Scanning electron microscopy of the jejunum in children with protein-energy malnutrition

Samples of jejunum from seven children dying from severe oedematous malnutrition were fixed with intralumenal glutaraldehyde in combination with external immersion, using a rapid autopsy protocol. Selected areas were post-fixed in osmium tetroxide, dehydrated with an ethanol series and critical point dried. After mounting on aluminium stubs, specimens were sputter-coated with a thin layer of gold and palladium. Scanning electron microscopy showed patterns ranging from subtotal villous atrophy, through partial villous atrophy with low ridges, to longer, taller ridges with cerebriform convolutions. In one case, villous height had been interpreted as normal on light microscopy. The scanning electron microscope revealed that the mucosa in this case was composed of ridges and leaf forms. Processing for scanning electron microscopy is simple. The specimens can be viewed and photographed in a relatively short time. In addition, the three-dimensional record provides clarification of ambiguities which often arise from routine histological sections.

Ultrastructure of voluntary muscle in childhood malnutrition

This paper is part of a study on the electron microscopy of protein-energy malnutrition, using a rapid autopsy protocol. Samples of voluntary muscle, obtained from eight children dying of severe oedematous malnutrition, were fised in glutaraldehyde within 75 minutes of death. Atrophy of myofibres, increased prominence of satellite cells, and segmental necrobiosis were seen by light microscopy. Electron microscopy showed variable depletion of myofibrils. In the most severe case, there was focal absence of myofibrils, also disorganized Z lines, and absent M bands. Residual atrophic myofibrils measured less than 0.1 µm in width. Other specimens showed sarcomere disorganization, mitochondrial swelling, glycogen depletion, sarcoplasmic oedema, and focal contractions of sarcomeres. Though non-specific, rigor may phosphates. These conditions may exist in severe malnutrition, complicated by terminal infection and metabolic disturbances

Age-specific incidence of cancer in Kingston and St Andrew, Jamaica, 1988-1992

During the period 1988 - 1992, a total of 4,030 malignant neoplasms were recorded in Kingston and St. Andrew, Jamaica. These comprised 1,829 males and 2,201 in females. Histological confirmation was obtained in 83.4 percent. The crude incidence rate for males was 128.5, and 136.2 for females. The age-standardized rates (ASR) were 179.9 for males and 166.1 for females. Age-specifics rates by site, sex and age are tabulated. Attention is drawn to increased incidence for cancers of prostate, larynx, bronchus and non-Hodgkin's lymphoma in males. There was also an increase in female breast cancer (crude rate 36.0; ASR 47.1). Invasive cervix cancer has shown no significant change in incidence. Neoplasms of the body of the uterus have increased (crude rate 7.6; ASR 9.5). The rise in cancer of breast and body of uterus suggests that the influence of exogenous oestrogens should be considered

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.