hypercaicemic AIL patients.
1. Introduction
Adult T-cell leukemia (ATL) was first
reported as a new clinical entity in 1977 in
Japan [1, 2]. The predominant physical
findings are skin involvement, such as
erythroderma and nodule formation due to
the infiltration of neoplastic cells,
lymphadenopathy, and
hepatosplenomegaly. The ATL cells are of
mature T-helper phenotype and have a
characteristic appearance with especially
indented or lobulated nuclei.
Hypercalcemia is common in patients with
ATL, and such patients often show
increased numbers of osteoclasts.
A type C retrovirus was isolated from
patients with cutaneous T-cell lymphoma
by Poiesz and colleasues in 1980 [3]. ThisHuman T-cell leukemia virus type-1
(HTLYV-1) is the causative agent of adult
T-cell leukemia (ATL). Hypercalcemia is
common in patients with ATL. These
patients rarely develop metastatic
calcification and acute pancreatitis. The
underlying pathogenesis of this condition
is osteoclast hyperactivity with associated
overproduction of parathyroid hormone-
related protein, which results in
hypercalcemia in association with bone
demineralization. The discovery of the
osteoclast differentiation factor receptor
activator of nuclear factor-«B ligand
(RANKL), its receptor RANK, and its
decoy receptor osteoprotegerin (OPG),
enhanced our understanding of the
mechanisms of ATL-associated
hypercalcemia. Macrophage inflammatory
protein-1-a, tumor necrosis factor-a,
interleukin-1, and interleukin-6 are
important molecules that enhance the
migration and differentiation of osteoclasts
and the associated enhanced production ofMaybe | missed that pathology lecture,
or maybe | was sleeping when the
terms were discussed.A For whatever
reason, | have always had a hard time
with dystrophic and metastatic
calcification.A | could remember that
one type of calcification was simply the
result of having a high calcium level, but
| couldn't really define the terms and
keep straight which one was which. If
you have had that problem, maybe this
will help clear it up once and for all.
Dystrophic calcification
This type of calcification is seen in areas
of necrosis. Some examples of lesions
with dystrophic calcification include:
atherosclerotic plaques, aging or
damaged heart valves, and tuberculous
lymph nodes.2. Metastatic Calcification Go to: >
The mechanism of calcification in the
viscera is categorized into two groups.
Metastatic calcification with hypercalcemia
occurs when calcium deposits in previously
normal tissue whereas dystrophic
calcification occurs in previously damaged
tissue. (1) Dystrophic calcification in
injured or necrotic tissue in a normal
serum calcium level, such as tuberculosis,
abscess, and hydatid disease. (2) Metastatic
calcification can be divided into malignant
and nonmalignant causes. Metastatic
calcification in malignancy is reported in
parathyroid carcinoma, multiple myeloma,
lymphoma, leukemia, hypopharyngeal
squamous cell carcinoma, synovial
sarcoma, breast carcinoma, and3. Acute Pancreatitis with Go to: »
Hypercalcemia
ATL associated with hypercalcemia and
acute pancreatitis was first described in
1984 by Hosokawa et al. [43], followed
later by other reports in 1990s [21, 44, 45].
Hypercalcemia is difficult to treat and can
be the cause of death in ATL [46, 47]. The
relation between hypercalcemia and acute
pancreatitis in patients with ATL was
suggested based on the observation of
pancreatitis in hypercalcemic renal
transplant recipients [48]. However, the
exact reason linking hypercalcemia and
acute pancreatitis in patients with ATL
remains to be elucidated. A plausible
theory [49] is the following sequence: high
serum calcium levels increase calcium
levels in pancreatic juice, which result in
accelerated calcium-dependent conversion
of trypsinogen to trypsin, leading to acute
pancreatitis. Another possibility involves
the high levels of nephrogenous cyclic
adenosine monophosphate [47], whichee
Dystrophic vs Metastatic Calcification
Dystrophic calcification is f
the deposition of calcium
salts in dead or
degenerated tissues
Serum calcium level
is normal
| Generally irreversible
Localized
Necrosis, infarct,
thrombi, dead parasites,
certain tumor or cyst
Increased binding of
| phosphates with necrotic
tissues which in turn
bind to calcium and thus
| forming calcium
phosphate precipitates
i
Generally better
d prognosis due to little
septicaemia
Metastatic calcification
is the deposition of
calcium salts in normal
Cui
Serum calcium level is
elevated
Reversible upon
correction of metabolic
disorder
Occurs in many tissues
throughout the body
Hyperparathyroidism.
resorption of bone tissue,
disorders of vitamin D,
renal failure, prolonged
immobilization.
aluminium intoxication
and milk alkali syndrome
Increased precipitation
of calcium phosphate
due to hypercalcemia at
otTae Take (ola)
lungs, stomach, blood
Nioitt 1 ial ket
Generally poor
prognosis due to
profound toxaemia