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Cirrhosis of the liver is frequently the last stage before liver failure. It is characterized by loss of the normal architecture with fibrosis. Cirrhosis can be broadly classified into two categories based upon the histologic and clinical-pathogenesis.

Central-Based Fibrotic Lesions Alcoholic fibrosis and cirrhosis
Cardiac fibrosis
Venous outflow obstruction such as Budd-Chiari syndrome and veno-occlusive disease
Portal-Based Fibrotic Lesions Chronic hepatitis and cirrhosis
Biliary tract disease including pirmary biliary cirrhosis, sclerosing cholangitis, inflammatory changes associated with idiopathic inflammatory bowel disease, and duct obstruction

The pathologist must establish the diagnosis from tiny needle core biopsies. Histologic clues to the diagnosis include:

Fragmented specimen with rounded edges
Reticulin fibers at the edge of fragments
Portal tracts absent
Irregular pattern of central veins
Twin plates
Enlarged nuclei (large cell change)
Caution with capsule on wedge biopsies (subcapsular fibosis normally present).

At times, the diagnosis may still be unclear. Pathologists may use the descriptive diagnoses such as probable or possible cirrhosis, or cannot exclude cirrhosis. If there is good clinical documentation of the duration of the cirrhosis of progression of the fibrosis, the term early cirrhosis has sometimes been used. If there is extensive fibrosis with minimal residual normal liver cells, the term end-stage cirrhosis has been used.


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Destruction of canals of Hering in primary biliary cirrhosis.

Saxena R, Hytiroglou P, Thung SN, Theise ND.

Lillian and Henry M. Stratton-Hans Popper Department of Pathology, Mount Sinai School of Medicine, New York, NY, USA.

Hum Pathol 2002 Oct;33(10):983-8 Abstract quote

The canals of Hering (CoH), converging from the hepatic lobule onto the portal tract, connect bile canaliculi to the interlobular bile ducts, and represent the most proximal portion of the bile drainage pathway with a cholangiocyte lining.

In this study we sought to ascertain whether this proximal pathway is involved by the disease process in primary biliary cirrhosis (PBC), which uniformly affects small bile ducts while sparing medium- and large-sized ducts. Ten biopsy specimens with early-stage PBC were compared with 6 normal control livers. Adjacent 4-micron-thick sections of routinely processed, formalin-fixed tissue were immunostained for CK19 and HLA-DR. Each terminal portal tract was assigned a stage: 0, normal; 1, bile duct damage or loss; 2, bile ductular proliferation; or 3, periportal fibrosis. The ratio of the number of CoH to number of portal tracts (i.e., the c/p ratio) was calculated for the control biopsies and individual portal tracts at each stage of PBC. The numbers of CoH were decreased in all stages of PBC (P <0.0001), with the fewest found around portal tracts at stages 0 and 1 and the most around portal tracts at stages 2 and 3, but never at normal levels. HLA-DR was expressed focally on bile ducts and CoH in PBC, but was absent in normal controls.

We conclude that CoH are destroyed in PBC in concert with the destruction of small bile ducts. This destruction appears to be an early event, because CoH numbers are lowest around stage 0 portal tracts, which still contain normal bile ducts.



Infarcted regenerative nodules in cirrhosis: CT and MR imaging findings with pathologic correlation.

Kim T, Baron RL, Nalesnik MA.

Department of Radiology, University of Pittsburgh Medical Center, 200 Lothrop St., Pittsburgh, PA 15213-2582, USA.

AJR Am J Roentgenol 2000 Oct;175(4):1121-5 Abstract quote

OBJECTIVE. The purpose of this article is to present the imaging findings and correlative pathologic findings of infarcted regenerative nodules in the cirrhotic liver.

CONCLUSION. Infarcted regenerative nodules exhibit a spectrum of imaging appearances in the cirrhotic liver and can resemble hypovascular hepatocellular carcinoma or other neoplasms on CT and MR imaging. Although uncommon, this abnormality must be included in the differential diagnosis of focal liver lesions in patients with cirrhosis, particularly in patients with a history of substantial gastrointestinal bleeding. Serial imaging may help differentiate these lesions from malignant tumors.



Frequent micronodular pattern
Mallory hyaline, especially centrilobular
Fatty change
Centrilobular sclerosis
Pericellular, perivenular fibrosis (chicken wire pattern)
Fairly uniform, diffuse process
Paucity of inflammation
Central-cental, central-portal bridging prominent

Analysis of histological and immunohistochemical patterns of the liver in posthepatitic and alcoholic cirrhosis by computerized morphometry.

Vizzotto L, Vertemati M, Gambacorta M, Sabatella G, Spina V, Minola E.

Department of Human Anatomy, Faculty of Medicine (LV, MV, GS, VS)

Mod Pathol 2002 Aug;15(8):798-806 Abstract quote

To assess the degree of fibrosis and the structural changes affecting parenchymal and extraparenchymal components in liver cirrhosis, a computerized morphometric model has been applied to liver specimens from patients with posthepatitic and alcoholic cirrhosis.

All specimens have been stained with chromotrope-aniline blue method and monoclonal antibodies against cytokeratin 7, CD31, and VIII factor. Volume fractions of parenchymal compartment and fibrosis have been determined stereologically on CAB slices; moreover, volume fractions of portal bile ducts and proliferated bile ductules, hepatocytes with biliary metaplasia, capillary units, and vascular structures have been measured. Volume fraction of fibrosis was higher in alcoholic cirrhosis when compared with the case of posthepatitic cirrhosis. Volume fractions describing parenchymal compartment showed a similar trend in both viral groups. The main differences were related to immunohistochemical stainings. Volume fraction of hepatocytes with biliary metaplasia was higher in hepatitis C virus-related cirrhosis, whereas volume fractions of biliary structures were more prominent in hepatitis B virus-related cirrhosis. Capillary units were more prominent in posthepatitic cirrhosis than in alcoholic cirrhosis. Interestingly, both forms of posthepatitic cirrhosis show similar features when compared with alcoholic cirrhosis.

Our computerized morphometric model well describes and quantifies the morphological alterations of the liver, and it could represent an adjunctive tool to evaluate the degree of dysplastic phenomena involving parenchymal and extraparenchymal components.


Metastatic Carcinomatous Cirrhosis and Hepatic Hemosiderosis in a Patient Heterozygous for the H63D Genotype

Mark L. Mitchell, MD, Marciana D. Filippone, MD, and Timothy F. Wozniak, MD

From the Departments of Pathology (Dr Mitchell) and Internal Medicine (Drs Filippone and Wozniak), Christiana Care Health System, Newark, Del.

Arch Pathol Lab Med 2001;125:1084–1087. Abstract quote

A 38-year-old woman had a mastectomy for infiltrating ductal carcinoma of the breast 3 years before her last admission and had received chemotherapy for known liver metastases.

She developed the rapid onset of liver failure with portal hypertension and died in a hospice. Autopsy revealed macronodular cirrhosis of the liver secondary to metastatic carcinoma of the breast with associated florid fibrosis. This rare lesion, previously called metastatic carcinomatous cirrhosis , was also found, in this case, to have marked hepatic hemosiderosis, and analysis of the patient's DNA showed heterozygosity for the H63D genotype. The possibility of cirrhosis-associated hemosiderosis secondary to an iron metabolism abnormality associated with the H63D mutation of the HFE gene is proposed.

Computed tomographic scans showed the development of cirrhosis during the 3-month period before the patient's last admission and suggested the possibility of a postnecrotic type origin.


Cryptogenic cirrhosis: clinicopathologic findings at and after liver transplantation.

Ayata G, Gordon FD, Lewis WD, Pomfret E, Pomposelli JJ, Jenkins RL, Khettry U.

Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.


Pathol 2002 Nov;33(11):1098-104 Abstract quote

The incidence of cryptogenic cirrhosis (CC) has decreased since the discovery of hepatitis C virus (HCV), still the etiology in 5% of cases with cirrhosis remains unresolved.

Our aims were to define the clinicopathologic features of CC at liver transplantation (LT), evaluate the post-LT course with outcome and define the possible pathogenetic mechanisms. 27/534 LT recipients (5%) over a period of 16.5 years were entered in the LT database as cases of CC. A detailed analysis of pre- and post-LT clinical and all liver pathology specimens was performed. Based on clinicopathologic findings, a more definite diagnosis was possible in 23 of 27 (85%): Nonalcoholic steatohepatitis (NASH) in 9 (33%), autoimmune liver disease (AILD) in 6 (22%), alcoholic liver disease in 4, secondary biliary cirrhosis in 2 and 1 each of hepatitis C and portal venopathy. 4/27 cases remained unresolved.

In the NASH group, native livers had focal steatosis, Mallory's hyalin, glycogenated hepatocytic nuclei, high-grade inflammation, and 3+ bile duct proliferation. Large cell dysplasia was more common in this group compared to other patients. Two patients had recurrence of NASH after LT. In AILD group native livers had little or no bile duct proliferation. Two patients had recurrence in AILD group. Of 27 patients 19 are alive (70%) with a follow-up of 407-3647 days. Based on the study results, the following conclusions were reached: (1) CC results from varying etiologies, which can be defined by a careful clinicopathologic analysis in a majority (85%) of cases; (2)

Nonalcoholic steatohepatitis (33%) and AILD (22%) are the common underlying causes of CC; and (3) Post-LT outcome for CC is disease dependent with, recurrent disease seen in both nonalcoholic steatohepatitis (22%) and autoimmune liver disease (33%).



Vitronectin in the cirrhotic liver: An immunomarker of mature fibrosis

George K. Koukoulis, MD
Jikun Shen, MD
Ismo Virtanen, PhD
Victor E. Gould, MD

Hum Pathol 2002;32:1356-1362

Vitronectin (Vn) is a multifunctional plasma glycoprotein produced by hepatocytes. Vn has been studied extensively as a cell adhesion molecule. However, its localization in the hepatic extracellular matrix has received relatively little attention.

Cryosections of 5 normal liver samples and of 20 specimens showing posthepatitic cirrhosis were stained by the avidin–biotin complex method with a well-characterized monoclonal antibody to Vn. The extent and intensity of immunostaining were assessed semiquantitatively (0, no staining; 1+, weak focal staining; 2+, strong focal staining; 3+, strong diffuse staining). Paraffin sections from the same samples were stained with Masson trichrome (MT) and Shikata orcein (Or) methods. Frozen samples from selected cases were analyzed by Western blotting. In the normal liver, 3+ staining was limited to portal vessels. The portal tract connective tissue showed minimal staining (0 to 1+). Cirrhotic septa showed strong staining (2+). Septa lacking significant inflammation and composed of dense connective tissue, as indicated by MT and Or stains, showed the strongest Vn reactions (3+). Immunoblotting data strongly correlated with Vn increase in cirrhotic livers. Vn immunoreactivity is markedly increased in the cirrhotic liver matrix, regardless of the documented decrease in plasma Vn. Binding to collagen, elastin, and proteoglycans is the current favored mechanism of Vn deposition in tissues. Previous studies in cirrhotic patients showed increased affinity of plasma Vn to collagen. Vn is also increased in aged skin, associated with dermal elastic fibers. In other tissues, Vn deposition reflects chronicity of injury.

Therefore, Vn immunoreactivity in liver can be considered a marker of fibrosis, especially of chronic/mature fibrosis, paralleling previous observations on enhanced orcein staining of cirrhotic septa. Immunolabeling of biopsy specimens with Vn and tenascin, a marker of ongoing remodeling or recently formed fibrous tissue, could be diagnostically helpful.


Diabetic hepatosclerosis: diabetic microangiopathy of the liver.

Harrison SA, Brunt EM, Goodman ZD, Di Bisceglie AM.

Liver Center, Department of Medicine, Saint Louis University School of Medicine, St Louis, MO 63110, USA.

Arch Pathol Lab Med. 2006 Jan;130(1):27-32. Abstract quote  

CONTEXT: Liver disease associated with diabetes mellitus is common and usually takes the form of simple steatosis or nonalcoholic steatohepatitis. After observing a noncirrhotic form of hepatic sinusoidal fibrosis in patients with long-standing diabetes mellitus who underwent liver biopsy, we set about to characterize this novel entity.

DESIGN AND SETTING: Cases with the hallmark histologic findings were gathered at Saint Louis University School of Medicine and the Armed Forces Institute of Pathology.

PATIENTS: The clinical records were examined in a systematic fashion. Results of light microscopy and prepared immunohistochemical stains were reviewed.

MAIN OUTCOME MEASURES: Clinical findings of patients with the histologic, detailed light microscopic, and immunohistochemical findings on biopsies.

RESULTS: Twelve patients were identified from biopsy findings; all had a history of long-standing diabetes mellitus and a noncirrhotic form of hepatic sinusoidal fibrosis not associated with nonalcoholic steatohepatitis. Most of these patients had a body mass index less than 25 kg/m2 and had substantial evidence of microvascular complications, including retinopathy, nephropathy, and peripheral and autonomic neuropathy. Alkaline phosphatase elevation was common. Liver biopsy specimens showed extensive dense perisinusoidal fibrosis, and immunostaining revealed basement membrane components in a perisinusoidal distribution. Features of nonalcoholic steatohepatitis were not present in the biopsy specimens.

CONCLUSIONS: We propose the term diabetic hepatosclerosis for this entity and suggest that it represents a form of diabetic microangiopathy affecting the liver. Further studies are needed to precisely characterize diabetic hepatosclerosis and to understand mechanisms of pathogenesis and the clinical significance

Liver pathology of idiopathic portal hypertension. Comparison with non-cirrhotic portal fibrosis of India. The Japan idiopathic portal hypertension study.

Okuda K, Nakashima T, Okudaira M, Kage M, Aida Y, Omata M, Sugiura M, Kameda H, Inokuchi K, Bhusnurmath SR, Aikat BA.


Liver 1982 Sep;2(3):176-92 Abstract quote

Morphological changes of the liver were studied in 24 autopsy cases of noncirrhotic portal hypertension of unknown etiology (idiopathic portal hypertension, IPH), and in 123 surgical biopsies from such patients.

For comparison, 15 whole-cut liver slices from autopsy cases of noncirrhotic portal fibrosis (NCPF) from India were also studied. Liver pathology was very similar in IPH and NCPF, characterized by phlebosclerotic changes and perivascular fibrosis of the portal vein system, and parenchymal atrophy perhaps secondary to portal circulatory insufficiency. The distribution of lesions was uneven, and despite marked fibrosis and occasional surface nodularity, there was no diffuse pseudonodule formation in the parenchyma. Surgical specimens showed similar changes except for more frequent portal cellular infiltrates, but the changes seen in one biopsy specimen were limited and not always diagnostic.

It seems that IPH of Japan and NCPF of India are the same disease, and perhaps hepatoportal sclerosis elsewhere is also the same disease.

Non-cirrhotic portal fibrosis (idiopathic portal hypertension): experience with 151 patients and a review of the literature.

Dhiman RK, Chawla Y, Vasishta RK, Kakkar N, Dilawari JB, Trehan MS, Puri P, Mitra SK, Suri S.

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

J Gastroenterol Hepatol 2002 Jan;17(1):6-16 Abstract quote

BACKGROUND: Non-cirrhotic portal fibrosis (NCPF), the equivalent of idiopathic portal hypertension in Japan and hepatoportal sclerosis in the United States of America, is a common cause of portal hypertension in India. The clinical features, portographic and histological findings, and management of 151 patients with non-cirrhotic portal fibrosis are presented.

METHODS: The disease is diagnosed by the presence of unequivocal evidence of portal hypertension in the definite absence of liver cirrhosis and extrahepatic portal vein obstruction (EHPVO). Retrospective analysis of records of 151 patients with NCPF was analyzed for the clinical presentation, physical findings, laboratory tests, radiological and histological findings, and for the outcome of treatment.

RESULTS: The disease is characterized by massive splenomegaly with anemia, preserved liver function and benign prognosis in a majority of patients. Splenoportovenography (SPV) showed massive dilatation of the portal and splenic veins, and the presence of collaterals. Twenty-four (15.9%) patients showed evidence of natural/spontaneous shunts (splenorenal 15, umbilical nine) on SPV; these patients had a lower incidence of variceal bleeding. Liver histology demonstrated maintained lobular architecture, portal fibrosis of variable degree, sclerosis and obliteration of small-sized portal vein radicles, and subcapsular scarring with the collapse of the underlying parenchyma. Piecemeal or hepatocytic necrosis was absent in all histology specimens. Three patients showed nodular transformation along with abnormal liver functions, and may represent late manifestation of NCPF where features are similar to those seen in patients with incomplete septal cirrhosis. In the initial part of the study, surgery (side-to-side lieno-renal shunt) was the preferred modality of treatment, however, endoscopic sclerotherapy or variceal ligation has now become the preferred first line of management of variceal bleeding.

CONCLUSIONS: The epidemiological and clinical features of NCPF have more similarity to IPH than has previously been documented. The development of spontaneous shunts tends to protect these patients from variceal bleeding.



Cachexia in liver cirrhosis.

Plauth M, Schutz E.

Klinik fur Innere Medizin, Stadtisches Klinikum, Auenweg 38, 06847, Dessau, Germany

Int J Cardiol 2002 Sep;85(1):83 Abstract quote

Patients with chronic liver disease exhibit a progressive loss of fat and muscle mass leading to mixed protein-energy malnutrition. The severe loss of muscle mass and body cell mass have convincingly been shown to carry a grave prognosis.

Cachexia is likely to progress due to increased requirements as a consequence of hypermetabolism on the one hand and reduced volitional food intake and malabsorption on the other. Hypermetabolism may be mediated by factors such as frequent episodes of endotoxinemia, an activation of the inflammatory cytokine and/or the beta-adrenergic system. Some of these factors may also be responsible for reduced appetite. Obviously, these mechanisms may also be operative in other disease entities but clearly, portal hypertension and portosystemic shunting pose the cirrhotic patient at a particular risk for such disturbances including that of malabsorption.

Apart from the established value of providing sufficient nutritious substrate to meet requirements the use of beta-adrenergic blocking agents and endotoxinemia lowering strategies seem worthwhile options that merit further clinical evaluation.


Reversibility of hepatitis C virus-related cirrhosis.

Pol S, Carnot F, Nalpas B, Lagneau JL, Fontaine H, Serpaggi J, Serfaty L, Bedossa P, Brechot C.

Hum Pathol. 2004 Jan;35(1):107-12. Abstract quote  

The aim of this retrospective study was to determine the potential reversibility of hepatitis C virus (HCV) cirrhosis with the combined antifibrotic effects of interferon-alpha and the increasing frequency of sustained virologic response.

Sixty-four HCV-cirrhotic immunocompetent patients who underwent antiviral therapies (interferon-alpha with or without ribavirin) and pretreatment and posttreatment liver biopsies were included (group 1). Resolution of cirrhosis was defined as a decrease in the fibrosis score from 4 to 2 or less by the Metavir score after blinded analysis by 2 independent pathologists. An additional group of 4 HCV-infected dialysis patients (group 2) who had received antiviral treatment, among whom 3 underwent a combined renal and liver transplantation allowing the analysis of the whole liver, was also studied. In 5 (all stage Child A) of the 64 cirrhotic patients (7.8%), the final biopsy showed only F2 to portal and periportal fibrosis with rare fibrous septa without nodule formation.

Four of these 5 were complete sustained responders (negative PCR and normal ALT), and 1 was a relapser. In group 2, reversibility of cirrhosis was observed in 3 of the 4 patients and was clearly shown in 2 patients by the analysis of the whole-liver examination at the time of the hepatectomy preceding the transplantation.

In conclusion, long-lasting suppression of the necroinflammatory activity of liver disease and/or antifibrogenetic effects of interferon-alpha may allow regression of cirrhosis.

Clinical course, predictive factors and prognosis in patients with cirrhosis and type 1 hepatorenal syndrome treated with Terlipressin: A retrospective analysis.

Colle I, Durand F, Pessione F, Rassiat E, Bernuau J, Barriere E, Lebrec D, Valla DC, Moreau R.

J Gastroenterol Hepatol 2002 Aug;17(8):882-8 Abstract quote

BACKGROUND AND AIM: Terlipressin has been proposed to treat renal failure in patients with type 1 hepatorenal syndrome (HRS). However, the predictive factors for improved renal function and survival are unknown in patients with type 1 HRS treated with terlipressin. The aim of the present retrospective study was to investigate the predictive factors and prognosis of patients with type 1 HRS treated with terlipressin.

METHODS: The clinical charts of 18 consecutive patients with cirrhosis and type 1 HRS treated with terlipressin were studied. The predictive factors for improved renal function and survival were identified using univariate analyses.

RESULTS: Improved renal function, indicated by a significant decrease in serum creatinine (61 +/- 4%), occurred in 11 (60%) patients. The only predictive factor for improved renal function was a Child-Pugh's score </=13 at the time of diagnosis of HRS (P = 0.02). Fifteen patients (83%) died at 45 days and the median survival was 24 days. Of the three patients who survived, two underwent successful orthotopic liver transplantation. Three predictive factors for survival were identified: absence of a precipitating factor for HRS (P = 0.012); improved renal function during terlipressin therapy (P = 0.05); and a dose of terlipressin >/=3 mg/day (P = 0.04).

CONCLUSIONS: In patients with type 1 HRS treated with terlipressin, patients with improved renal function had less severe cirrhosis (Child-Pugh >10 but </=13) than patients without. The predictive factors for survival were the absence of a precipitating factor for HRS, the terlipressin-induced improvement in renal function and a dose of terlipressin of at least 3 mg/day. These findings suggest that a randomized controlled trial investigating the effect of terlipressin on survival in patients with type 1 HRS should be performed.


Antibiotic prophylaxis for cirrhotic patients with gastrointestinal bleeding.

Soares-Weiser K, Brezis M, Tur-Kaspa R, Leibovici L.

Department of Medicine E, Rabin Medical Center - Beilinson Campus, Petah Tikva, Israel, 41900.

Cochrane Database Syst Rev 2002;(2):CD002907 Abstract quote

BACKGROUND: Bacterial infections are a frequent complication in patients with cirrhosis and gastrointestinal bleeding. Antibiotic prophylaxis seems to decrease the incidence of bacterial infections. Oral antibiotics, active against enteric bacteria, have been most often used as antibiotic prophylaxis in cirrhotic patients with gastrointestinal bleeding.

OBJECTIVES: This review aims to evaluate the effects of antibiotic prophylaxis in the prevention of bacterial infections in cirrhotic patients with gastrointestinal bleeding.

SEARCH STRATEGY: Electronic searches on The Cochrane Hepato-Biliary Group Controlled Trials Register (May 2001), The Cochrane Library (Issue 2, 2001), EMBASE (1980-2001), and MEDLINE (1966-2001); handsearching the references of all identified studies; contacting the first author of each included trial.

SELECTION CRITERIA: Randomised clinical trials comparing different types of antibiotic prophylaxis with placebo, no intervention, or another antibiotic to prevent bacterial infections in cirrhotic patients with gastrointestinal bleeding.

DATA COLLECTION AND ANALYSIS: Two reviewers independently appraised the quality of each trial and extracted the data from the included trials. Relative risks (RR) or average differences, with their 95% confidence intervals (CI) were estimated. The reviewers assumed an intention to treat basis for the outcome measures.

MAIN RESULTS: Eight trials evaluated the effects of antibiotic prophylaxis compared with placebo or no antibiotic prophylaxis in 864 patients. A significant beneficial effect on decreasing mortality (RR 0.73, 95% CI 0.55 to 0.95) and the incidence of bacterial infections (RR 0.40, 95% CI 0.32 to 0.51) was observed. No serious adverse events were reported. The trials showed no significant heterogeneity. Three additional trials evaluated the effects of antibiotics compared with a different regimen of antibiotics in 503 patients. Data could not be combined as each trial used different interventions. None of the examined antibiotic regimens was superior to the control regimen regarding mortality or the incidence of bacterial infections.

REVIEWER'S CONCLUSIONS: Antibiotic prophylaxis for cirrhotic inpatients with gastrointestinal bleeding is efficacious in reducing the number of deaths and bacterial infections, are well tolerated, and should be advocated.

Mod Pathol 2000;13:679-704.
Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Ninth Edition. Mosby 2004.
Sternberg S. Diagnostic Surgical Pathology. Fourth Edition. Lipincott Williams and Wilkins 2004.
Robbins Pathologic Basis of Disease. Seventh Edition. WB Saunders 2005.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
Fitzpatrick's Dermatology in General Medicine. 6th Edition. McGraw-Hill. 2003.
Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.

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Last Updated January 20, 2006

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