Brown atrophy

Brown atrophy In malnutrition, the liver shows a decrease in cell and nucleus size, glycogen depletion, pigment deposits, occasional siderosis as well as proliferation of Kupffer cells. The liver as a whole becomes smaller (by as much as two thirds of its normal weight). Due to its pigment deposits, particularly siderin, the liver takes on a brown colour. These changes have been subsmned under the term brown atrophy (H. Popper, 194S). 

Ischaemic hearts of 7 patients aged 48 to 63 years had increased mtDNA damage and OXPHOS gene expression, suggesting that mtDNA damage is associated with OXPHOS deficiency (Corral-Debrinski et al. 1991). Oxidative phosphorylation defects may also play a role in some other forms of cardiac disease as idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy, myocarditis, brown atrophy and coronary aAerosclerosis. 

In NRH, the liver is interspersed with numerous diffuse nodes, which are 1-3 mm in size (occasionally up to 3 cm) and yellow to yellowish brown in colour with blurred boundaries they consist of hyperplastic hepato-cytes. No fibroses or perinodal connective tissue septa are evident. The multilayered, disordered trabeculae do not have a lobular structure. (66, 69) CD 8" cytotoxic T cells infiltrate the acinus. The nodes lack central veins and bile duct proliferations. The intemodular parenchyma becomes atrophied due to pressure. It is possible by means of reticulin staining to demonstrate the nodes with the irregular trabeculae, whereas the altered vessels are best shown using elastica staining. The liver surface is smooth. (78) In the course of disease, presinusoidal, and later sinusoidal, portal hypertension with hepato-splenomegaly and oesophageal varices are usually observed. (64, 65, 67) (s. fig. 36.4)... 

BAT, in its cold/epinephrine-activated state compared to an atrophied or quiescent state, demonstrates increases in blood flow, lipoprotein lipase activity, triacylglycerol synthesis, 5 -deiodinase activity, and triiodothyronine-enhanced UCP gene expression. The processes of fatty acid uptake and triacylglycerol synthesis are essentially the same in both BAT and WAT. However, norepinephrine release by the sympathetic nervous system in acute cold exposure stimulates BAT to enhance expression and secretion of lipoprotein lipase to its sites in the vascular epithelium. Lipoprotein lipase releases fatty acids from passing chylomicrons and very low-density lipoproteins (Chapter 20), causing an influx of fatty acids into the brown adipocytes. 

J. Berth-Jones, R.A. Graham-Brown, D.A. Bums (1991). Lichen sclerosus et atrophi-cusa-review of 15 cases in young girls. Clin. Exp. Dermatol., 16(1), 14-17. 

Atrophy of the optic nerve appears to be a consistent finding. Pigmented macular protrusions have been observed by Hagbbrg et al. (1965). The spinal fiuid was found to be clear and colorless (Brown et al. 1954), and cells were not increased. Spinal fiuid protein was initially elevated (480 mg%) and later normal (51.3 mg%) in the case of Hagberg et al. The electroencephalogram in this patient showed lack of the normal basal rythmic activity and cortical activity. Ventriculography revealed marked dilatation of the ventricles with paper-thin walls and signs of underdevelopment of the cerebellum. Routine laboratory examinations were normal. Vacuolized lymphocytes were not seen. 

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