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Why Does Metabolic Acidosis Cause Abdominal Pain

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

What Is The Origin/mechanism Of Abdominal Pain In Diabetic Ketoacidosis?

What Is The Origin/mechanism Of Abdominal Pain In Diabetic Ketoacidosis?

Other than all papers I could find citing the depth of the keto-acidosis (and not the height of the blood glucose levels) correlating with abdominal pain, nothing else to explain how these two are linked. Decades ago, I was taught that because of the keto-acidosis causing a shift of intracellular potassium (having been exchanged for H+ protons of which in keto-acidosis there were too many of in the extracellular fluid) to the extracellular, so also the blood compartment, resulting in hyperkalemia, paralyzing the stomach, which could become grossly dilated - that’s why we often put in a nasogastric drainage tube to prevent vomiting and aspiration - and thus cause “stomach pain”. This stomach pain in the majority of cases indeed went away after the keto-acidosis was treated and serum electrolyte levels normalized. In one patient it didn’t, she remained very, very metabolically acidotic, while blood glucose levels normalized, later we found her to have a massive and fatal intestinal infarction as the underlying reason for her keto-acidosis….. Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body.Due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney metabolic acidosis leads to acidemia(blood pH is low (less than 7.35). Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia.Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In acute renal failure organic acid retention causes a fall in plasma bicarbonate by 1-2 mEq / L / day. In chronic renal failure acidosis primarily due to inability of the kidneys to form ammonia. Some compensation is achieved by buffering of acid anions by phosphates released from bones. In diarrohoeas like cholera stool bicarbonate loss may be 60 mEq/ L of stool. Causes of metabolic acidosis Normal Anion Gap Increased Anion Gap I Bicarbonate loss Proximal RTA,diarrhoea,Carbonic anhydrase inhibitorsPrimary hyperparathyroidism. Reduced renal excretion,Renal, failure, acute and Chronic. II Failure of Bicarbonate Regeneration Hypereninemic Hyperaldosteronism Potassium sparing diuretics. Accumulaiton of Organic acid, Lactic Acidosis, Keto-acidosis diabetic, alcoholic, starvation, infection, salicylates, ethylenglycol, Methanol. III Acidifying Salts :Ammonium ChlorideIysine hydrocholoride, agginineHydrocholoride. Undefined source :Methylmalonic aciduria, Bketolase deficiency. IV Latrogenic : Rapid hydration. Signs and Symptoms of metabolic acidosis Symptoms are not specific,Symptoms may include chest pain, palpitations, headache Continue reading >>

Metabolic Acidosis: Causes, Symptoms, Diagnosis, Treatment, Prognosis, Prevention

Metabolic Acidosis: Causes, Symptoms, Diagnosis, Treatment, Prognosis, Prevention

Acidosis- A medical condition in which the fluids present in the body start to develop increased amount of acidic content making the body fluids acidic. There are two types of Acidosis- Respiratory Acidosis and Metabolic Acidosis. Respiratory Acidosis occurs as a result of malfunction of lungs. Metabolic Acidosis occurs as a result of malfunction of the kidneys. In this article, we will look into about Metabolic Acidosis. We will look into the causes, diagnosis, and treatment of Metabolic Acidosis. As stated, Metabolic Acidosis is a medical disorder in which the body starts producing excessive amounts of acid and/or the kidneys are not able to remove enough acidic content from the body. If not corrected at the appropriate time, Metabolic Acidosis can lead to a medical condition called acidemia in which pH scale in the blood gets low as a result of the kidneys being unable to form bicarbonates in the body. Causes Of Metabolic Acidosis The amount of acid in the blood can is determined by measuring the pH. A lower value of the pH means that the blood is acidic and a higher value of pH means that rhe blood is basic. Ideal pH value in the blood should be around 7.5. There are many processes in an individual's body which produces acid. Usually, the lungs and the kidneys take care of the excess production of acid; however, if there is a malfunction of these organs it results in Acidosis. As stated, Metabolic Acidosis begins in the kidneys. It develops when the kidneys are not able to discard excessive acid or in cases when they discard too much basic content from the body. Metabolic Acidosis is of three types: Diabetic Acidosis: This occurs in poorly controlled diabetes patients. In this form, there is formation of excess ketones making the blood acidic. Hyperchloremic Acidosi Continue reading >>

Chronic Metabolic Acidosis Destroys Pancreas

Chronic Metabolic Acidosis Destroys Pancreas

Peter Melamed and Felix Melamed Biotherapy Clinic of San Francisco, USA *Corresponding Author: Biotherapy Clinic of San Francisco 2215 Post Street, Suite 1, San Francisco, CA 94115, USA Phone 1 415 3776643 Fax 1 415 4093909 [email protected] Visit for more related articles at JOP. Journal of the Pancreas Abstract One primary reason for the current epidemic of digestive disorders might be chronic metabolic acidosis, which is extremely common in the modern population. Chronic metabolic acidosis primarily affects two alkaline digestive glands, the liver, and the pancreas, which produce alkaline bile and pancreatic juice with a large amount of bicarbonate. Even small acidic alterations in the bile and pancreatic juice pH can lead to serious biochemical/biomechanical changes. The pancreatic digestive enzymes require an alkaline milieu for proper function, and lowering the pH disables their activity. It can be the primary cause of indigestion. Acidification of the pancreatic juice decreases its antimicrobial activity, which can lead to intestinal dysbiosis. Lowering the pH of the pancreatic juice can cause premature activation of the proteases inside the pancreas with the potential development of pancreatitis.The acidification of bile causes precipitation of the bile acids, which irritate the entire biliary system and create bile stone formation. Aggressive mixture of the acidic bile and the pancreatic juice can cause erratic contractions of the duodenum’s walls and subsequent bile reflux into the stomach and the esophagus. Normal exocrine pancreatic function is the core of proper digestion. Currently, there is no effective and safe treatment for enhancing the exocrine pancreatic function. Restoring normal acid-base homeostasis can be a useful toolfor pathophysi Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia. The precipitating factors, clinical features, evaluation, and diagnosis of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, and treatment of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr Continue reading >>

Acidosis: The Kiss Of Death!

Acidosis: The Kiss Of Death!

WHAT CAUSES A CONDITION CALLED "ACIDOSIS"? WHAT IS ACIDOSIS? Acidosis Definition: Acidosis is an increased acidity in the blood and other body tissue. Acidosis is said to occur when arterial pH falls below 7.35. The pH level of our blood affects every cell in our body. Chronic acidosis corrodes body tissue, and if left unchecked, will interrupt all cellular activities and functions. WHAT CAUSES ACIDOSIS? HIGH ACID-FORMING FOODS and DIETS all lead to ACIDOSIS. Living a fast-paced daily lifestyle, such as eating on the run and excessive over stimulation, will lead people to face a constant symptoms of indigestion and growing endangerment of over-acidification (Acidosis) of the body cells, which will interrupt cellular activities and functions. It is a major root of sickness and disease. Having our cells constantly exposed to an acidic environment leads to acidosis and then chronic acidosis and finally various forms of disease such as cancer and many more! Studies have shown that an acidic, anaerobic (which is also the lack of oxygen) body environment encourages the breeding of fungus, mold, bacteria, and viruses. As a result, our inner biological terrain shifts from a healthy oxygenated, alkaline environment to an unhealthy acidic one (acidic pH scale). This forces the body to constantly deplete its cellular energy to neutralize and detoxify these acids before they can act as poisons in and around the cells, ultimately changing the environment of each cell and finally compromising its immune system leaving it vulnerable to the ravages of disease to take a foothold in the body. When our body pH becomes overly acidic, it starts to set up defense mechanisms to keep the damaging acids from entering the vital organs. Modern Day Athletes and Acid-Forming Foods Unfortunately, Mo Continue reading >>

The Evaluation Of Acute Abdominal Pain In The Elderly Patient

The Evaluation Of Acute Abdominal Pain In The Elderly Patient

Abstract Obstetrician/Gynecologists frequently encounter older patients complaining of acute abdominal pain. Because of physiologic changes, medication use, and preexisting conditions, the elderly patient often does not manifest overt signs of disease. Also, while appendicitis is the most common cause of abdominal pain in the general population, biliary disease, small bowel obstruction and perforated viscus constitute the leading etiologies in the geriatric population. The older patient's physical findings often do not correlate with the severity of disease; however, mental status changes, hypothermia, bandemia, and metabolic acidosis are helpful indicators of significant derangement. Emergent abdominal pain, defined as hemodynamic instability such as that caused by massive hemorrhage, requires immediate surgery. Otherwise, the most effective work-up includes a detailed history and physical examination, and selective screening laboratory tests. When the diagnosis is still unclear, repeat physical examination, in-patient observation, and consultation should be considered. The decision of whether to perform diagnostic laparoscopy or laparotomy should be individualized after assessing the patient's entire clinical presentation and progress. Acute abdominal pain in the older patient is associated with low diagnostic accuracy, but high mortality. Therefore, as a primary care physician, the obstetrician/gynecologist must be proficient in the evaluation of acute abdominal pain in the elderly patient. Continue reading >>

Metabolic Acidosis; Gap Positive

Metabolic Acidosis; Gap Positive

Metabolic acidosis is defined by low serum pH (less than 7.35-7.45) and low serum bicarbonate. It occurs by one of three major mechanisms: 1. Increased endogenous acid (i.e., lactic acidosis, diabetic ketoacidosis). 2. Decreased renal acid excretion (i.e., renal failure). In determining the underlying etiology for a metabolic acidosis, the serum anion gap must be calculated by subtracting the major measured anions (chloride and bicarbonate) from the major measured cation (sodium). If the result is greater than 12 meq/L (which is the normal value for most laboratories), the acidosis is said to be an anion gap acidosis. The expected anion gap should is lower in hypoalbuminemia and should be corrected - for each decrease of 1gm/dl in albumin, the normal anion gap should be decreased by approximately 2.5 meq/L. A. What is the differential diagnosis for this problem? Anion gap acidosis can be the result from: 1. A fall in unmeasured cations (as seen in hypomagnesemia or hypocalcemia). The most common reasons for a rise in anions are ingestions, lactic acidosis, ketoacidosis and renal failure. Ingestions of multiple different toxins can result in unmeasured anions causing a metabolic gap acidosis. Most commonly salicylate and the alcohols (methanol and ethylene glycol) can lead to severe acidosis. The inhalant toluene may also be a culprit. Lactic acidosis is the most common cause of an elevated anion gap acidosis in hospitalized patients, occurring with decreased perfusion causing relative tissue ischemia. This leads to increased lactic acid production and impaired renal excretion with resultant acid accumulation (Type A lactic acidosis). Type B lactic acidosis occurs in patients without overt tissue and can be seen in diabetics on metformin, patients with hematologic and s Continue reading >>

Lactic Acidosis: What You Need To Know

Lactic Acidosis: What You Need To Know

Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>

Primary Hyperlipidemia, Acute Pancreatitis And Ketoacidosis In An Adolescent With Type 2 Diabetes

Primary Hyperlipidemia, Acute Pancreatitis And Ketoacidosis In An Adolescent With Type 2 Diabetes

Krisztina Lukacs1,2*, Laszlo Jozsef Barkai1, Nora Hosszufalusi1, Eva Palik1, Attila J Szabo2 and Laszlo Madacsy2 13rd Department of Medicine, Semmelweis University, 1125 Budapest, Hungary 21st Department of Pediatrics, Semmelweis University, 1083 Budapest, Hungary Citation: Lukacs K, Barkai LJ, Hosszufalusi N, Palik E, Szabo AJ, et al. (2016) Primary Hyperlipidemia, Acute Pancreatitis and ketoacidosis in an Adolescent with Type 2 Diabetes. J Diabetes Metab 7:651. doi:10.4172/2155-6156.1000651 Copyright: © 2016 Lukacs K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract A case is presented of a 15-year-old boy with a past medical history of hyperlipidemia and hypertension. He attended the emergency department with a 3-day history of vomiting, acute abdominal pain, and altered mental status. Laboratory data on admission revealed metabolic acidosis (pH: 7.12, BE: -20.8 mmol/L), high blood glucose level (32.1 mmol/L) and significant hyperlipidemia (cholesterol: 16.3 mmol/L, triglycerides: 21.1 mmol/L). Treatment with electrolytes and volume replacement and intravenous insulin successfully resolved the ketoacidosis, but the abdominal pain and hyperlipidemia remained. Abdominal US and CT scan showed severe necrotizing pancreatitis with a pseudocyst. The laboratory studies showed a Frederickson type V pattern hyperlipidemia. HbA1c was 14.3% (133 mmol/mol), indicating the presence of chronic glucose elevation. Based on the lack of islet cell antibodies and the normal fasting serum C-peptide level, type 2 diabete Continue reading >>

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