Middle-aged woman Case

A middle-aged woman was admitted to hospital suffering from sub-acute liver failure. She presented with jaundice, anorexia and vomiting and this progressed to grade II hepatic encephalopathy. Despite extensive investigation, the cause of her liver failure was not identified and she died three weeks after admission.

Post-mortem samples of liver and bone marrow were taken. Histological examination of the bone marrow showed abnormally large numbers of atypical plasma cells, an observation consistent with multiple myeloma. Slide A is an example of a normal liver (HE). Sections from the patient's liver were stained with HE (Slide B) or congo red (Slide C).

Slide A: the hepatic cells acquire large round nuclei with prominent chromatin. The irregular spaces which are between cords of the hepatic perenchmal cells are sinusoids, these are together with a discontinuous layer of endothelial cells, Kupffer cells line the sinusoids. The normal liver slide also shows central veins, which receive blood from surrounding sinusoids. The canals contain a branch of hepatic artery, portal vein, bile duct and a lymphatic vessel, these are visualised by the white dot like figure (Emanuel Rubin & John L. Farber 1998).

Slide B: the hepatomegaly of the liver is due to the perisinusoidal amyloid deposits. Atrophy of the hepatic cords with shrinkage that causes little functional impairment. Amyloid deposits are seen around the splenic follicles and in the space of Disse. The portal vein has an irregular shape; this is damaged by the invasion of amyloid deposits.

Congo red is stained with haematoxylin initially for 10 minutes to allow the differentiation of amyloid protein and normal cells. Haematoxylin shows epithelial cells, which is an orange-red colouring whereas the amyloid is shown as apple-green.

Polarised light is the preferred method for visualising congo red positively. Polarised light is a property of waves that illustrates the orientation of their oscillations. The apple-green birefrengence of congo red stain is visualised under polarised light. Amyloid protein depicts the β pleated sheet structure, which allows the congo red dye to bind.

From the case study, the middle aged women is suffering from sub-acute liver failure (SALF), from examination there is clear evidence that the middle aged women had grade II hepatic encephalopathy, this is because of the bone marrow showing large numbers of atypical plasma cells, which is consistent with multiple myeloma. The presence of liver involvement in multiple myeloma is visible on the slide B and C as hepatomegaly due to amyloid deposition. Grade II hepatic encepthalopathy is defined as SALF, it occurs 28 days and 72 days after the onset of jaundice

(Williams et al., 1993). The presence of liver involvement in jaundice is because of hepatic myeloma infiltrating and causing an extrahepatic obstructive jaundice. The most likely diagnosis of the middle aged women suffered from deposition of AL amyloid protein, this is because of the history of the women, she had multiple myeloma, and AL amyloid contains immunoglobulin light-chains (λ,κ) which are derived from plasma cells (Okabe et al., 1998). Amyloidoses can also be classified as primary or secondary, In case of the women she had primary, and this is because primary distorts immune cell function such as multiple myeloma which is present in the women's case history.

An 80 year-old woman presented with persistent nausea and abdominal discomfort. Endoscopic examination of the stomach revealed a red and inflamed mucosa with pale focal areas. A biopsy of one of the pale foci was taken and sections were stained with HE (Slide D) and with Alcian blue/PAS (Slide E). A control slide of normal gastric mucosa is provided as Slide F.

Slide F consists of short gastric pits which are open freely to the lumen. The whole surface consists orderly of surface mucous cells, the ultimate goal is to protect the stomach from self-digestion. Gastric glands are visible which comprise the volume of the mucosa beneath the pits. Lamina properia separates as seen on slide F separates the individual gland, most of the mucosal volume is occupied by secretory cells, which are mainly parietal and chief cells. The muscularis externa of the stomach is seen as the thickest along the tract. Gastric pits are also visible with their tubular shape and distinct glandular appearance. Beneath the gastric pits, the mucosa of the stomach is filled with closely associated tubular glands (Emanuel Rubin & John L. Farber 1998).

Slide D is of stomach which has encountered intestinal metaplasia, it shows partial replacement of the gastric mucosal epithelium. There are also signs of lamina propria and plasma cells involved in inflammation. The setting of inflammation is also distinguished by the presence of goblet cells; these are cells in which the cytoplasmic membrane and neucleus are distorted primarily by large vacuoles of acidic mucin.

By combining both Alcian blue / PAS it is possible to identify the major groups of mucins (full complement of tissue proteoglycans). Alcian blue in slide E is blocking the PAS reaction in acid mucins and so thus distinguishes between neutral and acid mucins. Acid mucins stain blue and the neutral mucins stain purple from the PAS, the resultant colour depends upon the dominant moiety (D.J Cook 2006). The purpose of Alcian blue / PAS in slide E is the fact that goblet cells are confirmed, Alcian blue stains the acid mucins of goblet cells blue whereas PAS stains all mucin red. As seen on slide E it is fairly distinguish to recognise an intestinal metaplasia, from mucin red colour given by PAS and blue acidic mucins by Alcian blue.

The importance of histological changes seen in patient suggests that the most likely cause of inflammation in the mucosa is a bacterium called H. Pylori. The evidence to suggest this is Slide E which is stained with Alcian blue / PAS. The stain differentiates between neutral and acetic muco-substances. H. Pylori is a gram-negative organism that inhibits a peculiarly protected niche closely applied to the surface epithelium beneath the mucous barriers where the pH approaches to neutral. Because the organism has its own acid buffering mechanism using its urease and ammonia production to neutralise hydrogen ions which gains access to its periplasmic place as seen on Slide E. The organism binds to the surface cells, and depending on its virulence, excerts cytopathic effects that leads to accelerated cell exfoliation (Underwood & Cross 2009). There is also evidence to suggest that blue colour which is shown on slide E is H. Pylori these are visualised as clear blue dots showing acid mucins by using Alcian bue. In case of the women she had intestinal metaplasia, in which H. Pylori does not colonise regions, few light blue bands around the mucosa suggest this.


Abraham L. Kierszenbaum (2002). Histology and Cell Biology. Missouri: Mosby Inc . 393-419.

D.J Cook (2006). Cellular Pathology An indroduction to techniques and applications. 2nd ed. Oxfordshire: Scion. 119-123.

Emanuel Rubin & John L. Farber (1998). Pathology. 3rd ed. Philadelphia: Lippincott Williams & Wilkins . 393-419.

J.C.E Underwood and S.S. Cross (2009). General and Systematic Pathology . Livingstone: Elsevier. 400-500.


O'Grady J G, Schalm S W, Williams R (1993). Acute liver failure: redefining the syndromes. Lancet. 342273-275.

Okabe M, Choi G H, Kudo M. et al (1998). Hepatic failure due to myeloma‐associated amyloidosis. J Gastroenterol. 33926-927.

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