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Blood, Vol. 93 No. 3 (February 1), 1999:
pp. 1062-1066
Long-Term Survival (10 Years or More) in 30 Patients With Primary
Amyloidosis
By
Robert A. Kyle,
Morie A. Gertz,
Philip R. Greipp,
Thomas E. Witzig,
John A. Lust,
Martha Q. Lacy, and
Terry M. Therneau
From the Division of Hematology and Internal Medicine and the Section
of Biostatistics, Mayo Clinic and Mayo Foundation, Rochester, MN.
 |
ABSTRACT |
The median survival in primary systemic (AL) amyloidosis is less
than 18 months. No published series of patients with AL amyloidosis have reported survival of more than 10 years. The records of all Mayo
Clinic patients with a diagnosis of AL amyloidosis between January 1, 1966 and March 1, 1987 were reviewed. Patients with secondary
amyloidosis, familial amyloidosis, senile systemic amyloidosis, and
localized amyloidosis were excluded. During the 21 years of the study,
841 patients with AL amyloidosis were seen. Of these, 29 were excluded
because the diagnosis was made at autopsy, and 2 others were excluded
because no follow-up data were available. Actuarial survival for the
810 patients was 51% at 1 year, 16% at 5 years, and 4.7% at 10 years. Thirty patients survived for 10 years or more after the
histologic diagnosis of AL amyloidosis; all received alkylating-agent
therapy. In 14 patients, the monoclonal protein disappeared from the
serum or urine. Of 10 patients with nephrotic syndrome, 4 had an
objective response. Congestive heart failure, older age, creatinine
value of 2 mg/dL or more, bone marrow plasma cell value of 20% or
more, platelet count of 500 × 109/L or less, and the
presence of peripheral neuropathy were underrepresented in the 10-year
survivors and are unfavorable prognostic features. Five percent
of patients with AL amyloidosis survived for 10 years or more.
© 1999 by The American Society of Hematology.
| |
INTRODUCTION |
THE MEDIAN SURVIVAL in 474 patients with
primary systemic (AL) amyloidosis was 13 months.1 Despite
the use of melphalan and prednisone, the median survival is still only
17 to 18 months.2 No published series of patients with AL
amyloidosis have reported survival of more than 10 years, and there
have been only infrequent case reports of patients surviving more than
a decade.3,4 This review was undertaken to report our
experience with patients with AL amyloidosis who have survived for 10 or more years and to identify any clinical or laboratory features that
predicted long-term survival.
| |
MATERIALS AND METHODS |
The records of all Mayo Clinic patients with a diagnosis of AL
amyloidosis who were seen between January 1, 1966 and March 1, 1987 were reviewed. Patients with secondary amyloidosis, familial amyloidosis, senile systemic amyloidosis, and localized amyloidosis were excluded.
Amyloidosis was confirmed histologically in all patients. Sections
stained with Congo red showed green birefringence when reviewed under
polarized light.5
The diagnosis of multiple myeloma was made on the basis of a bone
marrow containing more than 10% plasma cells, a monoclonal protein in
the serum, a monoclonal protein in the urine, or lytic bone lesions.
The clinical features of multiple myeloma were also present.
Serum protein electrophoresis was done on agarose gel with Ponceau S
staining. Immunoelectrophoresis or immunofixation was performed with
monospecific antisera to IgG, IgA, IgM, and  and  light chains.
All serum samples were screened by Ouchterlony immunodiffusion for
excess of IgD and IgE. Immunoglobulin levels were measured with
nephelometry. Electrophoresis and immunoelectrophoresis or
immunofixation were performed on urine concentrated by
ulrafiltration.6
Statistical analysis.
Many of the patients in the study were first referred to Mayo Clinic
some months after their initial diagnosis. A naive computation of the
survival curve for time from diagnosis will be biased upward in this
case. The method of Turnbull7 was used to compute the survival curve, corrected for the delayed entry.
Predictions of long-term survival were assessed with logistic
regression. Because a patient's characteristics measured at a delayed
entry date might differ from the patient's (unknown) values at
diagnosis, these comparisons used only subjects who were referred to
Mayo Clinic within 6 months of the initial diagnosis of AL amyloidosis.
All analyses were done with the SAS and S-Plus statistical
packages. All tests were two-tailed.
| |
RESULTS |
During the 21 years of the study, 841 patients with AL amyloidosis were
seen at Mayo Clinic. Of these, 29 were excluded because the diagnosis
was made at autopsy, and 2 others were excluded because no follow-up
data were available. Of the remaining 810 patients, 685 were seen at
Mayo Clinic within 6 months of the initial diagnosis of AL amyloidosis,
93 between 6 months and 2 years, and 32 more than 2 years after initial
diagnosis. Sixty-seven patients seen within 6 months are still alive
and under observation (Table 1). Overall
survival for the 810 patients was 51% at 1 year, 16% at 5 years, and
4.7% at 10 years (Fig 1).
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| Fig 1.
Survival for 810 patients with systemic amyloidosis seen
at Mayo Clinic between January 1, 1966 and March 1, 1987.
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Long-term survivors.
Thirty patients survived for 10 years or more after the histologic
diagnosis of AL amyloidosis; 19 of these were first seen at Mayo Clinic
within 6 months of diagnosis (Table 1). Comparison of these two groups
showed little difference between them
(Table 2). All but 1 of the 30 patients had
a monoclonal protein in the serum or urine, monoclonal plasma cells in
the bone marrow, or immunohistochemical proof of monoclonal light-chain
staining of the amyloid tissue. In the one exception, the diagnosis was made in 1970, immunoelectrophoresis and bone marrow biopsy were not
done, and the positive rectal biopsy specimen contained no additional
tissue for immunohistochemical studies. The ages of the survivors
ranged from 27 to 68 years (median, 54 years) at diagnosis of AL.
Fifty-three percent were male. Weight loss was present in 31%; 3 patients reported a loss of 40 pounds or more. The liver was palpable
in 31%. Only 3 patients had a liver palpable more than 5 cm below the
right costal margin. The spleen was not palpable in any survivor, and
lymphadenopathy was noted in only 2 patients. Macroglossia was present
in 20%. At the first Mayo Clinic visit, the median hemoglobin value
was 13.5 g/dL, and only 2 patients had a value less than 10 g/dL. The
median platelet value was 286 × 109/L; 24% of
patients had a platelet value more than 500 × 109/L.
Fourteen percent had an initial serum creatinine value of 2.0 mg/dL or
more. The median serum alkaline phosphatase value was 162 U/L (normal, < 309 U/L); 2 patients had a value twice normal. The serum albumin
value was less than 3.0 g/dL in 37%. Only 1 patient had a vitamin
B12 value less than 150 ng/L, and none had a serum carotene
value less than 50 µg/dL.
A monoclonal protein was found in the serum in 18 (64%) of 28 patients
tested; the monoclonal protein consisted of IgG in 7 patients, IgA in
3, IgM in 1, IgD in 1, in only 1, and in only 5. light
chains were found in 15 (83%) of 18 patients. Fifteen of the 28 patients who had serum protein electrophoresis had a  spike (range,
0.4 to 2.7 g/dL; median, 0.8 g/dL). Only 2 patients had a monoclonal
protein spike more than 2.0 g/dL. The urine contained a monoclonal
light chain in 16 (62%) of 26 patients tested; in 13 it was . The
size of the urine monoclonal spike ranged from 0.01 to 0.9 g/24 h in
the 16 patients. The 24-hour urine protein content ranged from 0.1 to
11.8 g/24 h (median, 0.5 g/24 h) in the 28 patients in whom it was
measured; 11 had a protein loss of more than 3.0 g/24 h.
A monoclonal protein was detected in the serum or urine in 24 (86%) of
the 28 patients in whom immunoelectrophoresis or immunofixation was
performed. Of the 6 patients without a monoclonal protein in the serum
or urine at diagnosis, a bone marrow biopsy specimen contained a
monoclonal population of plasma cells in 2, immunohistochemical stains
of the amyloid tissue were positive for a monoclonal light chain in 1, a monoclonal protein developed in the serum and urine in 2 patients
during the course of their illness, and no studies were done in 1 patient.
The interventricular septal thickness was 15 mm or more in 8 (36%) of
the 22 patients in whom it was measured. The ejection fraction was less
than 50% in 2 patients (44% and 45%).
Overt congestive heart failure was present in 2 patients at the time of
diagnosis. The first patient was a 62-year-old white man who had had
progressive dyspnea and paroxysmal nocturnal dyspnea for 1 year. He
also had periorbital purpura during this time and had lost 10 pounds.
The liver was palpable 3 cm below the right costal margin, and the
Tinel sign was positive. He had a small monoclonal light chain in
the serum and urine (300 mg/24 h). The bone marrow contained 20%
plasma cells. A rectal biopsy was positive for amyloid. He was treated
with melphalan and prednisone, and the light chain disappeared 13 months later. An endomyocardial biopsy was performed 6 years later
because the patient was doing so well. All four specimens showed
moderate amyloid deposition that was pericellular and nodular. Acute
leukemia subsequently developed, and the patient died 12.5 years after
diagnosis. Results of cytogenetic studies were normal on two occasions
before the diagnosis of acute leukemia. In the second patient, a
64-year-old white man, exertional dyspnea and paroxysmal nocturnal
dyspnea developed from congestive heart failure. Biopsies of the
tongue, rectum, and pleura were positive for amyloid. The
interventricular septal thickness was 13 mm. The urine contained a
small monoclonal light chain. He was treated with melphalan and
prednisone, and the light chains disappeared 7 months later. This
therapy was discontinued at 20 months (total melphalan dosage, 766 mg).
He subsequently required a pacemaker but is alive with compensated congestive heart failure 13 years after diagnosis.
Nephrotic syndrome was present in 10 patients (33%) when first
evaluated and developed in 1 other patient during the course of the
disease. Six patients had carpal tunnel syndrome at diagnosis, and only
2 had a sensorimotor peripheral neuropathy. Orthostatic hypotension was
present in 4 patients before diagnosis.
Bone marrow biopsy was positive for amyloid in 18 (64%) of the 28 patients in whom a bone marrow was done. Four of five liver biopsies
were positive for amyloid, and all four endomyocardial biopsies were
positive for amyloid. Subcutaneous fat aspiration was performed in only
3 patients, and all had positive results. All seven renal biopsies were
positive. Eleven (65%) of 17 rectal biopsies were positive for amyloid.
Chemotherapy.
All 30 patients received alkylating-agent therapy. One patient with an
IgM monoclonal protein received chlorambucil, and another patient was
given cyclophosphamide. The remaining 28 patients received melphalan
and prednisone. The duration of treatment ranged from 5 to 84 months
(median, 34.5 months). The total dose of melphalan ranged from 212 to
4,760 mg (median, 1,708 mg).
The monoclonal light chain disappeared from the urine in 13 patients
and from the serum in 5 patients. The monoclonal protein disappeared
from the serum or urine in a total of 14 patients. Of the 10 patients
with nephrotic syndrome, 4 had a reduction of more than 50% in
proteinuria and a normal serum creatinine value (1.1 mg/dL or less).
The serum albumin value increased 1.0 g/dL or more in 2 of the 3 patients who had an initial serum albumin value less than 3.0 g/dL.
The liver in the patient with marked hepatomegaly (14 cm below the
costal margin) became nonpalpable with therapy. The alkaline phosphatase value decreased from 379 to 113 U/L. One patient had a
ruptured spleen at diagnosis. Two of the 30 patients had an associated
multiple myeloma that required chemotherapy. In 1 patient, autopsy
results showed that the amyloidosis had disappeared. This patient had
presented with a nephrotic syndrome (24-hour urine protein value of 6.6 g/24 h and a serum albumin level of 1.2 g/dL), an IgG monoclonal
protein in the serum, and renal and bone marrow biopsies positive for
amyloid. At autopsy, there was no evidence of amyloid in any organ.
An acute nonlymphocytic leukemia developed in 3 patients, and 2 others
had a myelodysplastic syndrome. Cytogenetic studies revealed a monosomy
7 in 3 of the 4 patients in whom studies were done.
Of 18 deaths, the causes were cardiac in 9, infection in 3, renal
insufficiency in 2 (both patients voluntarily stopped dialysis), and 1 each from gastrointestinal bleeding, multiple myeloma and renal
failure, ventricular fibrillation (no evidence of amyloid at autopsy),
and an unrelated ruptured subclavian artery. Myelodysplasia or leukemia
contributed to death in 3 patients. Twelve patients are still alive and
under observation at 10 to 15.5 years. One patient had renal
transplantation and was doing well 7 years later (serum creatinine
value was 1.3 mg/dL and 24-hour urine protein value was 83 mg).
Comparison of long-term survivors with nonsurvivors.
Of the 685 patients seen at Mayo Clinic within 6 months of diagnosis,
599 died before 10 years; these patients were compared with the overall
group of 30 patients who survived 10 years or more after diagnosis and
with the 19 who were seen within 6 months of diagnosis and survived 10 years or more (Table 1). By logistic regression, the most significant
predictors of long-term survival were young age
(Fig 2) and initial platelet count.
Comparison of the 19 patients seen within 6 months of diagnosis who
survived 10 years or more and the overall group of 30 patients who
survived 10 years or more revealed no significant differences.
Congestive heart failure, older age, creatinine value of 2 mg/dL or
more, bone marrow plasma cell value of 20% or more, platelet value of 500 × 109/L or less, and the presence of peripheral
neuropathy were underrepresented in the 10-year survivors and are
unfavorable prognostic features.
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| Fig 2.
Status of 685 patients with primary systemic amyloidosis
seen at Mayo Clinic within 6 months of diagnosis, by age.
|
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Response to therapy.
The 19 long-term survivors were compared with 148 patients who received
melphalan and prednisone in a prospective study2 (Table 3). An objective protein response
was noted in 10 (53%) of the 19 patients who survived 10 years or more
and in 42 (28%) of the 148 patients in the prospective study
(P = .51). Although the percentages appear to differ, the
comparison must be adjusted for lead-time bias. The median time of
response was 258 days (8.5 months). Responders to chemotherapy at 8.5 months were not more likely to survive 10+ years than nonresponders
still alive at that time. In fact, responders are more likely to
survive 10+ years only by virtue of still being in the living cohort at
8.5 months. Thus, any patient still alive at 8.5 months is as likely to
survive 10+ years as a responder.
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|
Table 3.
Response to Therapy in Patients With Amyloidosis: A
Prospective Study and Survivors for 10 Years or More
|
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| |
DISCUSSION |
Long-term survival among patients with AL amyloidosis is uncommon. Only
two case reports of long-term survival have been published. The first
was a 72-year-old woman with an 18-year history of periorbital purpura.
Similar lesions appeared on the chest 10 years before the diagnosis of
AL amyloidosis. She had an IgG monoclonal protein in the serum and
a bone marrow containing 8% plasma cells. A skin biopsy was positive
for amyloid, and a rectal biopsy was negative. She had no evidence of
heart, kidney, skeletal, or neurologic system involvement.4
The second patient was a 43-year-old woman who presented in October
1981 with a 1-month history of paresthesias of her extremities. Results
of neurologic examination were consistent with a polyneuropathy. She
had an IgA monoclonal protein (1,300 mg/dL) and a bone marrow
containing more than 10% plasma cells. Biopsy of the sural nerve
revealed amyloid. She was treated with melphalan and prednisone for
several years. The IgA level subsequently increased to 2,900 mg/dL, and
the bone marrow was consistent with multiple myeloma. Another sural
nerve biopsy confirmed the presence of amyloid. She died of
cardiorespiratory failure 11 years after diagnosis.3
Of 841 patients with AL amyloidosis seen at Mayo Clinic from 1966 to
1987, 30 survived 10 years or more. In a comparison of the 19 patients
who survived 10 years or more and 599 who did not survive for 10 years
(both groups seen at Mayo Clinic within 6 months of diagnosis), we
found that younger patients and those with an initial platelet count of
500 × 109/L or more were more likely to survive 10 years. Congestive heart failure, older age, creatinine value of 2 mg/dL
or more, bone marrow plasma cell value of more than 20%, platelet
value of 500 × 109/L or less, and presence of
peripheral neuropathy were underrepresented in the 10-year survivors
and appear to be unfavorable prognostic features.
The finding of a better prognosis in younger patients with AL is
similar to our experience in multiple myeloma. In a series of 72 patients with multiple myeloma who were younger than 40 years, the
median survival was 54 months.8 However, it is difficult to
explain the possible benefit of thrombocytosis. In fact, one might
expect the opposite in that thrombocytosis would be associated with a
shorter survival because the increased platelet count may be due to
amyloid replacement of the spleen, resulting in hyposplenism producing
thrombocytosis. This finding is statistically significant but
clinically insignificant. The influence of multiple myeloma cannot be
ascertained because only 1 of the 30 patients had multiple myeloma at
the time of diagnosis of AL. In the second patient, multiple myeloma
developed 12 years after the diagnosis of AL and the patient died of
myeloma and renal insufficiency 3 years later.
This experience with 30 patients does not permit one to determine
whether high-dose therapy followed by stem-cell rescue is superior to
conventional chemotherapy with melphalan and prednisone. The selection
of patients for high-dose therapy is most critical. Unfortunately, the
decision to proceed with high-dose therapy must be made before the
patient has had an adequate trial of melphalan and prednisone because
alkylating therapy will damage the hematopoietic stem cells. One cannot
reliably identify patients who will respond to high-dose therapy.
Long-term survival in AL amyloidosis is rare. The factors affecting
long-term survival are generally unknown. The response rate to
conventional chemotherapy is low, and we hope that stem-cell transplantation9 or therapy with
4'-iodo-4'-deoxydoxorubicin10 will increase the
number of long-term survivors. Patients with AL amyloidosis should be
treated at institutions with ongoing amyloidosis trials in order to
make progress in this disease.
| |
FOOTNOTES |
Submitted April 16, 1998; accepted September 29, 1998.
Supported in part by Research Grant CA 62242 from the National
Institutes of Health.
The publication costs of this
article were defrayed in part by
page charge payment. This article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. section
1734 solely to indicate this fact.
Address reprint requests to Robert A. Kyle, MD, Mayo Clinic, 200 First
St SW, Rochester, MN 55905.
| |
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Top
Abstract
Introduction