Fatty Liver in Children

Nonalcoholic fatty liver disease (NAFLD), is an accumulation of fat in the liver. Over the last decade it has become the most common cause of chronic liver disease in children.
NAFLD is estimated to affect close to 10% of the American population aged 2 to 19 years, and this figure increases to 30-40% among obese children. Insulin resistance is almost a universal finding in pediatric NAFLD, and consequently, several of the clinical features associated with insulin resistance, such as, obesity, diabetes mellitus, dyslipidemia, hypertension, obstructive apnea, and gallstones are common comorbidities in children who suffer from NAFLD.

NAFLD includes a wide spectrum of liver damage ranging from simple, uncomplicated steatosis(fatty liver) to nonalcoholic steatohepatitis (NASH), to advanced fibrosis (scar tissue) that can lead to cirrhosis, which can lead to liver failure and loss of liver function.
The American Academy of Pediatrics has recommended that serum aminotransferases (ALT and AST), should be performed in all overweight children starting at the age of 10, if their BMI is >95% or between 85-95% with risk factors. The ALT and AST are to be checked in addition to fasting glucose and lipid profile.
The diagnosis of NAFLD requires:
1) Confirmation of diffuse fatty infiltration of the liver in imaging studies regardless of the AST and ALT levels, the most common use modality is a liver ultrasound.
2) Average daily ethanol consumption of less than 10 grams in the appropriate age group and social setting.
3) Appropriate exclusion other liver disease, such as viral hepatitis, Wilson’s disease, alpha-1-antitrypsin deficiency, autoimmune hepatitis, and studies to investigate standard metabolic/inborn error panel
4) Verification that medicine intake is not causing liver injury
5) Some patients may require a liver biopsy
Childhood obesity has more than doubled in children and quadrupled in adolescents in the past 30 years. In 2012, more than one third of children and adolescents were overweight or obese. The rising number of obese children explain the recommendation given by the American Academy of Pediatrics.
“The Natural History of Nonalcoholic Fatty Liver disease in Children: A Follow-Up Study for up to 20 Years” is a recent article published where 66 patients were monitored for up to 20 years in order to observe the natural history of NAFLD. The study revealed two important facts. Firstly, NAFLD in children is associated with a significant shorter long-term survival. Secondly, Two out of the 66 children followed developed liver cirrhosis.
The most common presenting symptoms are: abdominal pain, fatigue, hepatomegaly (enlarged liver), splenomegaly (enlarged spleen) and acanthosis nigricans.
Treatment for NAFLD and NASH:
• Lose weight, through a healthy diet, and increased physical activity. In most cases the liver injury is reversible if it is in the early stages and no scarring is present.
• Vitamin E have shown to improve fatty liver in some children. It is no yet clear why, it does not work for everyone, but genes and other risk factors might play a role.
Some useful Tips:
• Encourage your child to follow a healthy, portion-controlled diet, with low amounts of saturated fats and refined sugars.
• Avoid large portion sizes and sweetened drinks, like soda. Limit the amount of meals eaten at fast food restaurants, since this food is usually high in fat.
• See a dietician who will help guide healthy diet choices.
• Increase your child’s physical activity and outdoor play.
• Have the hepatitis A and B Vaccines updated, to avoid potential injury to the liver caused by these viral infections.

Acknowledgements:
I would like to thank Dr. Diana Lopez Garcia in the preparation of the article.

Pancreatic Cancer

By: Daniel Gelrud, MD

The pancreas is an important organ responsible for the production of enzymes necessary for the digestion of food and insulin (a hormone that controls sugar levels in the blood). Pancreatic cancer is a disease in which malignant cells form in the pancreatic tissues. The risk factors for developing pancreatic cancer include smoking, diabetes, obesity, chronic pancreatitis and certain inherited conditions.

Symptoms

Initially pancreatic cancer tends to be silent but as it grows symptoms develop. Unfortunately, by the time symptoms develop the cancer has probably grown outside of the pancreas. The symptoms will depend on the location of the cancer. If the tumor is in the body of the pancreas, the patient will have belly or back pain and weight loss. Pancreatic cancer of the head of the pancreas tends to cause weight loss, belly or back pain, jaundice (yellow skin and eyes), dark urine, itching or light colored stool.

Is Pancreatic Cancer Increasing?

Pancreatic cancer has a poor prognosis and its incidence has been increasing over the last 15 years. Although it is not clear why this is happening, pancreatic cancer ranks 4th in cancer related deaths. By 2030 it is believed that pancreatic cancer will fall shortly behind lung cancer as the second highest cause of cancer deaths.

There are several reasons for the increase in pancreatic cancer. Firstly, there has been a rise in obesity and diabetes which are both risk factors for the disease. Secondly, the incidence of colon and breast cancer has been decreasing because of effective screening practices. The incidence of colon cancer in older adults has decreased 30% over the last decade because of the increasing use of colonoscopy as a screening tool. Thirdly, the general population has a higher life expectancy and pancreatic cancer is more common later in life.

 How is Pancreatic Cancer Diagnosed?

The pancreas is a very difficult organ to image and obtain tissue from. This makes it very difficult to diagnose. After a patient develops symptoms suggestive of pancreatic cancer, your primary doctor will obtain a full history and physical exam and then he may order a CT scan or a MRI. After that the doctor will refer the patient to see a gastroenterologist with expertise in pancreatic diseases. A biopsy will be obtained using an Endoscopic Ultrasound (EUS) or with an ERCP (an endoscopic procedure that accesses the bile and pancreatic ducts). One of the main objectives for the imaging studies and EUS is to determine whether the cancer can be removed by surgery.

Treatments

The best treatment for pancreatic cancer depends on how far it has spread, or its stage. Early stages can be treated with surgery. When the tumor has spread beyond the pancreas, then surgery is not possible. Other treatment modalities such as chemotherapy and radiation therapy can extend survival.

Summary

Pancreatic cancer is a common cause of cancer related deaths and its occurrence has been increasing over the last 15 years. Early diagnosis is crucial and it is imperative to consult with a physician who has experience with pancreatic cancer.

 

Anal Fissure

An anal fissure is no more than a tear or cut of the anal skin below the dentate line in the anal canal, usually very small. This injury can cause severe and disabling pain to the patient. Symptoms include rectal bleeding, pain, and burning after defecation that could last from minutes to hours.

Fissures are mainly caused by trauma to the anal canal, such as, with the passage of hard stool. Other theories, such as ischemia to the posterior midline of the anus, have been entertained. Fissures are usually located in the posterior midline of the anus, but can also be seen in the anterior midline, and in both locations at the same time. When a fissure is located off the midline of the anus, the clinician should investigate for other potentially complicated disease processes, such as, Crohn’s disease, trauma, tuberculosis, syphilis, HIV/AIDS or anal carcinoma. The diagnosis of the fissure is usually suggested by the description of the patient’s symptoms, and is easily confirmed by physical examination. Usually, other means of examination such as a digital rectal examination and anoscopy are not required and actually could be very painful for the patient.

The treatment of an anal fissure usually goes directed towards relieving the hypertony of the internal sphincter muscle that is associated with the condition. Fiber supplements, stool softeners and laxatives are also prescribed as needed. The treatment is also divided into medical or surgical. With the medical therapy, the aim is to chemically induce a relaxation of the internal sphincter muscle, while the aim of the surgical therapy is to mechanically cause that same effect.

The medications more widely used for the treatment of anal fissures are topical anti-inflammatory agents, such as, hydrocortisone. In addition, sphincter relaxants such as, nitrate formulations, oral and topical calcium channel blockers, adrenergic antagonists, topical muscarinic agonists, phosphodiesterase inhibitors and the use of botulinum toxin with success cure rates that range from 50 to 80% are implemented.

 

Historically, surgical techniques, have had a high success rate to treat this condition. Techniques such as, anal dilatation and posterior sphincterotomy, have been largely abandoned due to their side effects in particular, fecal incontinence. The American Society of Colon and Rectal Surgeon’s practice parameters for the management of anal fissures recommends, Lateral Internal Sphincterotomy as the surgical treatment of choice in medically refractory anal fissures, in which a small portion of the left aspect of the internal sphincter muscle is divided to achieve the desired mechanical relaxation needed to help the fissure heal.

 

Despite the mixed results with medical therapy, it is our practice to step up treatment options. From the use of topical anti-inflammatories to sphincter relaxants to surgical therapies, treatment options depend on the patient’s potential risk for fecal incontinence.

Cáncer colorrectal: síntomas, factores de riesgo y prevención

El cáncer colorrectal es un cáncer común procedente del colon o recto. En los Estados Unidos es el tercer tipo de cáncer más común (excluyendo el cáncer de piel) y es la segunda causa principal de muerte por cáncer. Para el año 2014 se estima que aproximadamente 140.000 nuevos casos de cáncer colorrectal se producirán. Fuera del total de estos nuevos casos 50.000 resultaran en muerte. Aunque el cáncer colorrectal es muy común en los Estados Unidos es también uno de los más prevenibles debido al hecho de que existen muchas modalidades de cernimiento para detectarlo en una etapa temprana.

¿Cómo se desarrolla el cáncer colorrectal?

Se origina de células individuales del intestino grueso. A lo largo de la vida de una persona las células acumulan mutaciones en su código genético. Estas mutaciones hacen que las células crezcan con mas rapidez que las células adyacentes normales. Eventualmente estas células se expanden a un pequeño montículo en el interior del colon o recto. Este pequeño montículo se llama pólipo. No todos los pólipos se convertirán en cáncer, pero algunos, si se dejan crecer en el interior del colon por mucho tiempo, pueden transformarse en un cáncer. Este proceso en la mayoría de los casos es muy lento y puede tomar de 10 a 15 años. A veces el proceso puede llevarse a cabo más rápido, sobre todo cuando hay una fuerte historia familiar de cáncer colorrectal.

¿Cuáles son los signos y síntomas del cáncer colorrectal?

En la mayoría de los casos no hay síntomas específicos. Este suele ser el caso con los pólipos precancerosos y también los pequeños cánceres de colon. A medida que crece el cáncer muestras indicadoras comienzan a aparecer. Estos incluyen sangre en las heces, un cambio en los hábitos intestinales (estreñimiento progresivo), cambios en la forma de las heces, como heces más finas; también la pérdida de peso y fatiga. La fatiga puede ser un signo de anemia. La anemia es frecuente en el cáncer colorrectal debido a la pérdida de sangre lenta. A veces la anemia es la presentación inicial del cáncer colorrectal.

Los factores de riesgo para cáncer colorectal

Los factores de riesgo se pueden dividir en aquellos que no pueden ser controlados y aquellos que pueden ser controlados. Dentro de los factores que no se pueden controlar el principal de ellos es la edad. Cáncer colorrectal se vuelve más común con la edad. El riesgo comienza a aumentar después de los 40 años, incrementa de manera significativa a las edades de 50 a 60, y se duplica con cada década siguiente. Otros factores importantes que no pueden ser controlados incluyen antecedentes familiares de pólipos precancerosos o cáncer colorrectal, otros tipos de cáncer como el cáncer de útero, antecedentes personales de pólipos de colon rectal, enfermedad inflamatoria intestinal, y síndromes de cáncer hereditario como el síndrome de cáncer colorrectal hereditario sin poliposis. Los factores de riesgo que se pueden controlar incluyen factores que están vinculados a las cosas que uno normalmente puede hacer pero que aumentan el riesgo de cáncer colorrectal, como el consumo de una dieta rica en carnes rojas y carnes procesadas, cocinar carnes a altas temperaturas como en una parrilla (aumento de la temperatura puede crear toxinas que causan mutaciones en células), el estilo de vida sedentario, la obesidad, el tabaquismo y el consumo excesivo de alcohol.

 ¿Cómo se puede prevenir el cáncer colorectal?

Los estudios han encontrado que el incremento de peso corporal puede predisponer al cáncer colorrectal. Este enlace parece ser más fuerte en los hombres, particularmente cuando el aumento de peso está distribuido alrededor de la cintura. Otros estudios muestran que las dietas de bajo consumo en vegetales y granos enteros pueden predisponer al cáncer colorrectal. Finalmente pólipos precancerosos y el cáncer colorrectal se encuentran con mayor frecuencia en las personas con bajos niveles de actividad física. Para ayudar a prevenir el cáncer colorrectal se puede comenzar con la modificación del comportamiento. Aumente su actividad física. Episodios regulares de actividad vigorosa varias veces a la semana es tal vez más beneficioso que la actividad moderada en base regular. Coma más verduras, frutas y alimentos integrales y consuma menos carne roja y carne procesada. Haga como objetivo clave bajar de peso: aumente el ejercicio aeróbico y enfóquese en la pérdida de la grasa alrededor de la cintura. Por último, participe en un programa de cernimiento para cáncer colorrectal. La incidencia y la mortalidad de cáncer colorrectal se ha reducido en los últimos años posiblemente debido a los múltiples métodos de detección disponibles que son capaces de encontrar las lesiones precancerosas. La colonoscopía es el mejor método de cernimiento ya que puede ver todo el colon, detectar pólipos y removerlos durante el mismo procedimiento. Se recomienda que las personas con antecedentes familiares de cáncer colorrectal tengan su primera colonoscopía a los 50 años y si no hay pólipos precancerosos que se repita la colonoscopía cada 10 años. Los pacientes con una fuerte historia familiar de cáncer colorrectal deben someterse a su primera colonoscopía antes, y los pacientes con antecedentes de pólipos precancerosos deben tener su colonoscopía de seguimiento realizado a intervalos más cortos. Hable con su médico de atención primaria o sea referido a un gastroenterólogo para determinar cuándo y con qué frecuencia debe hacerse una prueba de cernimiento para cáncer colorrectal.

Colorectal Cancer: Symptoms, Risk Factors, and Prevention

Colorectal cancer (also known as CRC) is a common cancer originating from the colon or rectum. In the United States is a third most common cancer (excluding skin cancers) and it is the second leading cause of cancer death. For the year 2014 it is estimated that about 140,000 new cases of CRC will occur. Out of these new cases approximately 50,000 will result in death. Although CRC is very common in the United States it is also one of the most preventable due to the fact that many screening modalities are available to detect it at an early stage.  In this brief review will go over the signs and symptoms of colon cancer, risk factors for this disease, and the measures that can be taken to reduce the risk of colon cancer development.

 How Does Colorectal Cancer (CRC) Develop?

CRC originates from cells in the large bowel. Throughout the life of an individual cells accrue mutations in their DNA. Mutations make cells heartier and enable them to grow a little better than their normal surrounding cells. Eventually these cells expand into a little mound in the interior of the colon. This little mound is called a polyp. Not all polyps will turn into a cancer but some, if left inside the colon for long time, can transform into a cancer. This process in the majority of cases is very slow and can take anywhere from 10 to 15 years. Sometimes the process can take place quicker, particularly when there is a strong family history of CRC.

 What are the signs and symptoms of CRC?

In most instances there are no specific symptoms. This is usually the case for pre-cancerous polyps and small colon cancers. As the cancer grows telltale signs begin to appear. These include blood in the stool, a change in bowel habits (progressive constipation), changes in the shape of the stools such as thinner tools; weight loss, and fatigue. Fatigue can be a sign of anemia. Anemia frequently occurs in CRC due to slow blood loss. Sometimes anemia is the earliest presentation of CRC.

 

Risk factors for CRC

Risk factors can be divided into those that can’t be controlled and those that can be controlled.  Within the factors that cannot be controlled the main one is age. CRC becomes more common as people age. The risk begins to increase after the age of 40 and rises significantly at ages 50 to 60. The risk doubles with each following decade. Other important factors that cannot be controlled include a family history of polyps or CRC, other cancers such as uterine cancer, a personal history of colon rectal polyps, personal history of inflammatory bowel disease, and inherited CRC syndromes such as hereditary non-polyposis colorectal cancer syndrome (HNPCC). Risk factors that can be controlled include factors that are linked to things that you do that increase your risk for CRC such as consuming a diet high in red meats and processed meats, cooking meat at high temperatures such as in a grill (increased temperature can create toxins that cause mutations in cells), sedentary lifestyle, obesity, smoking, and excess alcohol use.

 

How can CRC be prevented?

Studies have found increase body weight can predispose to CRC. This link seems to be stronger in men, particularly when the increased weight is distributed around the waistline. Other studies show that consuming diets low in vegetables and whole-grain can predispose to CRC. Finally polyps and CRC are found more frequently in individuals with low levels of physical activity. To help prevent colon cancer start with behavior modification. Increase your physical activity. Scheduled episodes of vigorous activity several times a week maybe more beneficial than moderate activity on a regular basis. Eat more vegetables, fruits, and whole-grain foods and consume less red meat and processed meat. Make it a key goal to lose weight: increase your aerobic exercise and focus on losing the fat around the waistline. Lastly, participate in CRC screening programs. The incidence and mortality of CRC has dropped in the last several years, possibly due to multiple available screening methods capable of detecting precancerous lesions.  A colonoscopy is the best screening method since it can look at the whole colon, detect polyps, and remove them during the same procedure. It is recommended that people with no family history of CRC have their first colonoscopy at age 50. If no precancerous polyps are seen the colonoscopy can be repeated in 10 years. Patients with a strong family history of CRC should undergo their first colonoscopy sooner, and patients with a history of precancerous polyps should have their follow-up colonoscopy done at shorter intervals. Talk to your primary care doctor or get referred to a gastroenterologist to find out when and how often you should get screened for CRC

Do I Have IBS?

By: Pamela Garjian, MD

Irritable bowel syndrome is a functional gastrointestinal disorder that is common and can affect up to 20% of the adult population. It is predominantly seen in women, but also can occur in men. Symptoms might include abdominal pain, bloating, diarrhea, constipation and mucous. In fact there are a specific set of standards called the ROME III criteria that your physician might use to make the diagnosis. It includes abdominal pain at least 3 days per month out of the last 3 previous months, (and these symptoms must have started at least 6 months before). Additionally, a patient must have 2 or more of the following symptoms:

  • Improvement of pain with bowel movements
  • Change in bowel movements
  • Consistency or frequency

 

As opposed to another disease called inflammatory bowel disease (IBD), IBS is a multitude of GI symptoms where the intestinal tract is not damaged. Other associated IBS symptoms include feeling that a bowel movement is incomplete, passing mucus, predominant diarrhea, predominant constipation, or alternating diarrhea and constipation, bloating, and/or gas.

What causes IBS?                                                                                                                                                                                                                    

The cause of IBS is probably multifactorial. It is believed to include problems with the brain gut signal, motility disorders and contractions and spasms such as hyper or hypo-active gut, hypersensitivity of the intestines especially to stretching of the walls of the intestine, bacterial overgrowth possibly of the small intestine, genetics, food sensitivity, and disordered body chemicals. Some studies suggest that up to 60% of patients with IBS predominant diarrhea have had an infectious gastroenteritis preceding their symptoms. Essentially, IBS is a complicated disorder.

How is the diagnosis made?

The diagnosis of IBS is one of exclusion, which means that the doctor might run some tests to exclude other organic diseases such as gluten intolerance, lactose intolerance, inflammatory bowel disease, (which includes Crohn’s disease and ulcerative colitis), food allergies, sorbitol intolerance, H. pylori, gallbladder disease, ulcer disease, chronic constipation without IBS, eosinophilic enteritis, and infectious colitis. It is important that there are no “alarm symptoms” that might suggest a different diagnosis, such as fever, rectal bleeding, weight loss, anemia or low red blood cell count, family history of colon cancer, family history of celiac disease or inflammatory bowel disease. Tests might include a sigmoidoscopy, colonoscopy, stool studies, blood tests, and breath tests.

How is a treated?

Diet and lifestyle modifications may play a role and may be helpful for some patients. Certain diets have claimed to alleviate symptoms associated with IBS (Such as the FODMAP diet). However, this has caused much controversy because up to two thirds of patients with IBS will respond to dietary changes. Additionally, some foods are unpredictable because of their inconsistency in triggering IBS. Medication such as prescription anti-spasmodic medicines, over-the-counter probiotics, fiber, prescription antibiotics, and mental health therapy may all be helpful.

Diet and nutrition

Diet may play an important role in IBS and a food diary may be helpful and can help determine what triggers your symptoms. Furthermore, it is a possibility that a patient with IBS has an additional digestive problem such as lactose intolerance. A low FODMAP diet has been getting a lot of attention over the last several years and usually restricts gluten, fructose, sorbitol, sucrose, and lactose.   FODMAPs include foods such as wheat, barley, rye, legumes, mango, honey, pears, apples, mushrooms, cauliflower, onions, sugar-free candies, gum, garlic, and lactose. Although this is a very restricted diet, some studies suggest that it may be helpful. Other possible dietary restrictions can include low-fat or PALEO diet.

In summary

IBS is a common complicated constellation of many symptoms that may have several possible causes. Treatment needs to be tailored to the individual patient. Your gastroenterologist with your input, may be able to help you sort out these details. It is important however not to mistake a more serious organic illness as IBS. Furthermore if long-standing IBS symptoms change, then testing may be required to exclude another disease process. Consulting with your gastroenterologist is an important part of the diagnosis and treatment of this condition.

 

Hepatitis C Virus: Current Therapies and Beyond

The Hepatitis C Virus (HCV) is a major global public health concern. It is a serious and complex bloodborne virus which manifests itself through complications of the liver. If left untreated, it can cause significant and potentially fatal damage, possible hepatic carcinoma and other complications leading to transplantation.  The World Health Organization (WHO) estimates that 150 million people worldwide were chronically infected with HCV in 2011.  The virus is responsible for 350,000 deaths globally with 10,000 – 16,500 deaths each year in the United States.  Up to 90% of those infected with hepatitis C do not clear the virus and become chronically infected. In the United States, nearly 4 million people are chronically infected. The HCV virus is most commonly detected in people who are 40-60 years of age, reflecting higher rates of infection during the 1970’s – 1980’s.  Recently, both the Centers for Disease Control and Prevention (CDC) and the U.S. Preventive Service Task Force have encouraged HCV screening among baby boomers (those born between 1945-1965).

Treatment modalities for HCV have advanced incredibly in the last 25 years since HCV infection was identified in 1989.  We witnessed the first approved treatment with Interferon (IFN-a) in 1991, then seven years later, Ribavirin (an antiviral) was approved in combination with Interferon. Both of these drugs were revolutionary at the time because they inhibited viral replication.  However, although this was an incredible advancement there were several side effects such as fatigue, flu-like symptoms and depression.  Additionally, the body’s response to IFN-a, was not as efficient and effective as some had hoped. A decade would pass until we had an improved delivery method of Interferon. Pegylated Interferon (IFN-a) was introduced in 2001 and resulted in the interferon’s ability to stay in the body longer.  However, the side effects in treatment still persisted.

Fortunately, HCV treatment regimens saw a breakthrough in 2011 when the first direct-acting agents were approved in combination with Interferon and Ribavirin for genotype 1 HCV infection.  “We are now going to get into an era of using combinations of direct-acting antivirals”, said Luis Balart, MD, chief of gastroenterology and hepatology at Tulane University School of Medicine, in New Orleans. In December of 2013, the United Stated Food and Drug Administration (FDA) approved sofosbuvir (a nucleotide polymerse inhibitor of the HCV NS5B enzyme), as part of the first ever Interferon (IFN) free regimen for HCV. This was a major breakthrough because those who were not eligible for interferon due to contraindications now had a mode of treatment. Sobosbuvir was approved for use in combination with ribavirin for adults with HCV genotypes 2 or 3, and in combination with pegylated interferon (PEG-IFN) and ribavirin (RBV) for adults with HCV genotypes 1 or 4. This drug approval came several weeks after the approval of Simeprevir (a HCV NS3/4A protease inhibitor) which treated patients with HCV genotype 1 in combination with PEG-IFN and Ribavirin.

Despite the fact that the current standard of care for genotype 1 includes combination of PEG-IFN and ribavirin, the approval of these two new drugs represents a shift in the treatment paradigm for patients with chronic hepatitis C.  These two types of Direct Acting Antivirals (DAA’s) are playing a role in bringing about important therapeutic advances, particularly for IFN-free treatment modalities.

In the next 6 months to five years, a number of new DAA’s are expected to receive the FDA approval for hepatitis C.  According to Donald Jensen, MD, director of the Center for Liver Disease at the University of Chicago, “Five to 10 new HCV treatment regimens currently stand a good chance of being submitted for FDA approval in the next few years”. These new treatment modalities have a high sustained virologic response (SVR) rates, meaning that they have a high success rate. Not only are they effective at treating HCV but they are given in shorter duration with minimal side effects when compared to IFN based treatments. Moreover, the traditional risk factors thought to portend poor outcomes in HCV patients ( past treatment responses, gender, high baseline HCV RNA, advanced fibrosis/cirrhosis, and genotype-IL28B- non CC genotype) may have no effect with the new DAA agents.

“There are multiple, oral, interferon (IFN) free DAA regimens in late stage clinical trials with high SVR rates” said Mark Sulkowski, MD, Medical Director of the Viral Hepatitis Center in the Divisions of Infectious Diseases and Gastroenterology & Hepatology at Johns Hopkins School of Medicine, in Baltimore.  These include the Gilead-based regimen of sofosbuvir plus ledipasvir, with or without GS-9669; Abb Vie’s ABT 450/r plus ABT267 and ABT333; Boehringer Ingelheim’s faldaprevir plus deleobuvir, with or without PPI-668; Janssen’s simeprivir and samatasvir plus TMC647055/r; Merick’s MK 8742 plus MK 5172; Bristol-Myers Squibb’s daclatasvir plus asunaprevir and/or with BMS 791325. Not to mention the already filed and awaiting FDA’s “stamp of approval” for several DAA’s that will be on the market within the next 6 – 12 months

These new DAA’s can be classified into three groups: protease inhibitors, polymerase inhibitors and NS5A inhibitors.  All of the new agents target specific processes of the HCV life cycle.   The treatment strategy involving these new agents is to include drugs that attack at least two different HCV targets in a single regimen.   The challenge for the clinician will be to scrutinize the drug combinations and select the best regimen, such as assessing whether some populations may benefit from 8 or 24 weeks of therapy or the addition of ribavirin. However, the bottom line is that an extremely simple, safe, and effective therapy for HCV genotype 1 infection is here. Given the dramatic advances in the treatment of HCV infection, identification of patients with hepatitis C may provide an opportunity to cure patients and greatly reduce the health care burden associated with the complications of liver disease.

Finally, it is important to remember to ask your gastroenterologist if there are any new treatment options that are right for you. Gastro Health has been a long time leader in hepatitis treatment and expects to offer these new treatment combinations in the near future. At Gastro Health we remain up to date with current and future treatment remedies and offer quarterly support groups in order to effectively care for you and those you love.