Lymphocytic Interstitial Pneumonia

Introduction

Background

Lymphocytic interstitial pneumonia (LIP) is a syndrome of fever, cough, and dyspnea, with bibasilar pulmonary infiltrates consisting of dense interstitial accumulations of lymphocytes and plasma cells.

LIP may be associated with autoimmune and lymphoproliferative disorders, including rheumatoid arthritis, Hashimoto thyroiditis, myasthenia gravis, pernicious anemia, autoerythrocyte sensitization syndrome, chronic active hepatitis, common variable immunodeficiency, Sjögren syndrome, allogeneic bone marrow transplantation, lupus, and lymphoma. Pseudolymphoma represents a localized masslike variant of LIP.

LIP is also associated with infection via human immunodeficiency virus (HIV) type 1, Epstein-Barr virus, and human T-cell leukemia virus (HTLV) type 1.

Pathophysiology

Patients may have symptoms related to the above disorders.

HIV-related LIP may be part of a continuum of lymphocytic infiltrative disorders, such as pulmonary lymphoid hyperplasia in children and radiographically clear lymphocytic alveolitis in adults. Patients positive for HLA-DR5 and HLA-DR6 alleles are predisposed to developing a diffuse visceral lymphocytosis syndrome with LIP.

LIP has been reported to occur as part of immune reconstitution syndrome.

Frequency

United States

LIP is an uncommon disease. However, LIP is found in 22-75% of pediatric patients with HIV who have pulmonary disease. In contrast, among adult patients with HIV, LIP accounts for only 3% of HIV-related pulmonary pathology.

International

Small series have been reported in Europe, southwestern Japan, Africa, and the Caribbean basin.

Mortality/Morbidity

Mortality and morbidity data are inexact because of the lack of reported follow-up and the rarity of the disease.

• In the population who does not have HIV infection, half the patients improve with treatment but relapse is common. End-stage fibrosis may follow despite treatment. In the past, high mortality was reported in older patients.
• Patients with HIV-associated LIP display slower decline in CD4⁺ T-cell counts and longer survival than individuals who have HIV infection but do not have LIP.
• Patients with HIV infection but not LIP generally respond to treatment.

Race

• LIP has been found in every race and HIV risk group. Whether racial or geographic predispositions are crucial remains unclear.
• Many reports describe HIV and HTLV type 1–associated LIP among individuals of African ancestry.³
• LIP appears to cluster in southwestern Japan, where HTLV type 1 is endemic.

Sex

• LIP is more common in women when not associated with HIV infection.
• HIV-associated sicca syndrome occurs most often in males.⁴

Age

• Most cases not associated with HIV occur in the fourth and seventh decades of life, at an average age of 56 years.
• LIP is common only in children with HIV. In children with HIV infection, LIP has been designated an AIDS-defining illness by the US Centers for Disease Control and Prevention.

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Folic Acid Supplements May Fight Allergy Symptoms

With spring sneaking up on us, pollen is in the air and allergy sufferers everywhere are breathing a congested sigh of disdain. Even though outdoor barbeques, marathons, work-related outings, picnics, markets and festivals are planned throughout the summer, people who sneeze, cough, and generally feel miserable when the wind blows are not welcoming this change. Emerging research shows that B9—also known as folic acid—the component that keeps red blood cells healthy and has been shown to reduce birth defects associated with the spine may also help curb such miserable hot-weather symptoms. According to the Centers for Disease Control (CDC) about 25 million Americans are living with allergies due to their environment and asthma is the biggest portion of a chronic condition that children are afflicted by affecting 7 percent of all age groups throughout the United States.

The study was conducted at the Johns Hopkins Children’s Center, hoping to keep allergy symptoms (including asthma) at bay. By looking through the records of over 8,000 patients between the ages of 2 and 85, researchers tracked the folic acid levels against people with lung issues and allergy symptoms to find a pattern. Patients with higher blood levels of folic acid had less antibodies that trigger immunity response throughout the body.

The results were recently printed in The Journal of Allergy and Clinical Immunology and in a press release done by Johns Hopkins which lead researcher and pediatric allergist Dr. Elizabeth Matsui says that this is a breakthrough in allergy response, “Our findings are a clear indication that folic acid may indeed help regulate immune response to allergens, and may reduce allergy and asthma symptoms,” she adds that folic acid on its own won’t be a cure and more studies will eventually be done, “But we still need to figure out the exact mechanism behind it, and to do so, we need studies that follow people receiving treatment with folic acid before we even consider supplementation with folic acid to treat or prevent allergies and asthma.”

Even if popping B9 supplements may not help prevent this year’s allergy season, it is good to know that there is hope for the future. Usually found in leafy, green vegetables (also rich in vitamin K), nuts, beans, grains, and cereal products, healthy men and women are supposed to ingest 400 micrograms per day.

Believed to be the first study of its kind linking folic acid to allergy symptoms, these findings are new and exciting. More specifics of the findings include records like patients with lower folic acid levels in their blood (also known as folate levels) incur a 40 percent higher risk of wheezing than people with higher levels. Other risks involved with low folate levels are a 30 percent higher risk of developing allergies, 31 percent higher risk of allergy symptoms, and 16 percent higher risk of asthma.

Funded by the National Institutes of Health (NIH), the next step to the study is to use a controlled experiment using a placebo group alongside patients with both allergies and asthma.

Scientists decree that folic acid is not a cure-all and will not be ready for use as an allergy preventative for at least a few years. Although a lot of allergies are based on the type of landscape you live around, but if you are prone to allergen sensitivity, you will most likely find something to trigger the effects. Asthma is more tricky but because this is a rising condition among children, it merits research and this discovery seems to be shedding light that may eventually help. If folic acid is not already consciously part of your on your shopping list, it may be helpful to stock up on foods already rich in the nutrient…just in case.

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Everything Is Coming Up Rose Hips

Growing up I did not have any allergies, but a check-up with my pediatrician at age 12 confirmed an allergy when I told my doctor that cantaloupe melon makes the roof of my mouth itch uncontrollably. After I was told to stop eating cantaloupe (and the rest of the ripe, sweet melon family including avocado), I reluctantly went home with a food allergy. With a huge focus the past few years on the dangers of peanut allergies, from taking the tiny dangerous bags off of airplanes to banning peanuts and peanut butter-related items from school cafeterias across the globe, a food allergy awareness week is just the thing to kick start more campaigns to keep meals at their safest.

Starting today, Saturday May 10, to the following Saturday May 16th, Food Allergy Awareness Week takes place ensuring consumers safer ways to avoid the high or low profile foods that spark your family’s allergic needs. The Food Allergy and Anaphylaxis Network (FAAN) created the Food Allergy Awareness Week in May of 1997 in order to use the media coverage to educate.

This year’s theme is “Take Action, Prevent Reactions.” Schools, communities, and outreach organizations will be taking part in trying to spread the word about this growing hidden danger. You can download posters, fliers, statistics and other promotional and informational materials from the FAAN website to help with your local efforts.

FAAN’s goal for 2009 is to get proclamations from all 50 states that legislation will declare Food Allergy Awareness Week to promote it on a larger scale. With 4 percent of the population suffering from food allergies and around 50,000 emergency visits per year, this is becoming a widespread problem. So far communities across the country have been helping to get states on board and the FAAN has already convinced Connecticut, Georgia, Maine, Nebraska, Illinois, Nevada, Wisconsin, and Texas to sign on to proclamations. To make and send a proclamation, find a template on the FAAN website and send it to your governor for approval.

In terms of education, there are educational DVDs and children’s books aimed at making sure school-aged children are aware of the dangers of bringing banned foods to school and making sure to keep their lunches to themselves if they happen to have an allergy. There are also cookbooks for the healthy and safe at-home chef in order to keep those food allergies at bay.

By reminding consumers with allergies to “CAP It,” the FAAN tries to get people to remember three simple steps to keeping healthy: Carry your medicine; Avoid your allergen; and Plan ahead to prevent reaction. The CEO of FAAN, Julia Bradsher, says that although food allergies are a pain, they need to be managed, “Food allergies can be challenging to manage, but we know that reactions can be prevented by taking a few simple steps….Adults and children with food allergies and their families can empower themselves every day by taking steps to safeguard against reactions. By sharing their knowledge with others during Food Allergy Awareness Week and throughout the year, we hope to reduce the number of reactions and save lives.”

With over 30,000 members worldwide, FAAN is developing quite a fan base and they hope to become better known in your state when new proclamations are announced. Affecting around one of every 25 Americans and countless friends and families, food allergies are lurking inside millions of people from the playground to the boardroom, so take action now and stay safe.

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Researchers Say U.S. Obesity Epidemic Due to Overeating

The debate about whether the chicken or the egg came first has had some steep competition in recent years—what’s to blame for the obesity epidemic in America? Some experts say it’s genetics, some say environmental chemicals are to blame, others say it’s our slothful lifestyle filled with hours of television and video games. But Australian researchers say the rise in obesity is due almost entirely to overeating, and they have the numbers to prove it.

For their study, Professor Boyd Swinburn of Deakin University in Victoria, Australia and colleagues calculated how much adults need to eat in order to maintain a stable weight and how much children must eat to maintain a normal growth curve under normal living conditions. Then, using national food supply data from the 1970s and the early 2000s, they figured out how much Americans were actually eating. From this information, the researchers could predict how much weight Americans would be expected to gain over the 30-year period had food intake been the only influence. Next they used NHANES data on population weight during that time period to determine how much weight was actually gained.

According to the researchers, the predicted and actual weight increase in children matched exactly, indicating that the increase in caloric intake alone could explain the additional pounds. Adults gained less than the data predicted—18.9 pounds versus 23.8 pounds—which “suggests that excess food intake still explains the weight gain, but there may have been increases in physical activity over the 30 years that have blunted what would otherwise have been a higher weight gain,” Swinburn noted.

“There have been a lot of assumptions that both reduced physical activity and increased energy intake have been major drivers of the obesity epidemic. Until now, nobody has proposed how to quantify their relative contributions to the rise in obesity since the 1970s,” said Swinburn. “This study demonstrates that the weight gain in the American population seems to be virtually all explained by eating more calories. It appears that changes in physical activity played a minimal role.” He added that the findings would “probably be similar” for other developed countries as well.

Swinburn said that for the U.S. population to revert to the leaner 1970s levels, children would have to cut their daily caloric intake by about 350 calories—the equivalent of a can of fizzy drink and a small portion of French fries, and adults by about 500 calories—about the same as a Big Mac burger. Alternatively children would have to walk an extra two-and-a-half hours a day, and adults for nearly two hours. “Getting everybody to walk an extra two hours a day is not really a feasible option for countering the epidemic,” Swinburn said. “We need to limit our expectations of what an increase in physical activity can achieve.” In short, Americans must eat less, he said.

However, Swinburn emphasized that the findings in no way seek to negate the value of physical activity. “We absolutely need to continue to promote increased physical activity and a healthy diet because they are both obviously beneficial factors in terms of obesity,” he said. “But when it comes to placing priorities, I think it needs to be on reducing energy intake. It’s particularly important for policymakers to focus on the energy intake side of the equation.”

Other experts agree with the study’s conclusions. “We have long suspected that the decrease in physical activity seen during the past 30 years is playing a minor role in the change in body weight,” said Dr. Robert Lustig, an obesity researcher at the University of California San Francisco. “This was inferred by the fact that virtually all studies of increased exercise in obesity did not translate into weight loss.” He added that exercise plays an essential role in the obesity epidemic, not because it reduces excess weight, but because it improves health. For example, twenty minutes of jogging burns the equivalent of a chocolate chip cookie, he said. Therefore, Americans “need a complete overhaul of our diet if we are to solve the obesity epidemic,” Dr. Lustig said.

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Child Hunger a Growing Issue in the U.S.

Based on the 2005-2007 data from the U.S. Census Bureau and the Agriculture Department, at least 17 percent of children across America have the potential to go hungry. Children who lack proper nourishment during their developmental stages of life risk long-term affects, such as developmental, behavioral, and academic problems. Children are a key component to our future, and nourishment is significant to children prospering, both mentally and physically.

Thousands of children go hungry across the United States daily. The government has developed ways to ensure school-aged children are provided nutritious meals each school day. However, it may be hard for the government to extend this assistance to children aged five and under, which are not in school. A new study recently conducted by a non-profit anti-hunger group called Feeding America, concentrated primarily on hunger in children below the age of five. The group found that approximately 17 percent of children in this age group are at risk of going hungry. They found that 11 states actually had more than 20 percent of children under five who were at risk of going hungry. They included the top state of Mississippi, then North Carolina, Ohio, Kentucky, Texas, New Mexico, Kansas, South Carolina, Tennessee, Idaho and Arkansas. Feeding America operates centers to feed the hungry around the U.S

According to Dr. John Cook, an associate professor of pediatrics at Boston Medical Center and lead researcher of the report, hunger is based on two main factors across each state, the states level of employment and poverty rates, as well as the offerings of food and income assistance programs. Hunger seems to be a major problem across the U.S that continues to need attention. The newly released study was not based on data gathered during this new downturn in the economic market, which probably mean the numbers are currently even worse than expected. Vicki Escarra, president and chief executive of Feeding America said, "These children without the availability of nutrition don't have the chance to spring back." She noted that her organization is currently lobbying for additional federal funding for food bank programs to target young children.

This new data should help us be more aware of our hunger situation here in the United States. Children are not just going hungry in other countries, but there are over 12 million children at risk of going hungry here in the U.S. each day. It is very important for communities to support their local food banks and charities that target these groups and look to our government for more financial support and food for our hungry children. Without food and nutrition in their developmental stages in life, children may be left with impairments and the lifelong affects of childhood hunger.

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Esophageal Stricture

Introduction

Background

Disease processes that can produce esophageal strictures can be grouped into 3 general categories: (1) intrinsic diseases that narrow the esophageal lumen through inflammation, fibrosis, or neoplasia; (2) extrinsic diseases that compromise the esophageal lumen by direct invasion or lymph node enlargement; and (3) diseases that disrupt esophageal peristalsis and/or lower esophageal sphincter (LES) function by their effects on esophageal smooth muscle and its innervation.

Many diseases can cause esophageal stricture formation. These include acid peptic, autoimmune, infectious, caustic, congenital, iatrogenic, medication-induced, radiation-induced, malignant, and idiopathic disease processes.

The etiology of esophageal stricture can usually be identified using radiologic and endoscopic modalities and can be confirmed by endoscopic visualization and tissue biopsy. Use of manometry can be diagnostic when dysmotility is suspected as the primary process. CT scan and endoscopic ultrasound are valuable aids in the staging of malignant stricture. Fortunately, most benign esophageal strictures are amenable to pharmacological, endoscopic, and/or surgical interventions.

Because peptic strictures account for 70-80% of all cases of esophageal stricture, peptic stricture is the focus of this article. A detailed discussion of possible benign and malignant processes associated with esophageal stricture and its management is beyond the scope of this article.

Pathophysiology

Peptic strictures are sequelae of gastroesophageal reflux–induced esophagitis, and they usually originate from the squamocolumnar junction and average 1-4 cm in length.

• Two major factors involved in the development of a peptic stricture are as follows:
  • Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patients with peptic strictures compared with healthy controls or patients with milder degrees of reflux disease. A study by Ahtaridis et al (1979) showed that patients with peptic strictures had a mean LES pressure of 4.9 mm Hg versus 20 mm Hg in control patients. LES pressure of less than 8 mm Hg appeared to correlate significantly with the presence of peptic esophageal stricture without any overlap in controls.
  • Disordered motility resulting in poor esophageal clearance: In the same study, Ahtaridis et al (1979) demonstrated that 64% of patients with strictures had motility disorders compared with 32% of patients without strictures.
• Other possible associated factors include the following:
  • Presence of a hiatal hernia: Hiatal hernias are found in 10-15% of the general population, 42% of patients with reflux symptoms and no esophagitis, 63% of patients with esophagitis, and 85% of patients with peptic strictures. This suggests that hiatal hernias may play a significant role.
  • Acid and pepsin secretion: This does not appear to be a major factor. Patients with peptic strictures have been demonstrated to have the same acid and pepsin secretion rates as gender-matched and age-matched controls with esophagitis but no stricture formation. In fact, some authors believe that alkaline reflux may play an important role.
  • Gastric emptying: No good evidence suggests that delayed emptying plays a role.

Frequency

United States

Gastroesophageal reflux affects approximately 40% of adults. Strictures are estimated to occur in 7-23% of untreated patients with reflux disease.

Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of esophageal stricture. Postoperative strictures account for about 10%, and corrosive strictures account for less than 5%.

The overall frequency of initial and subsequent dilations for peptic stricture appears to have decreased gradually since the introduction of proton pump inhibitors (PPIs) in the market in 1989. This has been borne out by data at the author's institution and in 2 large community hospitals in Wisconsin. It is also in keeping with the general experience of gastroenterologists in the United States.

Mortality/Morbidity

The mortality rate is not increased unless a procedure-related perforation occurs or the stricture is malignant. However, the morbidity for peptic strictures is significant.

• Most patients undergo a chronic relapsing course with an increased risk of food impaction and pulmonary aspiration.
• Frequently, coexistent Barrett esophagus and its attendant complications occur.
• The need for repeated dilatation potentially increases the risk of perforation.

Race

Peptic strictures are 10-fold more common in whites than African Americans or Asians.

Sex

Peptic strictures are 2- to 3-fold more common in men than in women.

Age

Patients tend to be older, with a longer duration of reflux symptoms.

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Esophageal Spasm

Introduction

Background

Broadly, esophageal spasm can be subdivided into 2 distinct entities: (1) diffuse esophageal spasm (DES), in which contractions are uncoordinated, and (2) nutcracker esophagus, in which contractions proceed in a coordinated manner, but the amplitude is excessive.

Symptoms can include dysphagia, regurgitation, and noncardiac chest pain. Because of the vague symptoms and difficulty in diagnosis, esophageal spasm often is not diagnosed and is undertreated. Many patients with manometric and radiologic aberrations may not have any appreciable symptoms.

Currently, manometry is the best diagnostic modality. Treatment includes calcium channel blockers, botulinum toxin, nitrates, tricyclic antidepressants, dilatation, myotomy, and esophagectomy. Research is ongoing to unlock the underlying causes to improve our diagnostic capabilities and therapeutic regimens in the future.

Pathophysiology

The esophagus is comprised of 2 layers of muscle, the inner circular and the outer longitudinal layers. Arbitrarily, the esophagus can be divided into 3 zones, each with separate yet integrated anatomy and physiology.

Esophageal zones

Upper zone: Comprised entirely of striated muscle, this zone initiates the contractions that propel the food bolus down the esophagus. The upper esophageal sphincter (UES), named the cricopharyngeus muscle, is located in the upper zone.

Middle zone: Comprised of striated and smooth muscles, the inner circular muscle layer and the outer longitudinal muscle layer work in conjunction to propel the food bolus.

Lower zone: The lower segment is the lower esophageal sphincter (LES). This sphincter is a thickening of the smooth muscle that is contracted tonically to prevent reflux. At rest, the pressure in the LES is usually 15-25 mm Hg. For food to pass into the stomach, the LES relaxes.

Upper esophageal sphincter

When functioning properly, the esophagus can detect the presence of a food bolus at the UES and then coordinate progression of the food down the esophagus to the stomach. When this does not occur in a coordinated fashion, the patient can develop symptoms of esophageal spasm.

The UES is contracted tonically. Manometric evaluation of the UES reveals constant spiking activity. As food is sensed at the UES, the laryngeal muscles contract to move the cricoid cartilage anteriorly. The tonic contraction of the UES is inhibited, opening the UES to allow passage of food. The inner circular muscles and longitudinal muscles of the remainder of the upper zone then propel the food. To propel the food, the longitudinal muscles must contract, followed immediately by contraction of the circular muscles. At the end of the upper zone, the initial wave dies out as another wave starts, propelling the food down to the middle zone. The nucleus solitarius in the brainstem controls swallowing in the upper zone.

Esophageal middle zone

The middle zone propels the food bolus from the upper zone to the lower zone. This segment consists of 2 muscle layers, an inner circular and outerlongitudinal layer.

In the middle zone, the striated muscle transitions to smooth, or involuntary, muscle. The wave propagates down the esophagus by coordinated contractions. Again, the longitudinal muscles must contract before the circular muscle contracts. Furthermore, contraction of the muscles must proceed caudally in an organized manner. If the muscle contraction is not orderly, the food bolus cannot progress.

Two forces propel the food from cephalad to caudad. First, gravity pulls the food caudally. The organized contractions of the muscles propel the food caudally. If a myotomy is performed, the contractions will be ineffective. Only gravity forces the food caudally. Thus, patients who have had a myotomy are more likely to have dysphagia.

Lower esophageal sphincter

The lower zone is comprised of the LES. This is a condensation of the smooth muscles. Tonically, this muscle is contracted and must relax to allow food to pass. Failure of the LES to relax to allow a food bolus to pass is termed achalasia (see Achalasia).

Diffuse esophageal spasms

Simplistically, DESs occur when the propagative waves do not progress correctly. Usually, several segments of the esophagus contract simultaneously, preventing the propagation of the food bolus. The usual presentation is intermittent dysphagia with occasional chest pain. Myotomy, which is performed only in extreme cases, can relieve the uncoordinated contractions.

Nutcracker esophagus

Nutcracker esophagus occurs when the amplitude of the contractions exceeds 2 standard deviations from normal. The contractions proceed in an organized manner, propelling food down the esophagus. These patients often present with chest pain, but they present with dysphagia less often than patients with DES.

Because the progression of the contractions occurs normally, patients often do not benefit from a myotomy. Even though the increased amplitude of the contractions can be demonstrated using manometry, the symptoms often do not correlate with the manometrically documented contractions.

The symptoms of DES and nutcracker esophagus may overlap and can be distinguished only by motility study.

Frequency

United States

The true incidence of esophageal spasm cannot be determined. The symptoms range from mild to severe. Patients with mild symptoms often do not seek medical attention. Because of the similarity of symptoms of reflux disease and esophageal spasm, many patients may be misdiagnosed with reflux. Furthermore, reflux and spasm can occur concomitantly.

International

Because the symptoms are mild (or even absent) in many patients, true incidence is not known.

Mortality/Morbidity

• Mortality is very rare, but morbidity can be significant.
• 
  
• Morbidity arises from an inability to eat, secondary to the pain, and the subsequent decline in nutritional status. The pain can be incapacitating, preventing normal activity and leading to considerable psychological challenges and impairment in the patient's quality of life.
• 
  
• The chest pain can mimic cardiac, pulmonary, or rheumatological chest pain, instigating appropriate workup.

Race

• This condition seemingly is more common in whites.

Sex

• This condition may be more common in women than in men.

Age

• This condition is rare in children, and incidence increases with age.

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