

Liver specimens obtained immediately after death from eight severly malnourished children were examined by electron microscopy, and compared with seven liver biopsy specimens from children who recovered from malnutrition. The liver cells from the fatal cases showed mitochondrial swelling, with coarse densities in the matrix, cholestasis, depletion of the endoplasmic reticulum and Golgi apparatus, diminished glycogen stores, prominent lipid deposits and focal cytoplasmic degradation. The nucleoli were enlarged. There was marked reducation in peroxisomes. In contrast, the biopsies from recovering children showed good cellular organisation, and a normal frequency of peroxisomes. Multiple factors, including sepsis, may lead to depletion of peroxisomes. Loss of peroximes may interrupt beta-oxidation of long-chain fatty acids and accentuate the accumulation of lipid. Moreover, a reduction in the concentration of catalase may remove one avenue for the detoxification of free radicals. As the concentration of other anti-oxidants, notably glutathione, is also reduced, free radical damage may occur, leading to lipid peroxidation of membranes, mitochondrial damage, pump failure and influx of water and electrolyted into the cell.

The exocrine pancreas in kwashiorkor and marasmus. Light and electron microscopy

Histological sections of pancreas and liver from 65 cases of children dying from childhood malnutrition were reviewed. The extent of pancreatic atrophy and fibrosis was compared with fatty change in the liver. Pancreatic atrophy was common, and often associated with severe fatty change in the liver, but also occurred in marasmic children with scanty liver fat. Pancreatic fibrosis, when present, was only of mild degree. Among 16 patients with marasmus, fibrosis was only seen in one pancreas. Fibrosis was recorded in 8/25 cases of kwashiorkor, and in 7/24 cases diagnosed as marasmic-kwashiorkor. Electron microscopy of the pancreas was performed in seven cases, using tissue collected at immediate autopsy. Atrophy and variable amounts of degranulation of acinar cells were seen. There was often disorganization of the endoplasmic reticulum with intracisternal sequestration. Mitochondrial swelling was consistent with terminal anoxia. Centro-acinar cells were prominent. Some acini were dilated and contained fibrillar material. These findings support the pioneer paper by Blackburn and Vinijchaikul (1969) and underlie the importance of pancreatic atrophy in the pathology of protein-energy malnutrition.