Extracellular Deposition and Amyloidosis
Extracellular Deposition
Definition: An abnormal element deposited around cells.
Main Types:
Hyalinosis
Calcium
Amyloid
Mucin
Uric acid
Hyaline Degeneration (Hyalinosis)
Definition: An alteration within cells or in extracellular spaces that gives a homogeneous acellular glassy pink appearance in H&E stained sections.
Usage: A descriptive histologic term rather than a specific marker for cell injury.
Characteristics:
Produced by various alterations and does not represent a specific pattern of accumulation.
Types of Hyalinosis
Intracellular Hyalinosis:
Examples:
Plasma cell (Russel bodies)
Hepatocytes (Mallory bodies)
Renal tubule cell
Extracellular Hyalinosis:
Examples:
Old scar
Uterine fibroid
Blood vessels of systemic hypertension (HT)
Pathological Calcification
Definition: A common process in diverse disease states, resulting from abnormal deposition of calcium salts, along with smaller amounts of iron, magnesium, and other minerals.
Classification of Pathological Calcification
Types:
Dystrophic Calcification:
Features: Normal calcium metabolism but deposits in injured or dead tissue, such as areas of necrosis.
Initiation: Extracellular deposition of crystalline calcium phosphate.
Metastatic Calcification:
Features: Associated with hypercalcemia and can occur in normal tissues, often due to parathyroid hormone excess.
Commonly Affected Tissues: Blood vessels, kidneys, lungs, gastric mucosa.
Additional Conditions Related to Calcification
Calcinosis:
A disorder of unknown cause characterized by calcification of skin and subcutaneous tissues; may be localized or generalized.
Often involves tendons, fascia, muscles, and nerves.
Pathologic (Heterotropic, Extraosseous, Soft Tissue) Ossification:
Characterized by the formation of bone tissue away from bones; an example is myositis ossificans after a suprachondylar bone fracture.
Amyloidosis
Definition: A disorder characterized by extracellular deposition of various fibrillary proteins in organs, leading to tissue damage and functional compromise.
Association: Linked with several inherited and inflammatory disorders.
Cause of Name: The term comes from 'amylose' because of the starch-like appearance.
Nature of Amyloid
Composition:
90% is fibril protein.
10% is a glycoprotein called P component.
Role of Macrophages: Important in amyloidosis through proteolytic cleavage of precursor proteins into amyloid fibrils.
Types of Amyloid Fibril Proteins: Various types exist.
Pathogenesis of Amyloidosis
Causes of Protein Deposition:
Excessive production of proteins prone to aggregation.
Mutations result in improperly folded proteins that aggregate.
Defective or incomplete proteolytic degradation of extracellular proteins.
Mechanism:
Excessive production of amyloidogenic proteins.
Mutant proteins lead to aggregation due to inability to fold correctly.
Monoclonal B-lymphocyte proliferation and macrophage activation contribute through cytokines such as Interleukins 1 and 6.
Fibril Formation: Monomers assemble to form $\beta$-sheet structures, leading to significant amyloid formation.
Chemical Composition of Amyloid
Diversity: Biochemically heterogeneous with at least 30 different proteins.
Common Forms:
AL (Amyloid Light Chain): Comprised of complete immunoglobulin light chains.
AA (Amyloid-Associated): Derived from SAA (Serum Amyloid Associated) protein synthesized in the liver.
β-Amyloid Protein (Aβ): Comes from proteolysis of the amyloid precursor protein.
Characteristic Stains of Amyloid
Staining Reactions:
Iodine: Brown color when added to fresh tissue containing amyloid.
H&E Stain: Amyloid stains red.
Methyl Violet: Shows metachromasia and appears pink.
Congo Red Stain: Appears orange-red with apple-green birefringence under polarized light.
Electron Microscopy (EM): Amyloid appears as non-branching fibrils, 7.5-10 nm wide.
X-ray Diffraction: Exhibits $\beta$-pleated sheet structure.
Classification of Amyloidosis
Categories:
Systemic (Generalized) Amyloidosis:
Plasma cell proliferations (Primary Amyloidosis)
Reactive systemic amyloidosis (Secondary Amyloidosis)
Hemodialysis-associated amyloidosis
Hereditary Amyloidosis (e.g., Familial Mediterranean fever)
Other hereditary types (familial amyloidotic neuropathies, systemic senile amyloidosis).
Localized Amyloidosis:
Affects specific organs such as the brain (senile cerebral), endocrine organs (medullary carcinoma of thyroid, islets of Langerhans).
Primary Amyloidosis
Overview: Most common form of amyloidosis.
Causes: Clonal proliferation of plasma cells.
Prevalence: Occurs in 5% to 15% of multiple myeloma cases.
Light Chain Distribution: λ light chains are approximately six times more likely to form amyloid than κ light chains.
Reactive Systemic Amyloidosis
Distribution: Systemic; composed of AA protein.
Common Causes: Rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, and certain cancers (e.g., renal cell carcinoma).
Infectious Causes: Tuberculosis, chronic osteomyelitis.
Heredofamilial Amyloidosis
Examples: Familial Mediterranean fever; characterized by excessive IL-1 production.
Protein Involvement: Deposition of amyloid derived from mutant transthyretin (TTR).
Hemodialysis-Associated Amyloidosis
Risk Factor: Long-term hemodialysis for renal failure can lead to amyloid deposits derived from β2 microglobulin.
Localized Amyloidosis
Definition: Limited to a single organ or tissue; often affects lung, larynx, skin, urinary bladder, and tongue.
Composition: Typically consists of AL protein.
Endocrine Amyloid
Examples: In endocrine tumors (e.g., medullary carcinoma of the thyroid), amyloid protein is procalcitonin produced by tumor cells.
Aging Related: Amyloid derived from normal TTR in older individuals leading to restrictive cardiomyopathy and arrhythmias.
Alzheimer's Disease: Involves β2-amyloid protein (Aβ).
Morphology in Amyloidosis
Affected Organs:
Kidneys: The most common and serious involvement.
Gross: Enlarged kidney with possible ischemic changes.
Cut Section: Pale gray waxy amyloid spots with sharp borders.
Microscopy: Amyloid deposits in glomeruli and tubules, pink and refractile in H&E, with orange-red birefringence in Congo red.
Liver:
Gross: Enlarged and firm with pale gray amyloid streaks.
Microscopy: Deposits in walls of arterioles and venules, leading to pressure atrophy of liver cells.
Spleen: Characterized by two patterns:
Sago Spleen: Amyloid deposits in walls of central arterioles, moderate splenomegaly with mottled cut surface.
Diffuse Amyloid Spleen: Amyloid in walls of sinusoids, marked splenomegaly with uniformly pale gray cut surface.
Heart:
Patterns: Localized or part of generalized amyloidosis.
Gross: Moderate cardiac enlargement, subendocardial amyloid deposits.
Complications: Potential heart failure due to amyloid causing pressure atrophy of myocardial fibers.
Clinical Features of Amyloidosis
Initial Symptoms: Nonspecific, such as weakness, weight loss, lightheadedness, or syncope.
Later Symptoms: Related to renal, cardiac, and gastrointestinal involvement, leading to:
Progressive obliteration of glomeruli causing renal failure and uremia.
Cardiac amyloidosis leading to conduction disturbances and potentially fatal arrhythmias.
Gastrointestinal symptoms possibly leading to malabsorption and diarrhea.
Tongue Involvement: Can hamper speech and swallowing due to inelasticity.
Vascular Amyloidosis: Causes fragility and may lead to bleeding.
Diagnostic Procedures
Common Biopsies: Kidney, rectal, or gingival tissues when systemic amyloidosis is suspected.
Testing: Serum and urine protein electrophoresis and immunoelectrophoresis for cases of AL amyloidosis.
Prognosis
Generalized Amyloidosis: Generally poor outlook.
Reactive Systemic Amyloidosis: Better prognosis depending on control of underlying conditions; rare occurrence of amyloid resorption after treatment.
Affect on Tissues: Amyloid deposits cause tissue injury and dysfunction by exerting pressure on cells without causing an inflammatory response.
References
Robbins, Cotran & Kumar Pathologic Basis of Disease, 11th Edition.
Anderson’s Pathology, 10th Edition.
Boyd’s Pathology, 10th Edition.