The company has begun negotiating settlements with individual plaintiff’s firms, David S. Ratner, a lawyer with Morelli Ratner, said in a phone interview. “It’s been going on for a few weeks,” he said.

Mr. Ratner, a member of a steering committee of lawyers for the drugs’ users, said he did not know which specific firms were involved in the settlements.

More than 3,000 patients have claimed that the drugs caused heart attacks and strokes. Celebrex, in the same class of medicines as Merck’s recalled Vioxx, is Pfizer’s third-best-selling drug. The product, which is still on the market, generated $2.3 billion in sales in 2007, a 12 percent increase from the previous year.

The Wall Street Journal reported on Friday that Pfizer had reached settlements with three law firms representing more than 200 of the thousands who sued over the drugs. Firms have been offered $40,000 to $50,000 a client to resolve Bextra cases and as much as $200,000 a client for Celebrex, The Journal reported, citing an unidentified lawyer.

Pfizer withdrew Bextra in April 2005 after it was tied to a potentially fatal skin condition.

The first Bextra trial, due to begin May 5 in federal court in San Francisco, was postponed until May 29, according to court records.

Ray Kerins, a Pfizer spokesman, declined to comment on pending litigation.

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Genetic studies suggest that a defective, leaky skin barrier is the initial cause in up to half of eczema cases seen by doctors.

Topical drugs that reduce inflammation are still the mainstay of treating rashes, but new genetic findings highlight the importance of keeping the skin barrier intact by frequent use of moisturizers.

For millions of people who suffer from chronic eczema, life can become a hellish existence in which patches of dry skin become red and inflamed and constantly cry out: scratch me!

“It’s like having poison oak or poison ivy 24 hours a day, seven days a week, forever,” said Vicki Kalabokes, chief executive of the nonprofit National Eczema Association in San Rafael, Calif.

The best treatments, like prescription creams and ointments that tamp down inflammation, can provide some relief. Antihistamines may aid nighttime sleep, and a good skin-care routine of slathering on moisturizers and avoiding irritating soaps also helps. But for many patients who still scratch through the night and hide crusted, oozing infections under long sleeves and pants, the medical world has little more to offer.

That could change, thanks to recent research that has led to new thinking about why chronic eczema happens. In a sort of chicken-versus-egg turnabout, researchers have challenged the prevailing dogma that chronic eczema is mainly an allergic disease that leads to skin dryness and rashes. Instead, a growing number of experts believe that a structural defect of the skin is the primary culprit, instigating the immunologic problems seen in patients.

For decades, allergists embraced the idea that eczema arose from an immune overreaction inside the body, leading to inflammation and cracked, itchy skin. Skin cracking, in turn, let in more allergens, irritants and microbes that further fueled the cycle. The theory was supported by the observation that eczema sufferers show high blood levels of an immune defense protein called IgE and often develop immune-related ailments like asthma, food allergies and hay fever.

Many dermatologists, on the other hand, have argued that allergies do not cause chronic eczema. Over the last decade, some proposed that an intrinsic defect of the skin occurs first and then causes immunological weirdnesses. In other words, trouble develops from the outside in.

The major breakthrough came in 2006, when Irwin McLean, a geneticist at the University of Dundee in Scotland, and Dr. Alan Irvine, a pediatric dermatologist at Our Lady’s Hospital for Sick Children in Dublin, Ireland, reported that chronic eczema was rampant among families carrying a defective gene for filaggrin, a skin protein that serves as a natural moisturizer. Without it, the usually impervious barrier formed by the skin is compromised by cracking.

“Our work has really said, ‘Look, it’s not all just about the immune system,’ ” Dr. Irvine said.

The flawed gene fails to produce filaggrin, which normally pulls together protein filaments and flattens out dead cells to form the skin’s outermost layer. The molecule also holds water in, moisturizing the barrier.

About one-third to half of all children and adults with moderate to severe chronic eczema have a nonfunctioning filaggrin gene, Dr. Irvine said. Researchers have identified nearly 40 filaggrin mutations, including variations specific to Asian populations. And evidence suggests that the risk of childhood asthma is nearly doubled in those who inherit one of these mutations, but only after eczema arises first.

With a dry, filaggrin-deficient barrier, almost anything on the patient’s skin — dust mites, pollen, food proteins or bacteria — can easily get through, said Dr. Jon M. Hanifin, a dermatologist at Oregon Health & Science University in Portland who was not involved in the genetic work. The new thinking is that the foreign intrusions activate immune cells to respond and crank out IgE, causing the inflamed skin lesions. That process may also prime the immune system to overreact to specific allergens, leading eventually to asthma, hay fever and food allergies.

The genetic findings could help explain why chronic eczema has grown increasingly common in industrialized countries in the past two decades, Dr. Irvine said. Environmental factors like increases in pollutants or use of soaps, air conditioning and central heating may dry out or irritate a defective skin barrier.

But debate rages on over how much of eczema may still originate from allergic disease. It is unclear whether a leaky skin barrier is always the initial culprit. Many people who do not have a filaggrin mutation still get eczema, and eczema does not occur in everyone who carries the genetic defect, noted Dr. Donald Leung, an immunologist at the National Jewish Medical and Research Center in Denver.

While a genetic skin barrier defect is important, he said, the immune and environmental factors also play key contributing roles in this complex disease. Dr. Leung’s own research has revealed that inflammation itself can reduce filaggrin levels in the skin.

On the other hand, mutations in additional skin barrier genes may yet be discovered.

It may be possible to create eczema drugs enhancing filaggrin production. For now, the genetic studies magnify the need to protect the dry, damaged skin barrier — and keep out irritants and allergens — by hydrating it and keeping it intact. That means that along with using anti-inflammatory medications, it is crucial for eczema patients to follow the basic advice on moisturizing to prevent flare-ups, Dr. Hanifin said.

For infants, the research even raises the possibility of prevention.

“It points up to us that maybe we can reduce the impact of asthma and allergic rhinitis by treating the skin in kids with eczema early,” he said, “by moisturizing right from day one.”

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