EXHIBIT 99.1



COMPANY CONTACT:                             MEDIA CONTACTS:
---------------                              --------------

Andrew Wiseman, Ph.D.                        Virginia Amann or Trista Morrison
Sr. Director of Business Development         Atkins + Associates
La Jolla Pharmaceutical Company              for La Jolla Pharmaceutical Company
858-646-6615                                 858-527-3490
andrew.wiseman@ljpc.com                      tmorrison@irpr.com


     RESULTS FROM TWO RIQUENT(TM) TRIALS SHOW LUPUS PATIENTS WITH SUSTAINED
           REDUCTIONS IN ANTIBODIES TO dsDNA HAVE FEWER RENAL FLARES

SAN DIEGO, MARCH 31, 2003 -- La Jolla Pharmaceutical Company (Nasdaq: LJPC)
announced today that additional analyses of data from its Phase 3 and Phase 2/3
studies of Riquent(TM) for the treatment of lupus renal disease demonstrate
statistically significant correlations between reductions in antibodies to
double-stranded DNA (dsDNA) and a reduced risk of renal flare in lupus patients
(Phase 3: p < 0.0001, Phase 2/3: p = 0.0004). Furthermore, the Phase 3 trial
results demonstrated that Riquent lowers levels of antibodies to dsDNA in a
statistically significant manner (p < 0.0001), although the trial did not reach
statistical significance for its primary endpoint, time to renal flare. These
results were presented by Matthew Linnik, Ph.D., Chief Scientific Officer and
Executive Vice President of Research of La Jolla Pharmaceutical Company at the
Biomarkers for the Assessment of Systemic Lupus Erythematosus Conference in
Bethesda, MD.

In the Phase 3 study, renal flares occurred approximately one fifth as often in
patients with sustained reductions in antibodies to dsDNA compared with patients
with unchanged or increasing antibodies. Patients with sustained reductions were
defined as those who had 10% or more reduction in antibodies to dsDNA for
two-thirds or more of all observed values. Renal flares are episodes of
inflammation that can cause kidney damage and failure.

PHASE 3 STUDY RESULTS: In patients with sustained reductions, renal flares
occurred in only 4% or 5 of 121 patients compared with patients who did not
experience sustained reductions, where renal flares in occurred in 20% or 36 of
177 patients (p < 0.0001). Twice as many Riquent-treated patients had sustained
reductions (80 of 145 or 55%) compared with placebo-treated patients (41 of 153
or 27%).

PHASE 2/3 STUDY RESULTS: In patients with sustained reductions, renal flares
occurred in only 3% or 2 of 67 patients compared with patients who did not
experience sustained reductions, where renal flares occurred in 21% or 26 of 122
patients (p = 0.0004). Four times as many Riquent-treated patients had sustained
reductions (54 of 92 or 59%) compared with placebo-treated patients (13 of 97 or
13%).

The results of both studies also confirm the correlation between increasing
levels of antibodies to dsDNA and the occurrence of renal flares in lupus
patients (Phase 3: p<0.0001 and Phase 2/3: p<0.0007).

"Few diseases are as frustratingly enigmatic as lupus, but today, one more piece
of this medical puzzle appears to have fallen into place. These results indicate
that antibodies to dsDNA are correlated with renal disease in lupus and that
lupus patients with reduced levels of antibodies to dsDNA have a lower risk of
renal flare," said Steve Engle, Chairman and CEO of La Jolla Pharmaceutical
Company.

"Although one of the strongest indicators of lupus is the presence of antibodies
to dsDNA and many have suspected that these antibodies are a key cause of renal
disease in lupus patients, the proof has been elusive," added Engle. "These
encouraging findings, in two of the largest and longest controlled trials
conducted in lupus, appear to demonstrate the pathogenic nature of antibodies to
dsDNA. For lupus patients, this may be a critical step forward in understanding
the cause of their disease."

ANTIBODIES TO dsDNA AND COMPLEMENT C3: Additional data from the two trials also
demonstrate an inverse relationship between levels of antibodies to dsDNA and
levels of complement C3 (p < 0.001). Complement C3 is a protein that contributes
to inflammation and often decreases during a renal flare and increases following
treatment for flare. Following treatment with Riquent, antibodies to dsDNA
decreased and C3 levels increased, which is consistent with a positive
biological effect.

In the Phase 3 study, 298 patients were enrolled and treated for up to 22
months. In the Phase 2/3 study, 189 patients were enrolled and treated for up to
18 months. In both studies, a validated Farr assay was utilized to measure
antibodies to dsDNA. The assays were run at a central laboratory to ensure
consistency and blood samples were collected on a weekly to monthly basis.

BIOMARKERS FOR THE ASSESSMENT OF SYSTEMIC LUPUS ERYTHEMATOSUS: Approximately 100
lupus clinicians, researchers and patients are meeting to discuss the potential
use of lupus biomarkers such as antibodies to dsDNA to assess disease activity
and as indicators of response to therapy. The conference is co-sponsored by the
Lupus Foundation of America, the Alliance for Lupus Research, The Lupus Research
Institute, and Rheuminations, Inc. Invited speakers include experts from
academia, the National Institutes of Health, the healthcare industry and the
Food and Drug Administration.

BACKGROUND INFORMATION

EPIDEMIOLOGY OF LUPUS AND ANTIBODIES TO dsDNA: About 90% of individuals
diagnosed with lupus are women, and 80% of those afflicted develop the disease
between the ages of 15 and 45. Approximately 50% of lupus patients will develop
renal disease, which is a leading cause of death in lupus patients. The presence
of antibodies to dsDNA is an important criterion for the diagnosis of lupus and
antibodies to dsDNA are rarely found in normal subjects. Up to 80% to 90% of
lupus patients test positive for the presence of antibodies to dsDNA. The use of
concomitant immunosuppressive agents to treat the symptoms of lupus may
significantly reduce the production of antibodies to dsDNA, making their
detection more difficult.

PATHOLOGY OF ANTIBODIES TO dsDNA: First observed in 1967, large amounts of
antibodies to dsDNA can be extracted from kidneys of lupus patients and these
antibodies often have a much higher affinity for dsDNA than antibodies in the
circulation. Antibodies to dsDNA are thought to be highly pathogenic and are
specific to lupus. Antibodies to dsDNA have been shown to bind directly to
kidney membrane structures. Some antibodies to dsDNA bind directly to DNA-like
components of the kidney membrane, which may lead to increased organ damage.
These antibodies form immune complexes that lodge in the kidney where they can
cause tissue damage.


RENAL DISEASE AND ANTIBODIES TO dsDNA: In lupus patients, high levels of
antibodies to dsDNA usually correlate with active renal disease. While these
antibodies are present in the majority of patients with lupus, rises in
antibodies to dsDNA are believed to predict a worsening of disease. Some
published clinical studies in lupus have shown similar results to what was
presented today and others have not. Some studies did not use a central
laboratory to control variability, sampled too infrequently, did not use the
Farr assay or did not use a validated assay.

CURRENT THERAPIES TO CONTROL LUPUS DISEASE: Immunosuppressive drugs used today
to control lupus can suppress the entire immune system, including the production
of antibodies to dsDNA. Immunosuppressive agents can be associated with poor
tolerability, significant toxicity and organ damage and limit their usage.
Infections due to immunosuppression are a leading cause of death in lupus.

La Jolla Pharmaceutical Company is a biotechnology company developing
therapeutics for antibody-mediated autoimmune diseases afflicting several
million people in the United States and Europe. The Company is developing
Riquent(TM), formerly known as LJP 394, for the treatment of lupus kidney
disease, a leading cause of sickness and death in patients with lupus. The
Company is also developing LJP 1082 for the treatment of antibody-mediated
thrombosis, a condition in which patients suffer from recurrent stroke,
deep-vein thrombosis and other thrombotic events. The Company's common stock is
traded on The Nasdaq Stock Market under the symbol LJPC. For more information
about the Company, visit its Web site: http://www.ljpc.com.

Except for historical statements, this press release contains forward-looking
statements involving significant risks and uncertainties, and a number of
factors, both foreseen and unforeseen, could cause actual results to differ
materially from our current expectations. Forward-looking statements include
those which express a plan, belief, expectation, estimation, anticipation,
intent, contingency, future development or similar expression. Although we
expect to meet with the regulatory authorities to discuss the results of our
Phase 3 trial of Riquent(TM), there is no guarantee that a meeting with the
regulatory authorities can be held in a timely manner, or at all, or that our
meetings with them will result in us being able to continue to develop Riquent.
Our analyses of clinical results of Riquent, previously known as LJP 394, our
drug candidate for the treatment of systemic lupus erythematosus ("lupus"), and
LJP 1082, our drug candidate for the treatment of antibody-mediated thrombosis
("thrombosis"), are ongoing and could result in a finding that these drug
candidates are not effective in large patient populations, do not provide a
meaningful clinical benefit, or may reveal a potential safety issue requiring us
to develop new candidates. The clinical results from our recently completed
Phase 3 clinical trial of Riquent are unlikely to be sufficient to obtain
regulatory clearance to market Riquent either in the U.S. or Europe. We likely
will be required to conduct additional clinical studies to demonstrate the
safety and efficacy of Riquent before we can seek to obtain marketing approval.
. There is no guarantee, however, that we will have the necessary resources to
complete any additional trial, that we will elect to conduct an additional
trial, or that any additional trial will sufficiently demonstrate the safety and
efficacy of Riquent. Our blood test to measure the binding affinity for Riquent
is experimental, has not been validated by independent laboratories, may require
regulatory approval, and may be necessary for the approval and the
commercialization of Riquent. Our other potential drug candidates are at earlier
stages of development and involve comparable risks. Analysis of our clinical
trials could have negative or inconclusive results. Any positive results
observed to date may not be indicative of future results. In any event,
regulatory authorities may require additional clinical trials, or may not
approve our drugs. Our ability to develop and sell our products in the future
may be affected by the intellectual property rights of third parties. Additional
risk factors include the uncertainty and timing of: obtaining required

regulatory approvals, including delays associated with any approvals that we may
obtain; the clear need for additional financing; FDA approval of our
manufacturing facilities and processes; the increase in capacity of our
manufacturing capabilities for possible commercialization; successfully
marketing and selling our products; our lack of manufacturing, marketing, and
sales experience; generating future revenue from product sales or other sources
such as collaborative relationships; future profitability; and our dependence on
patents and other proprietary rights. Readers are cautioned to not place undue
reliance upon forward-looking statements, which speak only as of the date
hereof, and we undertake no obligation to update forward-looking statements to
reflect events or circumstances occurring after the date hereof. Interested
parties are urged to review the risks described in our Annual Report on Form
10-K for the year ended December 31, 2002, and in other reports and registration
statements that we file with the Securities and Exchange Commission from time to
time.

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