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5615

Doctor Claims To Irreversibly Change Eye Color From Brown to Blue

Did you ever thought about the possibility of changing your eyes color to blue? If yesterday this was only just a dream, a doctor made it true by showing he can permanently change a person eye color in under 30 seconds.

Doctor Gregg Homer, who works at Stoma Medical Center in California, uses a special kind o laser to change the eye color from brown (the most common type of eye color) to blue, using his Lumineyes technology. The laser works by burning the brown color pigment also know as melanin contained in the upper layer of the iris the result beeing baby blue eyes within two to three weeks.

The Lumineye technology shaves one layer of brown pigment leaving one blue layer instead. You can see the results below, in a patient on the lower half of the eye.

Brown To Blue Eyes

Brown To Blue Eyes

Doctor Gregg Homer and his technology can provide a powerful alternative for contact lenses for people who want light colored eyes. The down side is that the procedure is irreversible as the iris can not regenerate and turn brown again.

Stroma medical is now in the human clinical testing stage, but lacks half a million euros to complete, but all is up to schedule according to Dr Homer, and the procedure will be probably available in the United States within 18 months and all around the world in about three years, at a cost of three thousand euros.

Doctor Homer has been already contacted by hundreds of possible clients. “They say the eyes are the window to the soul”.

CEO of Stromal Medical, Doug Daniels was sceptical at first when Doctor Homer first told him about his procedure. Eye color is an inherited characteristic, and brown eyes are the most common color type. A blue pigment does not normally exist in nature,  people with blue eyes actually have lower concentrations of melanin (pigment) in the front of the iris thus their eyes are blue. People with higher concentration of melanin in the front of the iris have dark coloured eyes.

Brown To Blue Eyes

Brown To Blue Eyes

In 2008, scientists from the Copenhagen University showed that all blue-eyed people are the descendants of a singer ancestor carrying a mutation for blue eyes that lived ten thousand years ago. Before that all humans had brown eyes according to Proffessor Eiberg (study leader). This mutation is not considered either bad or good, but part of the many mutations that shape our daily life as hair color, nose length, predisposition to certain diseases and so on.

Proffesor Eiberg stated at the time that : “‘It  simply shows that nature is constantly shuffling  the human genome, creating a  genetic cocktail of human chromosomes and trying out different changes as it  does so”

9925

Hypoglycemic coma represents the extreme manifestation of hypoglycemia, it is announced by loss of consciousness or, in other words, the patient’s inability to act appropriately to manage hypoglycemia without the intervention of others. Coma is characterized by a total inability to regain consciousness.

Hypoglycemia is a syndrome caused by decreased plasma glucose concentration below the level for which the human body is adapted . Biochemical criteria of hypoglycemia for adults are: from breakfast (on an empty stomach) <3.3 mmol / l in plasma or serum, and <2.8 mmol / l in capillary blood (glucose in the blood plasma and serum is 15% higher than in capillary blood) and the postprandial hypoglycemia (over 3-4 hours after glucose load) – in plasma and serum <2.8 mmol / l and  in capillary blood <2.2 mmol / l.

Hypoglycemia without clinical manifestations can be seen in healthy individuals or in the case of reactive hypoglycemia. Hypoglycemia is dangerous on short term periods and evolves worse than hyperglycemia, as glucose is the primary energy substrate for brain tissues.

Clinical Forms Of Hypoglycemia

Hypoglycemia signs and symptoms may occur on an empty stomach or  3-4 hours after eating (postprandial).

  • Fasting hypoglycemia (starvation)
  • Postprandial hypoglycemia (reactive or functional)

In the first case plasmatic hypoglycemia occurs only when hungry for over 5 hours. In the second case hypoglycemia occurs only in response to meals, and usually occurs within 5 hours after. Hunger hypoglycemia means that a pathological process is associated with decreased plasma glucose, while symptoms suggestive of postprandial hypoglycemia are often found in the absence of diseases that could be recognized.

Affected organs and systems: the central nervous system suffers mainly  from hypoglycemia, the cardiovascular system, other – depending on the underlying cause, which induced hypoglycemia.

Hypoglycemia Incidence And Prevalence

Hypoglycemia found in 1.5 -3: 1000 newborns, in the major risk groups the prevalence is much higher. The transient hypoglycemia occurs in 2 of 3 new born babies and also in 80-90% of babies born from mothers who suffer from insulin-dependent diabetes or have suffered from gestational diabetes. Approximately 10-20% of children from the high risk groups, develop stable severe hypoglycemia.

Prevalence

Hypoglycemia prevalence in adults is not known because many patients solve this problem alone, without resorting to medical help. Age and sex predominance is also unknown.

Hypoglycemia

Hypoglycemia

Hypoglycemia Signs And Symptoms

Neurological symptoms – slow decrease in glucose levels : marked fatigue, extreme hunger sensation, vertigo, headaches, confusion, visual disturbances (diplopia), paraesthesia, convulsions, coma, which is installed quickly. Adrenenergic symptoms – predominantly caused by sudden decrease of glucose levels: sweating, irritability, restlessness, tremors in the extremities, tachycardia, irregularity of heart contractions, hypertension, hyperreflexia, muscle hypertonia.

Complications – cerebral edema.

Hypoglycemia Causes

The postprandial hypoglycemia causes are:

  • Hyperinsulinism (exaggerated insulin secretion response)
  • Hereditary fructose intolerance
  • Galactosemia
  • Sensitivity to leucine
  • Idiopathic hypoglycemia (hypoglycemia with unknown cause)

The main causes of fasting hypoglycemia installation may be either due to low production of glucose or excessive use of glucose.

The causes of  fasting hypoglycemia are:

  • Hormonal deficits: hypopituitarism, glucagon deficiency, adrenal insufficiency, catecholamine deficiency
  • Enizimatic defects: glucose-6-phosphatase, liver phosphorylase ,pyruvate – carboxylase, glycogen synthase; deficit of substrates: ketosis hypoglycemia in children, malnutrition, muscle atrophy, advanced pregnancy.
  • Liver disease: acute fulminant hepatitis, hepatic congestion, severe forms of liver cirrhosis
  • Uremia
  • Hypothermia
  • Some drugs, alcohol, propranolol, salicylates
  • Sulfonylureas
  • Autimmune diseases with insulin or insulin receptor antibodies
  • Insulinoma (insulin secreting tumor of the pancreas)

Hypoglycemic coma causes

In diabetes type 1

  • Insulin overdose
  • Inadequate food intake, too long interval between injection and meal
  • Intense and prolonged exercise
  • Suppression of  certain medications
  • Alcohol abuse.

In diabetes type 2

  • Sulfonamides overdose, especially with generation 2 sulfonamides (which determine a long and severe hypoglycemia), and insulin overdose;
  • Additional drugs (coumarin, phenylbutazone, sulfonamides, b-blockers)
  • Travelling and diminished food intake.

Hypoglycemia Risk factors

Older age, renal disease, cardiovascular failure, gastroenteritis, alcoholism, poor nutrition, mental disorders (intentional overdose of insulin with suicidal purpose).

Hypoglycemia Diagnosis

Hypoglycemia diagnosis is not difficult to establish. The difficult part to achieve is to identify the cause of hypoglycemia. Diagnosis of severe hypoglycemia in diabetes mellitus is established on the patient history, collected from the patient or family diary data from and on the clinical signs: sudden onset of symptoms, irritability, sweating, hunger, headache. Hypoglycemic coma occurs frequently during the night, during sleep, with signs that should alert the family members: noisy breathing, convulsions and sweating. With rapid determination of blood glucose using a  home glucometer, the diagnosis of hypoglycemia is specified in minutes.

Hypoglycemia

Laboratory investigations

  • Hypoglycemia <2.8 mmol / 1.
  • High levels of insulin
  • Increasing levels of peptide C
  • Alkaline reserve and normal pH.
  • Cetonuria and glycosuria do not refute the diagnosis of hypoglycemic coma

Hypoglycemia Prognosis

Diagnosed early and treated properly severe hypoglycemia can have a good prognosis. Possible cerebral functional disorders can be detected only by fine psychological tests. If hypoglycemia lasts more than 5-10 hours, and the blood sugar levels are very low (lower than 25 mg / dl) total recovery may be possible only after a prolonged period of treatment (several hours).

Serious two complications can occur: stroke or myocardial infarction, leading to increased mortality and post-hypoglycemia encephalopathy, massive retinal hemorrhage or loss of vision, which severely affects the patient’s quality of life.

Hypoglycemic coma mortality varies according to age, 5% in young adults and reaching up to 25% in the elderly persons with multiple complications

5711

New Drug Shows Promise In Refractory Hodgkin’s Lymphomas

A new drug, called brentuximab vedotin, used in infusion, was released for the treatment of relapsed or refractory Hodgkin’s lymphoma and for systemic anaplastic large cell lymphoma. This new drug is a product that combines a monoclonal antibody, called brentuximab and a antimitotic agent, called monomethyl auristatin (vedotin). The mechanism of action of this new drug consist in fact that this medication is targeting CD30 receptors, which are foundon  the tumor cells and then will release the toxic chemotherapeutic agent.

Brentuximab vedotin is indicated in patients with Hodgkin’s lymphoma, which has not progressed after they received an autologous stem cell transplant, and in patients who were ineligible for stem cell transplant, but who have failed at least 2 multiagent chemotherapy regimens. This new drug also may be used in patients with anaplastic large cell lymphoma who have failed at least 1 chemotherapy treatment.

The drug was study in clinical trials in which, brentuximab vedotin was administered intravenously at a dose of 1.8 mg/kg over the course of 30 minutes once every 3 weeks, in patients with Hodgkin’s lymphoma and anaplastic large cell.

Results from the first clinical trial showed that from a total number of 102 patients with Hodgkin’s lymphoma, 73% of patients with Hodgkin’s lymphoma achieved an objective response to brentuximab vedotin therapy, including 32% with complete remission and 40% of patients with Hodgkin’s lymphoma achieved partial remission. Average response duration was 6.7 months.

Hodgkin's lymphoma

Hodgkin’s lymphoma

Results from the second clinical trial showed that from a total number of 58 patients with anaplastic large cell lymphoma, 57% achieving complete remission and 29% a partial remission. Average response duration was 12.6 months.

Hodgkin’s lymphoma is a highly curable disease, but about 20% of patients become refractory or resistant to treatment and for this reason, the responses seen in refractory patients with Hodgkin lymphoma have been very impressive and the researchers predicted that will be seen better results if this drug will be used in patients with less advanced Hodgkin lymphoma, or if it be used in combination with others chemotherapy agents.

Most commonly side effects, that were reported about brentuximab vedotin therapy, with a incidence about 20%, included: neutropenia, peripheral sensory neuropathy, fatigue, nausea, anemia, upper respiratory tract infection, diarrhea, fever, rash, thrombocytopenia, cough and vomiting. In pregnant women, this drug may have teratogenic effect and can cause fetal harm. Also, caution is advised in patients who are receiving concomitant treatment with strong cytochrome P 450 isoenzyme 3A4 inhibitors.

However, the use of this new drug in patients with refractory Hodgkin lymphoma and in patients with anaplastic large cell lymphoma, might be just the beginning of a new treatment scheme and in the future it should be possible that the standard treatment for lymphomas should include brentuximab.

3425

TNF Inhibitors May Increase The Risk Of Developing Skin Cancer

Tumor necrosis factor inhibitors, like Etanercept (Enbrel) and Infliximab (Remicade), which are used in the treatment of rheumatoid arthritis, are increasing the risk for developing skin cancer, said a team of researchers.

A new study showed that the risk for developing skin cancer is about one third higher in patients with rheumatoid arthritis who are treated with tumor necrosis factor alpha (TNF) inhibitors than for patients with rheumatoid arthritis who are treated with disease-modifying antirheumatic drugs (DMARDs), like methotrexate or leflunomide.

TNF Alfa Inhibitor

TNF Alfa Inhibitor

The study was made on 20.648 patients diagnosed with rheumatoid arthritis. Some of this patients were treated with TNF-inhibitors and some of them with DMARDs. The incidence of skin cancer was 18.9/100 patients,in patients treated with TNF inhibitors and 12.7/100 patient, in patients treated with DMARDs. The risk for developing skin cancer was greater in male patients who were older and  had used in the past nonsteroidal anti-inflammatory drugs or glucocorticoids, or had others malignancies.

The researchers concluded that patients with rheumatoid arthritis who are treated with TNF-alpha inhibitors, may have a higher risk to develop skin cancer. This result should lead the rheumatology specialists to follow up the patients with rheumatoid arthritis who are treated with TNF inhibitors, for skin cancer and precancerous lesions, by sending them to a dermatologist for a complete skin exam, at least once a year.

This is an observational study and therefore may be over interpreted. Many studies, to date, on this subject showed that the risk of developing skin cancer is similar to the risk found in the general population. Although this new study shows a relationship between consumption of TNF inhibitors and skin cancer development, but the researchers dose not know if between this two entities exist a causal relationship. In the future, researchers hope to bring more information on this issue and if is necessary to introduce screening programs to prevent skin cancer in rheumatoid arthritis patients who are treated with TNF inhibitors.

10404

Migraine Symptoms, Causes, Treatment And Prevention

A migraine is defined as an intense head pain (headache), with a duration of 4 to 72 hours with a repetitive nature. A person who has migraines, can not perform normal daily activities . Although migraines are uncomfortable and interfere with the normal course of life, they do not cause long term damage. Migraines can be considered a disease and should be treated as such. It is important to be consulted by a specialist.

Migraine

Migraine

Causes

  • Familial aggregation (genetic transmission), has been shown for migraines. However it is not known exactly why some people are more prone to migraines than others
  • Expansion or narrowing of cerebral vessels (aneurysms, vascular stenosis ), which can cause intense headaches secondary to various chemical changes at this level (the chemical changes can cause inflammation, swelling and pain).

Symptoms

Symptoms of migraine may vary from case to case, often preceded by warning signs (the aura). Symptoms usually occur with typical aura about 30 minutes before the migraine attack itself and is characterized by headache that increases in intensity and with a degree of visual disturbances (the patient sees black spots or bright flashes). Other signs are a feeling of numbness or tingling in the arms, hands or face during the aura. However, most people do not have an aura before a migraine. These symptoms are :

– throbbing headache on one side of the skull;
– moderate to severe headache;
– increased headache along with routine physical activity;
– nausea, vomiting;
– sensitivity to light (photophobia) or audible stimuli, sometimes even to certain odors.

Evolution

A day or two before the migraine appears, the persons affected by these disease report different signs, marked fatigue, drowsiness, selective appetite for certain foods (for example  chocolate), irritability or anxiety.

“The Aura”

An alarming 30% of people who suffer from this disease, present before the migraine sets in, some warning signs, called “the aura”. The aura sings install in approximately 5-20 minutes and are characterized by the appearance of visual disturbances such as intense light flashes, black spots, feeling the distortion of images. Also, there may be sensory disturbances numbness, tingling in the hands, arms or face.
In rare cases the patient can not describe in words the sensations experienced.

Risk factors

  • Family history of migraine;
  • Sex :  women have an increased risk of developing migraine headaches three times higher than men;
  • Teens and young adults;
  • Diseases such as, depression, anxiety, depression, asthma or epilepsy.
Affect of Drugs

Affect of Drugs

Initial treatment

Acetaminophen (Paracetamol) or non-steroidal anti-inflammatory drugs  (Aspirin, Ibuprofen). Most experts recommend using NSAIDs, initially, before using other drugs that may have more side effects.

Main treatment

  • Serotonin receptor agonists (triptans) are drugs that are used when trying to reduce the headache quickly;
  • Ergotamine derivatives such as Cafergot, are also used to treat migraines but not as effective as triptans.

Drugs used to prevent migraine episodes

  • Beta-blockers that produce relaxation of vascular muscle;
  • Calcium channel blockers that reduce the narrowing of blood vessels;
  • Antidepressant medications, or tricyclic antidepressants like amitriptyline are also useful in preventing migraine episodes;
  • Anti-convulsive drugs such as topiramate has recently been approved as a pharmaceutical associations anti-migraine medication.

Prevention

Patients who suffer from this disease can achieve effective prevention by avoiding certain trigger factors, such as:

  • consumption of chocolate, mono-sodium glutamate, red wine and caffeine;
  • Sleep excess or insufficient sleep;
  • Irregular meals or no meals;
  • Weather and barometric changes (decrease or increase in atmospheric pressure);
  • Stress and intense emotions;
  • Strong odors or cigarette smoke;
  • Bright, intense light including reflection.

24766

Obesity – Risk Factors, Complications And Associated Diseases

Obesity is a disease characterized by weight gain due to adipose tissue and is defined by a value of body mass index (BMI) > 30 kg/m².

In clinical practice, assessing the weight status is made by weighing the patient and calculating the body mass index:

  • BMI = W / H² (W = weight, H = height).

According to BMI values, the World Health Organization classifies weight status as:

  • Underweight: BMI < 18.5 kg/m²;
  • Normal weight: BMI = 18.5 kg/m² – 24.9 kg/m² ;
  • Overweight: BMI = 25kg/m² – 29.9 kg/m²;
  • Obese: BMI > 30 kg/m².
Obesity

Obesity

Because BMI does not give indications on the distribution of adipose tissue in the body, the latter is assessed by measurement of some anthropometric parameters:

  • Abdominal circumference, it is correlated with abdominal fat mass. As waist circumference is greater, the higher the risk of cardiovascular morbidity and mortality is. Values of abdominal circumference greater than 94 cm in men and 80 cm in women, is the criterion required for defining the metabolic syndrome;
  • Waist-hip index represents the ratio of abdominal girth and pelvic girth;
  • Abdominal index represents the ratio of waist circumference and height (normal = 0.5).

The weight of a subject is related to the ideal weight and can be calculated by the Broca’s formula:

  • Ideal weight = Height (cm) – 100 (in men);
  • Ideal weight = Height (cm) – 105 (in women).

Obesity Risk Factors

Etiopathogenesis of obesity is not fully elucidated, but is believed to be multifactorial, the risk factors involved are:

  • genetic factor: studies on twins, adopted children and the familial studies support the role of genetic factors in the pathogenesis of obesity;
  • Age: although obesity may occur at any age, the risk increases with age;
  • Sex: women generally have a higher BMI then men;
  • Physiological circumstances: pregnancy, puberty, menopause, andropause;
  • Socio-economic conditions: obesity affects mostly the social groups with low economic possibilities and low cultural level;
  • Sedentary life;
  • Psychological factors: depression, psychological traumas;
  • Disturbance of eating behavior: hypercaloric diet, some jobs (chefs, confectioners). Food preferences, in particular, hiperlipidic food, have little effect on satiety, which favors the installation of obesity. Increased consumption of sweets promotes weight gain both by caloric intake, and by hyperinsulinemia and hypoglycemia, responsible for the increase of food intake. Rare and high-calorie meals can lead to the development of obesity;
  • Certain medicines: in the presence of genetic predisposition, antipsychotics (chlorpromazine, haloperidol), antidepressants (doxepin, lithium salts), antiepileptics (carbamazepine), beta blockers, corticosteroids, isoniazid, insulin, sulfonylureas, may encourage the development of obesity.
Obesity

Obesity

Obesity Pathogenesis

Obesity consists in the increase of total mass of adipose tissue, caused by hyperplasia or hypertrophy of adipocytes, which are overloaded with triglycerides.Normal adult body works after the first principle of thermodynamics, according to which energy intake is equal to energy of consumption. Increased energy intake and decreased energy consumption will lead to a surplus energy which will be stored in the body as fat.

In subjects prone to obesity and obese:

  • Adipocytes: these cells in obesity, have an increased volume and a greater number, have a higher turn-over of triglycerides and secrete an increased amount of leptin, resistin, proinflammatory cytokines, plasminogen activator inhibitor, angitensinogen. These substanete, in high concentrations increase the atherogenic and diabetogenic risk. Simultaneously, in the obese people is reduced secretion of adiponectin, a substance with a protective role against atherogenesis and type 2 diabetes mellitus;
  • Insulin: in general in obese, there is an increase insulin secretion, which stimulates hepatic synthesis of triglycerides and decreased HDL-cholesterol production;
  • Liver and skeletal muscle: in basal conditions, in people with obesity, the takeover of fatty acids by the liver and skeletal muscle is higher than in people with normal weight.

Morphopathology

In men with normal weight, body fat is 12% -20% of body weight, while in women is between 20% and 30%.

From the morphological point of view, obesity has two types:

  1. Hyperplasic obesity, characterized by an increased number of fat cells, which are maintaining their normal diameter. Clinic, this type of obesity has an early onset, before 18 years or before 20 years, and is usually gynoid and resistant to treatment;
  2. Hypertrophic obesity, characterized by hypertrophy of adipocytes, in the sense that the number of adipocytes is smaller, but fat cell diameter is larger than normal. Disposition is predominantly android, often begins in adulthood and is associated with diabetes mellitus, hyperlipidemia, hypertension and coronary artery disease.
  3. Mixed obesity, combines the characters of the two types of obesity above.
Obesity in Men vs. Women

Obesity in Men vs. Women

Obesity Classification

Etiopathogenic criteria:

  • Primary obesity: which includes most of the cases, it is a category that remains after the exclusion of secondary obesity and particular obesity;
  • Secondary obesity: endocrine (hypothyroidism, Cushing’s syndrome, male hypogonadism, polycystic ovary syndrome in women, growth hormone deficiency), tumors or other lesions involving the hypothalamic areas of appetite control.

Clinical criteria:

  • Android obesity, characterized by waist-hip index > 0.85 in women and > 0.95 in men and the abdominal index > 0.5. Adipose tissue accumulation occurs predominantly in the upper half of the body. These patients have hyperinsulinemia, diabetes mellitus, dyslipidemia, hyperuricemia, coronary artery disease, hypertension. This type of obesity is hypertrophic, and the treatment offers slightly better results;
  • Gynoid obesity, characterized by waist-hip index <0.85 in women and <0.95 in men and the abdominal index <0.5. Adipose tissue accumulation occurs predominantly in the lower half of the body (pelvis, thigh). It is associated with varicose veins and arthritis. This type of obesity is hyperplasic and resistant to treatment.

Severity criterion:

According to BMI, obesity has three grades:

  • Grade I: BMI = 30 kg / m² – 34.9 kg / m²;
  • Grade II: BMI = 35 kg / m² – 39.9 kg / m²;
  • Grade III: BMI > 40 kg / m².

Obesity evolutive criteria:

  • Dynamic obesity, represents the growth phase, weight gain phase or accumulation phase;
  • Static obesity, when the maximum weight is reached.
Obesity Evolutive Criteria

Obesity Evolutive Criteria

Obesity Complications And Associated Diseases

Among pathological states associated with obesity, some may be considered complications and other related diseases.

Cardiovascular complications:

Obesity, particularly the android is associated with increased cardiovascular risk, due to atherosclerosis. This risk grows with the increasing of BMI and waist circumference.

  • Hypertension, the disease often associated with obesity, increases the cardiovascular risk. Weight loss will reduce blood pressure, independent of other factors;
  • Atherosclerosis, the most severe manifestation beeing the coronary manifestation (coronary artery disease) and the cerebral manifestation (cerebral vascular accident or stroke);
  • Heart failure, due to coronary disease. This pathology associated,aggravates the significance of obesity.

Obesity metabolic complications:

Obesity, in particular the abdominal one is associated with insulin resistance and hyperinsulinemia.

  • Diabetes mellitus type 2: association of type 2 diabetes and obesity is known, because of insulin resistance and hyperinsulinemia. 80% of patients with type 2 diabetes are overweight or obese;
  • Dyslipidemia: obesity is associated with a series of plasma lipid abnormalities, including hypertriglyceridemia, low HDL-cholesterol levels and increased LDL-cholesterol and VLDL-coloesterol levels, which have atherogenic potential;
  • Hyperuricemia;
  • Metabolic syndrome.

Digestive complications:

Respiratory complications:

  • Mixed ventilatory dysfunction, predominantly restrictive, evolving to respiratory failure;
  • Pickwick syndrome, characterized by extreme obesity, intense daytime somnolence, hypoxemia, hypercapnia, cyanosis, and right ventricular dilatation with the picture of decompensated chronic cor pulmonale;
  • Sleep apnea, manifested by periods of apnea more than 10 seconds during sleep, often associated with cardiac arrhythmias.

Osteoarticular complications:

  • Arthrosis in the major joints of the lower limbs and spine.

Venous circulatory disorders:

Oncological diseases:

Genitourinary complications:

Psychiatric complications:

Skin complications:

  • Bacterial infections;
  • Fungal infections.

Obesity Evolution And Prognosis

Obesity Evolution And Prognosis

Obesity Evolution And Prognosis

Obesity has a progressive evolution (dynamic phase), as long as there is a surplus of energy. At one point, the patient is no longer gaining weight (static phase), because in most cases, when  maximum weight is achieved, the appetite is reduced. Regression to the ideal weight is possible especially in patients with android, moderate overweight. This is achieved by changing eating habits, exercise and if is necessary medical treatment and surgery. Obesity is a disease with poor prognosis, associated morbidity and mortality are correlated with the level of weight excess.

4632

Gastrodudenal Ulcer

Gastroduodenal ulcer is a common disorder of the stomach and duodenum (first portion of the small intestine) characterized by the ulcerated  mucosa of the stomach lining and that can penetrate into surrounding organs (pancreas frequently, hepatic pedicle) and in some cases even erode blood vessels giving all sorts of bleeding complications.

Symptoms

Ulcer disease manifestations are:

  • Pain and burning in the epigastric and right upper abdominal wall  ( in the chest )
  • Loss of appetite
  • Vomiting
  • Weight loss
  • Fatigue

In most cases peptic ulcer disease is also caused by Helicobacter pylori, a germ of the gastric and duodenal mucosa.

Causes

During treatments with anti-inflammatory drugs (NSAIDs), especially long term usage can lead to secondary gastroduodenal ulcer.

Commonly used NSAIDs include:

  • Aspirin
  • Ibuprofen
  • Phenylbutazone
  • Naproxen

Under normal circumstances the stomach has several defense mechanisms that protect it from  harmful effect of drugs, acidity and other pathogen agents.

NSAIDs can overcome any defense mechanisms and cause ulceration of the stomach lining.  In most cases the disease is non-symptomatic and complications are responsible for sending the patient to the hospital : upper gastrointestinal bleeding, ulcers in acute flare with intense pain, ulcer perforation with generalized peritonitis.
If a patient is diagnosed with gastroduodenal ulcer, anti-inflammatory treatment should be interrupted immediately.

NSAIDs

NSAIDs

Treatment

For wound healing and ulcer symptoms relief the patient will be treated with:

  • antacids to neutralize acid secretion
  • anti-secretory drugs (proton pump inhibitors or H2 receptor antagonists) to reduce acid secretion.
  • other classes of anti-ulcer drugs that have the effect of forming a protective film on the gastric mucosa, stimulating wound healing for example bismuth based drugs.
    In patients with ulcers that have an infection with Helicobacter pylori the treatment plan will contain antibiotics.
Gastroduodenal Ulcer

Gastroduodenal Ulcer

Surgery may be necessary when common forms of treatment are not satisfactory and overcomed or other complication occur like bleeding, perforation, pyloric stenosis. Any patient treated with NSAIDs, who accuses any symptoms of the gastroduodenal tract, must be consulted by a physician and appropriate therapy should be instituted imediately to prevent further serious complications

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