scholarly journals Distinct Types of Lipofuscin Pigment in the Hippocampus and Cerebellum of Aged Cheirogaleid Primates

2013 ◽  
Vol 296 (12) ◽  
pp. 1895-1906 ◽  
Author(s):  
Emmanuel P. Gilissen ◽  
Ludmilla Staneva-Dobrovski
Keyword(s):  
Lipofuscin Pigment

scholarly journals Lipofuscin Accumulation in Cortisol-Producing Adenomas With and Without PRKACA Mutations

2017 ◽  
Vol 49 (10) ◽  
pp. 786-792 ◽  
Author(s):  
Anna Angelousi ◽  
Eva Szarek ◽  
Vincent Shram ◽  
Electron Kebebew ◽  
Martha Quezado ◽  
...  
Keyword(s):  
Laser Scanning ◽  
Cushing Syndrome ◽  
Visual Fields ◽  
Laser Scanning Microscopy ◽  
Detection Methods ◽  
Confocal Laser ◽  
Lipofuscin Accumulation ◽  
Lipofuscin Pigment ◽  
Lipofuscin Granules ◽  
Hematoxylin Eosin

AbstractThe adrenal cortex accumulates lipofuscin granules with age. Lipofuscin accumulation is also seen in adrenocortical tumors associated with Cushing syndrome (CS), particularly those with PRKAR1A mutations, such as in primary pigmented nodular adrenocortical disease (PPNAD). We investigated the presence of lipofuscin in cortisol-producing adenomas (CPAs) responsible for CS with and without the PRKACA (pLeu206Arg) somatic mutation. Ten paraffin-embedded sections of CPAs from cases with overt CS with (n=4) and without (n=6) a PRKACA mutation were microscopically examined through three detection methods, the hematoxylin-Eosin (H & E) staining, the Fontana Masson (FM) staining using light microscopy, and lipofuscin autofluorescence, using confocal laser scanning microscopy (CLSM). Sections were examined quantitatively according to the intensity of the pigmentation, as well as qualitatively based on the total number of granular pigments at all visual fields per tissue slide. Tissues from CPAs were compared to peritumoral adjacent tissues (n=5), to Conn adenomas (n=4), and PPNAD (n=3). CPAs had significantly higher number of lipofuscin-pigment granules compared to peritumoral adrenal tissue and Conn adenomas (46.9±9.5 vs. 3.8±4.8, p=0.0001). The presence of the PRKACA mutation did not increase the chances of pigmentation in the form of lipofuscin granules within CPAs associated with CS. Thus, all CPAs leading to CS accumulate lipofuscin, which presents like pigmentation sometimes seen macroscopically but always detected microscopically. PPNAD caused by PRKAR1A mutations is the best known adrenal lesion leading to CS associated with intense lipofuscin pigmentation and this was confirmed here; CPAs harboring PRKACA mutations did not have statistically significantly more pigmentation than CPAs without mutation, but a larger study might have shown a difference.

The human placenta does not contain lipofuscin pigment

Placenta ◽  
1984 ◽  
Vol 5 (5) ◽  
pp. 459-464 ◽  
Author(s):  
M. Haigh ◽  
L.E. Chawner ◽  
H. Fox
Keyword(s):  
Human Placenta ◽  
Lipofuscin Pigment

Lipofuscin pigment can be used as a prognostic marker in prostatic adenocarcinoma

2006 ◽  
Vol 10 (5) ◽  
pp. 257-262 ◽  
Author(s):  
Mandana Mahmoodi ◽  
Shunli Zhang ◽  
Sadia Salim ◽  
J. Steve Hou ◽  
Fernando U. Garcia
Keyword(s):  
Prognostic Marker ◽  
Prostatic Adenocarcinoma ◽  
Lipofuscin Pigment

Diurnal rhythm of lipofuscin pigment in neurocytes of certain nuclei of mouse hypothalamus∗

1982 ◽  
Vol 13 (2) ◽  
pp. 147-156 ◽  
Author(s):  
H. Lach ◽  
K. Dziubek ◽  
S. Krawczyk ◽  
W. Szaroma
Keyword(s):  
Diurnal Rhythm ◽  
Lipofuscin Pigment

scholarly journals THE IN VITRO PREPARATION AND HISTOCHEMICAL PROPERTIES OF SUBSTANCES RESEMBLING CEROID

1951 ◽  
Vol 94 (6) ◽  
pp. 549-562 ◽  
Author(s):  
W. G. Bruce Casselman
Keyword(s):  
Fatty Acids ◽  
Blood Cells ◽  
Periodic Acid ◽  
Vitamin E Deficiency ◽  
Silver Carbonate ◽  
Relative Lack ◽  
Unsaturated Lipids ◽  
Lipofuscin Pigment ◽  
Ceroid Pigment

Substances possessing the same histochemical properties as the ceroid in cirrhotic livers of rats fed choline-deficient diets have been prepared from various unsaturated fats, fatty acids and their esters by autoxidation but could not be obtained from hydrocarbons or saturated fats or fatty acids. The formation of ceroid-like substances occurred first on surfaces or at interfaces in the reaction mixtures. It was inhibited by antioxidants and was accelerated by the addition of tissues, blood cells, erythrocytic stroma, or hemoglobin, by emulsification, by increasing the surface exposed to the air, and by increasing the temperature. Histochemical studies provided much evidence that the following properties of ceroid might be attributed to the products of the autoxidation of unsaturated lipids: insolubility in organic solvents, sudanophilia, yellowing by concentrated nitric acid, positive periodic acid-Schiff's reaction, basophilia, acid fastness, positive hernofuscin reaction, and reduction of diammine silver carbonate and alkaline potassium permanganate. The normal reactivity of cells or tissues embedded in ceroid was effectively masked by the pigment, apparently, initially at least, by preventing the reagents' gaining access to them. It is suggested that the iron sometimes demonstrated in ceroid may be that of blood cells or tissue fragments incompletely masked by the ceroid. It is concluded that whenever conditions are such that unsaturated fats accumulate in tissues to such an extent that a relative lack of biological anti-oxidants results, autoxidation of the fats and their conversion to ceroid pigment are favored, and that ceroid and the lipofuscin pigment of vitamin E deficiency may be fundamentally similar.

A Histopathologic Pattern of Centrilobular Hepatocyte Injury Suggests 6-Mercaptopurine-Induced Hepatotoxicity in Patients With Inflammatory Bowel Disease

2012 ◽  
Vol 136 (6) ◽  
pp. 618-622 ◽  
Author(s):  
Ricard Masia ◽  
Daniel S. Pratt ◽  
Joseph Misdraji
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Massachusetts General Hospital ◽  
Periodic Acid ◽  
Nodular Regenerative Hyperplasia ◽  
Periodic Acid Schiff ◽  
Hepatocyte Injury ◽  
Lipofuscin Pigment ◽  
Inflammatory Bowel ◽  
Therapeutic Doses

Context.—Hepatotoxicity is an important side effect of thiopurine analog treatment for inflammatory bowel disease. A variety of histopathologic findings have been observed in patients with inflammatory bowel disease with thiopurine-induced hepatotoxicity, including nodular regenerative hyperplasia, vascular injury, and cholestasis. Objective.—To describe the histologic features shared by 3 cases of thiopurine-induced hepatotoxicity in patients with inflammatory bowel disease. Design.—We identified 3 patients with inflammatory bowel disease who developed hepatotoxicity due to 6-mercaptopurine from the educational files of the Department of Pathology at Massachusetts General Hospital (Boston). Histology slides (stained with hematoxylin-eosin, trichrome, periodic-acid Schiff with diastase digestion, and iron stains) and patients' medical records were reviewed retrospectively. Results.—All 3 patients were receiving 6-mercaptopurine monotherapy at therapeutic doses, had normal thiopurine metabolite levels, and presented with elevated aminotransferase levels. Biopsies from all 3 cases exhibited a pattern of centrilobular hepatocyte injury characterized by ceroid-laden macrophages, hepatocyte anisonucleosis, and increased lipofuscin pigment, as well as centrilobular steatosis. Aminotransferase levels trended downward and either normalized or remained at borderline elevated levels after 6-mercaptopurine dose was reduced (in 1 patient) or discontinued (in 2 patients). Conclusions.—Recognition of a pattern of centrilobular injury enables pathologists to suggest thiopurine-induced liver injury as the cause of elevated aminotransferases in patients with inflammatory bowel disease.

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