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Prednisolone is used for treating allergies, arthritis, breathing problems (eg, asthma), certain blood disorders, collagen diseases (eg, lupus), certain eye diseases (eg, keratitis), cancer (eg, leukemia), endocrine problems (eg, adrenocortical insufficiency), intestinal problems (eg, ulcerative colitis), swelling due to certain conditions, or skin conditions (eg, psoriasis).

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Prednisolone (Cortan) as known as: Adelcort, Adelone, Aersolin d, Ak-pred, Alertine, Alpicort, Apicort, Aprednislon, Bisuo a, Blephamide, Bronal, Capsoid, Cetapred, Chloramphecort-h, Compesolon, Cor tyzine, Corotrope, Cortan, Cortico-sol, Cortisal, Cortisol, Danalone, Decortin h, Delta-cortef, Deltacortenesol, Deltacortril, Deltahydrocortisone, Deltapred, Deltastab, Dermol, Dermosolon, Deturgylone, Dhasolone, Di-adreson-f, Dojilon, Dontisolon, Econopred, Emsolone, Encortolon, Estilsona, Fenicort, Fisiopred, Fisopred, Flo-pred, Frisolona forte, Glucortin, Gupisone, Hefasolon, Hexacorton, Hexy-solupred, Hydrocortancyl, Hydrocortidelt, Infectocortikrupp, Inflanefran, Inflanegent, Insolone, Intalsolone, Key-pred, Klismacort, Kohakusanin, Lenisolone, Lepicortinolo, Lidomex kowa, Linola-h n, Locaseptil-neo, Lygal, Mecortolon, Mediasolone, Medopred, Meprisolon, Metacortandralone, Meti-derm, Meticortelone, Minisolone, Nurisolon, Ocupred, Oftalmol, Omnipred, Ophtapred, Optipred, Optival, Orapred, Orapred odt, Panafcortelone, Paracortol, Parisilon, Pediacort, Pediapred, Pednisol, Precodil, Precortalon aquosum, Pred-clysma, Predacort, Predalone, Predate s, Predcor, Predenema, Predfoam, Predicort, Predinga, Predlone, Predmix, Prednefrin, Prednesol, Predni, Predni h tablinen, Predni-pos, Prednicortil, Prednigalen, Prednihexal, Predniliderm, Predniocil, Prednip, Prednis, Prednisolon caproate, Prednisolona, Prednisolonacetat, Prednisolonpivalat, Prednisolonum, Prednisolut, Prednizolons, Predohan, Predonema, Predonine, Predsim, Predsol, Predsolets, Preflam, Prelon, Prelone, Premandol, Prenin, Prenolone, Preson, Prezolon, Rectopred, Redipred, Riemser, Scheriproct, Scherisolona, Sintisone, Solone, Solpren, Solu-dacortina, Solu-decortin, Soluble prednisolone, Solupred, Sopacortelone, Sophipren, Spirazon, Spiricort, Sterolone, Ultracortenol, Vasocidin, Walesolone, Wysolone, Youmeton

Deltasone - drug review: dosage, side effects, action, buy Deltasone

Deltasone Deltasone review

Deltasone is a brand name for the drug predisone, in the steroid classification of drugs. It is used to reduce swelling. but also lowers the immune system. It comes in tablets and is prescribed for several different problems. These can include endocrine disorders when the body does not produce enough of its own prednisone. rheumatic disorders such as arthritis. collagen diseases, dermatologic diseases such as severe psoriasis. allergies. ophthalmic disorders, respiratory disorders, hematologic disorders, neoplastic diseases, edematous states, gastrointestinal diseases such as ulcerative colitis. asthma. lupus, and nervous system disorders, especially those associated with flare-ups of multiple sclerosis.

Some of the side effects of Deltasone include fluid retention, congestive heart failure. loss of potassium, insomnia. nausea or vomiting. dizziness. fatigue, joint pain. increased hunger or thirst, high blood pressure. muscle weakness, loss of muscle mass, rupturing tendons, peptic ulcer. pancreatitis, abdominal distention, fragility of skin, increase sweating, convulsions, vertigo. menstrual irregularities, glaucoma. or headache. Other side effects may include salt and water retention, and lowered immune system effectiveness for some people. Some people may also experience an allergic reaction to Deltasone; this is rare, but contact your doctor or go to the emergency room if you experience difficulty breathing, swelling of the throat, face, lips. or tongue. or hives. sudden weight gain, severe headache, or blurred vision. Other conditions are rare but can be more frequent with higher doses of Deltasone, such as acne. increased hair growth, cataracts, roundness of the face, or behavior or mood changes.

As with all steroids, it is very important not to stop taking prednisone suddenly. Your doctor will prescribe your Deltasone in such a way that you reduce your dosage gradually before finally ending treatment. Deltasone should be taken with food or milk so that it does not upset your stomach. You should not take other medications while taking Deltasone unless you have first discussed them with your doctor. This includes herbal and natural treatments, as well as other prescriptions.

There are some people who should not take Deltasone, or who should take special precautions if they do. You should not take it if you have a serious bacterial, viral, or fungal infection. since Deltasone can weaken your body’s ability to fight these infections. You should also discuss it with your doctor if you have kidney disease, liver disease, high blood pressure or heart disease, ulcerative colitis, diverticulitis. stomach ulcers. hypothyroidism, a psychiatric condition, osteoporosis. myasthenia gravis (or muscle weakness), diabetes mellitus, or any other medical conditions. These conditions may require an adjusted dosage of Deltasone.

No studies have been done to determine whether Deltasone is safe for use by pregnant women, so extreme caution should be used in prescribing this or any steroid for someone who is pregnant. The benefits of Deltasone treatment should be weighed against any possible harm to the developing fetus. This is also true if you are nursing a baby, since it is known that Deltasone passes into breast milk. Of you are pregnant or nursing and do take Deltasone, your child should be monitored carefully for signs of hypoadrenalism.

Deltasone has the following structural formula:

• Molecular formula of deltasone is C21H26O5
• Chemical IUPAC Name is 17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-7,8,9,10,12,13,14,15,16,17- decahydro-6H-cyclopenta[a]phenanthrene-3,11-dione
• Molecular weight is 358.428 g/mol
Deltasone available. 1mg tablets, 2.5mg tablets, 5mg tablets, 10mg tablets, 20mg tablets, 50mg tablets

Generic name:Prednisone

Brand name(s): Adasone, Ancortone, Betapar, Bicortone, Cartancyl, Colisone, Cortab, Cortan, Cortancyl, Cortidelt, Cotone, Dacorten, Dacortin, Decortancyl, Decortin, Decortisyl, Dehydrocortisone, Dekortin, Delcortin, Dellacort, Deltacortene, Deltacortisone, Deltacortone, Deltison, Deltisona, Deltisone, Deltra, Diadreson, Econosone, Encorton, Encortone, Enkorton, Fernisone, Fiasone, Hostacortin, Incocortyl, Juvason, Lisacort, Metacortandracin, Meticorten, Nisona, Nizon, Novoprednisone, Nurison, Orasone, Panafcort, Panasol, Paracort, Parmenison, Pehacort, Precort, Predeltin, Prednicorm, Prednicort, Prednicot, Prednidib, Prednilonga, Prednison, Prednisona, Prednisonum, Prednitone, Prednizon, Prednovister, Presone, Pronison, Rectodelt, Reserpine, Retrocortine, Servisone, Sone, Sterapred, Sterolin Liq, Supercortil, Ultracorten, Ultracortene, Winpred, Wojtab, Zenadrid

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Prednisone Dosage

Prednisone Dosage

Glucocorticosteroids like prednisone, are important components of the treatment regimen for certain inflammatory and autoimmune diseases. The current article gives a brief overview of prednisone dosage in the context of certain crucial conditions and diseases.

Prednisone is a type of glucocorticoid prodrug, and serves as an anti-inflammatory and immunosuppressive agent. It forms a part of the treatment for certain allergic conditions, rheumatoid arthritis, pulmonary tuberculosis, lupus, multiple sclerosis, and adrenal insufficiency diseases like Addison's disease. Recent research has shown that apart from its ability to reduce fatigue, pain and swelling in the joints, it also slows down the damage of affected joints.

In the past, corticosteroids, simply referred to a 'steroids,' were considered to be miracle drugs. This was due to the results of study conducted in 1948, wherein a group of patients suffering from arthritis were given corticosteroid injections daily. The improvement in their condition was so spectacular, that people believed a cure for arthritis had been found. However, as corticosteroid usage became widespread over the years, and its side effects began emerging, it became clear that high doses of corticosteroids taken over prolonged periods of time had many disadvantages. As a result, physicians began prescribing the drug more conservatively, and many people with arthritis were so scared that they often refused to be treated with it.

Prednisone, the brand names of which include, Deltasone, Cortan, Meticorten, Liquid Pred, Panasol-S, Orasone, Sterapred, and Prednicen-M, is a corticosteroid that is most commonly prescribed for treating arthritis. This drug is 4-5 times more potent than cortisol. 5 mg or prednisone is equivalent to the amount of cortisol produced by the body in one day.

The range for prednisone dosage in adults is 5 to 60 mg per day. Generally, prednisone treatment begins with a high dose which is gradually reduced over a period of few weeks. The treatment is then stopped or continued as a low-dose therapy, depending on the individual case. The generally recommended, adult and pediatric doses for certain diseases and conditions have been summarized below.

2 mg/kg (tapered over 4-8 weeks)

Prednisone may also be prescribed to individuals who need to undergo imaging techniques, like CT scan, that involve the use of intravenous dyes. Prednisone is generally prescribed in three doses, with the first dose being prescribed 24 hours before administration of the intravenous dye. The objective behind such a dosage is to prevent the occurrence of any allergic reaction to the dye.

Note: The precise dosage depends on the condition to be treated, its etiology, as well as other factors like age, weight, severity of symptoms, and medical history of the patient.

While it is not clear if a daily dose of 3 mg has any clinically significant toxic effects, it is known that a daily intake of more than 5 mg may increase the risk of cataracts, osteoporosis. Higher doses may even lead to decreased wound healing capacity and increased susceptibility to infections due to suppression of immune system.

Corticosteroids and Cortisol

Corticosteroids are actually drugs that are related to cortisol, which is a hormone synthesized naturally in the body by the adrenal cortex. Cortisol helps to control the balance of salt and water in the body, and regulates the metabolism of proteins, fats, and carbohydrates.

Cortisol is also produced by the body to deal with stress. When a stressful condition occurs, the pituitary gland, which is located at the brain's base, releases adrenocorticotropic hormone (ACTH) which, in turn stimulates the adrenal glands to secrete cortisol. This extra dose of cortisol helps the body to cope with daily stress, as well as more stressful conditions like emotional problems, surgery, trauma, or infection. When there is an end to the stressful condition, the secretion of the hormone gets back to normal.

The adrenal glands normally secrete about 20 mg of cortisol in a day, usually during the morning hours, but they can secrete five times more if required.

How do Glucocorticosteroids Work?

Glucocorticosteroids function by binding to a protein receptor called Glucocorticoid Receptor (GR), which is present in the cytosol of many cells. Through this receptor, glucocorticoids activate the anti-inflammatory genes leading to a suppression of the inflammatory response, and alleviation of the inflammatory symptoms. It also suppresses cell-mediated immunity and other vital processes of the immune system. This renders the patient more susceptible to infections.

Many patients suffering from arthritis and autoimmune hepatitis are prescribed with a long term dose of prednisone. However, it is essential for the concerned medical expert to compare the beneficial effects of this drug along with its side effects. In addition, it is also advisable to evaluate the alternative treatment options, in order to ensure an optimum and safe treatment.

Disclaimer: This Buzzle article is for informative purposes only, and should not be used as a substitute for professional medical advice.

Last Updated: February 6, 2013

Haemoglobinopathies thalassemia, prophyrias and sickle cell disease

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Cuts, Scrapes and Puncture Wounds: Read About Treatment

Cuts, Scrapes (Abrasions), and Puncture Wounds

John P. Cunha, DO, FACOEP

John P. Cunha, DO, is a U.S. board-certified Emergency Medicine Physician. Dr. Cunha's educational background includes a BS in Biology from Rutgers, the State University of New Jersey, and a DO from the Kansas City University of Medicine and Biosciences in Kansas City, MO. He completed residency training in Emergency Medicine at Newark Beth Israel Medical Center in Newark, New Jersey.

William C. Shiel Jr. MD, FACP, FACR

Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.

  • First Aid Sprains & Strains Slideshow
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Quick Guide First Aid Pictures Slideshow: Caring for Wounds

Cuts, scrapes (abrasions), and puncture wounds facts
  • Washing a cut or scrape with soap, and water and keeping it clean and dry is all that is required to care for most wounds.
  • Cleaning the wound with hydrogen peroxide and iodine is acceptable initially, but can delay healing and should be avoided long-term.
  • Apply antibiotic ointment and keep the wound covered.
  • Seek medical care within 6 hours if the bleeding does not stop, as the wound might need stitches .
  • A delay can increase the rate of wound infection.
  • Any puncture wound through tennis shoes or sneakers has a high risk of infection and should be seen by a doctor.
  • Any redness, swelling, increased pain. fever. red streaking, or pus draining from the wound may indicate an infection that requires medical care.
What is the best first aid for a cut or scrape?

The first step in the care of cuts, scrapes (abrasions) is to stop the bleeding. Most wounds respond to direct pressure with a clean cloth or bandage. Hold the pressure continuously for approximately 10 to 20 minutes. If this fails to stop the bleeding or if bleeding is rapid, seek medical assistance.

Next, thoroughly clean the wound with soap and water. Remove any foreign material in the wound, such as dirt, or bits of grass, which may lead to infection. Tweezers can be used (clean them with alcohol first) to remove foreign material from the wound edges, but do not dig into the wound as this may push bacteria deeper into the wound or injure subcutaneous (under the skin) structures. The wound may also be gently scrubbed with a washcloth to remove dirt and debris. Hydrogen peroxide and povidone-iodine (Betadine) products may be used to clean the wound initially, but may inhibit wound healing if used long-term.

Cover the area with a bandage (such as gauze or a Band-Aid) to help prevent infection and dirt from getting in the wound. A first aid antibiotic ointment (Bacitracin, Neosporin. Polysporin) can be applied to help prevent infection and keep the wound moist.

Continued care to the wound is also important. Three times a day, wash the area gently with soap and water, apply an antibiotic ointment, and re-cover with a bandage. Change the bandage immediately if it gets dirty or wet.

Medically Reviewed by a Doctor on 2/10/2015

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  • UPDATE 1-WHO halves sugar intake advice to 5 percent of daily intake

    UPDATE 1-WHO halves sugar intake advice to 5 percent of daily intake

    * Draft guideline suggests adult limit of 6 teaspoons a day

    * Poor diets linked to obesity, tooth decay, chronic disease

    * WHO expert "more intense action" needed on sugary drinks (Adds quotes, details from press briefing)

    By Kate Kelland, Health and Science Correspondent

    LONDON, March 5 (Reuters) - Adults should eat less than the equivalent of 6 teaspoons of sugar a day if they are to avoid health risks such as weight gain and tooth decay linked to sugary diets, the World Health Organisation said on Wednesday.

    Issuing draft guidelines calling for a new sugar limit of less than 5.0 percent of daily energy intake, the United Nations health agency said its recommendations were based on "the totality of evidence regarding the relationship between free sugars intake and body weight and dental caries".

    "Obesity now affects half a billion people in the world, and it is on the rise in all age groups and particularly in low- and middle-income countries," said Francesco Branca, the WHO's director of nutrition for health and development, adding that free sugars were a key culprit in that epidemic.

    Free sugars include monosaccharides and disaccharides that are added to foods by manufacturers, cooks or consumers, and sugars naturally present in honey, syrups, fruit juices and fruit concentrates.

    Five percent of total energy intake is equivalent to around 25 grams - or around 6 teaspoons - of sugar a day for a normal weight adult.

    "WHO recommends reduced intake of free sugars throughout the life-course," the agency said in a statement.

    It said the 5.0 percent level should be a target for people to aim for - calling it a "conditional recommendation" - but also reiterated a "strong recommendation" that sugar should account for no more that 10 percent of total energy intake.

    "There is increasing concern that consumption of free sugars - particularly in the form of sugar-sweetened beverages - increases overall energy intake and may reduce the intake of foods containing more nutritionally adequate calories," it said.

    This can lead "to an unhealthy diet, weight gain and increased risk of non-communicable diseases (such as heart disease, diabetes and cancer)."

    Non-communicable, or chronic, diseases are the world's leading causes of ill health and death, killing more than 36 million a year with more than 90 percent of these premature deaths in poorer countries.

    Asked whether he would characterise sugar as "the new tobacco" in terms of its threat to public health if consumption levels are not reduced, Branca said sugar was one key risk factor which, combined with others like fat, salt and lack of exercise, could be compared to smoking.

    Research published last month in the journal JAMA Internal Medicine suggested the risk of dying of heart disease is higher among people who eat a larger percentage of their calories from added sugars. And the risk was also higher for people who had seven or more sweetened drinks a day.

    "The consumption of sugar-sweetened beverages has to be done with great care - particularly in children," Branca said. "This is an area where more intense action needs to be taken."

    Branca acknowledged the new guidelines "may not be popular amongst sugar producers" but said the WHO would resist any unjustified pressure or lobbying from the food and sugar industries to change them.

    "If pressure comes on the organisation we are very well equipped to deal with (it)," he said. "I don't anticipate any problem in that regard." (Reporting by Kate Kelland, editing by Ralph Boulton)

    Oral involvement in a case of AA amyloidosis: a case report

    Oral involvement in a case of AA amyloidosis: a case report Introduction

    Deposition of amyloid fibrils derived from circulating acute-phase reactant serum amyloid A protein causes systemic amyloidosis, a serious inflammatory disorder. We document a male patient who developed reactive amyloidosis (AA type), most likely secondary to his long standing periodontitis.

    Case presentation

    A 67-year-old Turkish man complained of pain in his oral cavity (burning mouth) especially on the tongue, and had difficulty chewing and swallowing foods. A careful dental/periodontal examination was performed, including assessment of plaque, gingival condition and periodontal probing depths on all his remaining teeth. Prosthetic rehabilitation was provided three months after the completion of his periodontal and surgical therapy. The concentration of serum inflammatory markers including erythrocyte sedimentation rate, white blood cell count, fibrinogen and high sensitive C-reactive protein were measured at baseline, at the second and sixth weeks, and at three and six months after the periodontal and surgical therapy.


    Oral examination revealed a few papules on the dorsum of the tongue with two slightly painful, small ulcers, localized on the vestibule of the mouth. The mean probing depth was 9.10 ± 0.84 mm. Biopsies of the tongue, buccal mucosa and retromolar trigone were performed and amyloid deposits were found. The serum inflammatory markers improved more dramatically at the second week of periodontal therapy than any other time intervals.

    Amyloidosis may manifest as periodontal destruction that leads to severe chronic periodontitis. Proper periodontal treatment may alleviate systemic inflammatory mediators caused by the amyloidosis.

    Electronic supplementary material

    The online version of this article (doi: 10.​1186/​1752-1947-4-200 ) contains supplementary material, which is available to authorized users.


    Reactive systemic AA amyloidosis, with a sustained acute phase response (APR), can complicate chronic inflammatory disorders. AA amyloid fibrils are derived from the acute-phase reactant serum amyloid A protein (SAA) through a process of cleavage, misholding, and aggregation [ 1 ]. Renal disease is a frequent manifestation of the systemic amyloidosis and a major cause of morbidity [ 1 ]. SAA is an apolipoprotein constituent of high-density lipoprotein that is synthesized by hepatocytes under the transcriptional regulation of pro-inflammatory cytokins [ 2 ]. Sustained overproduction of SAA is a prerequisite for the development of AA amyloidosis. Amyloidosis affects a small proportion of patients that present with chronic inflammatory disorders [ 3. 4 ]. The etiologies for this disease remain unknown. The activation pattern of SAA protein in the presence of inflammation is similar to that of C-reactive protein (CRP) [ 5 ]. The level of SAA increases during acute and chronic infections [ 6. 7 ]. It has been shown that patients with chronic periodontitis display signs of a sub-clinical systemic inflammatory condition [ 8 ]. Furthermore, treatment of advanced periodontitis by full-mouth tooth extraction reduced systemic levels of cardiovascular risk and inflammatory reaction [ 9 ].

    Cross-sectional studies have demonstrated that plasma levels of inflammatory markers such as CRP, fibrinogen, IL-6 and leukocyte counts increase in periodontitis patients when compared to periodontally healthy patients [ 9. 10 ]. Some studies have shown that effective periodontal therapy reduced levels of CRP [ 11 ]. This implies that inflammatory reaction triggered by periodontitis contributes to the whole-body inflammatory burden.

    Secondary amyloidosis, representing approximately 45% of all cases of systemic amyloidosis, has been associated with various chronic inflammatory conditions such as rheumatoid arthritis, sarcoidosis, Crohn's disease, ulcerative colitis and tuberculosis [ 12 ]. Secondary amyloidosis has also been linked to malignant diseases such as Hodgkin's disease and mesothelioma [ 12 ]. In addition, familial Mediterranean fever (FMF), an autosomal recessive disease, primarily affects the population in the Mediterranean basin [ 13 ]. FMF is characterized by recurrent episodes of fever and serosal inflammation along with a very intense APR. The most important complication of FMF is secondary amyloidosis [ 13 ]. Mutation analysis of Mediterranean fever gene (MEFV) can be helpful in confirming the diagnosis for patients with an atypical presentation. Infection or inflammatory diseases may cause AA amyloidosis even without obvious infection or inflammation [ 14. 15 ]. The progression of secondary amyloidosis depends on the nature and status of the underlying chronic inflammatory disease. For example, secondary amyloidosis-associated tuberculosis has been shown to undergo remission when the chronic infection has been eliminated [ 16 ].

    Histopathologic examination of amyloid is essential for the diagnosis and classification of amyloidosis [ 17. 18 ]. The sensitivity and specificity of the histopathologic diagnosis depend on the biopsy site and the adequacy of the tissue sample [ 19. 20 ].

    Case presentation

    Our patient is 67-year-old Turkish man, a primary school graduate, and a forest ranger who lives in a rustic area. He was fully informed about the study and written consent was obtained from him prior to examination. In his medical examination he explained that his gums started bleeding at a very early age. At age 24, he started to smoke since he thought smoking would help to stop bleeding. Currently, he smokes 1-1.5 packs a day. At age 30, he started to experience difficulty in eating and complained of tooth mobility and gum bleeding. He claimed that his teeth ached a lot and as a result the teeth were extracted by a non-dentist or himself. Consequently, at the age of 50 to 60, he lost most of his teeth. At age 25, he was diagnosed with periodontitis. Nonetheless, he had not seen a dentist for this problem or performed any personal oral hygiene.

    Our patient complained of pain in the oral cavity especially on the tongue, buccal mucosa and had difficulty in chewing and swallowing solid food for six months.

    His past medical history was significant for a tonsillectomy as a child. All the symptoms in his medical reviews were negative. Spirometric pulmonary tests were normal. High resolution computed tomography (HRCT) showed minimal emphysematous areas over both apices and non-specific sequelae (Figure 1 ). Head and neck examinations were normal. Magnetic resonance imaging of the tongue revealed no sign of abnormality. He underwent extensive tests to identify the etiologies associated with systemic amyloidosis. Tests such as rectal biopsy, bone marrow biopsy, echocardiogram, abdomen tomography, serum and urine protein electrophoresis as well as liver function test were all normal. However, our patient was diagnosed as chronic renal failure with proteinuria and hypoalbuminemia (Table 1 ). Renal biopsy showed AA type amyloidosis.

    High resolution computed tomography (HRCT) showed minimal emphysematous areas over both apices and non-specific sequalae .

    The effect of periodontal therapy on the inflammatory markers and some laboratory data

    ESR: erythrocyte sedimentation rate (< 10 mm/hour); WBC: white blood cell; Fibrinogen; Serum albumin; hs-CRP: high sensitive C-reactive protein (< 3 mg/L); RF: rheumatoid factor; MEFV: Mediterranean fever gene mutation; FVC: forced vital capacity; FEV1: forced expiratory volume in a second; FEF 25-75: forced expiratory flow 25%-75%; HRCT: high resolution computed tomography

    Clinical examination revealed poor oral hygiene and heavy plaque accumulation. Our patient was almost completely edentulous. The mean periodontal probing depth was 9.10 ± 0.84 mm (range 8-10 mm) in his remaining teeth. The tongue was diffusely enlarged (macroglossia) and clear red appearance and bilateral white plaques bleeding easily by gentle removing, and irregular translucent papules were present (Figure 2 ). Based upon our patient's history, these papules developed spontaneously or after minor trauma. The enlarged tongue has interfered with speech and swallowing, and caused sleep apnea. In addition, two painful, small flat-based ulcers with erythematous halos and a white ulcer bed were detected, localized on the right and left buccal mucosa.

    The tongue was diffusely enlarged (macroglossia), and bilateral white plaques and irregular translucent papules are seen .

    Cultures from the plaques on the tongue and oral cavity were all negative for bacteria and fungi. The biopsies were obtained from the tongue, buccal mucosa and retromolar trigon. Secondary amyloidosis (AA type), was diagnosed by histological and immunohistochemical findings (Figure 3 ).

    Histopathologic examination findings: the Congo red method was used to detect amyloid in tissue sections. Amyloid was identified as the AA type on immunohistochemical testing with the use of monoclonal antibodies specific to SAA. (A) Hematoxylin and eosin staining of the biopsy specimen shows homogen, eosinophilic material (×20, hemotoxylin and eosin). (B) The amorphous extra-cellular material stains positively with Congo red (×2.5, Congo red). (C) This Congo red-positive material appears apple-green when viewed under polarized light (×20 Congo red-positive material appears apple-green when viewed under polarized light). (D) Extra-cellular and peri-vascular deposits of amyloid reveal positive immunoreactivity with an antibody against amyloid A (×40).

    Our patient received comprehensive periodontal therapy, which included careful oral hygiene instructions, curettage combined with non-surgical and surgical therapy. Serum inflammatory markers and some laboratory data improved dramatically at the second week of the periodontal therapy more than at any other time interval (Table 1 ). Restorative treatment started after his periodontal condition was stabilized (around three months after periodontal therapy). Intra-oral radiographs showed poor bone density (Figure 4 ).

    Radiographic findings from the patient described in this case report. Diffuse osteopeny in mandibular and prominence trabeculation of maxilla are present.

    Histopathologic examination findings

    The Congo red method was used to detect amyloid in tissue sections [ 21 ]. Amyloid was identified as the AA type on immunohistochemical tests with the use of monoclonal antibodies specific to amyloid A [ 18 ].


    Our patient was 67-year-old man, a heavy and current smoker. He suffered severe chronic periodontitis and chronic renal failure. Our patient complained of pain in the oral cavity especially on the tongue, buccal mucosa and had difficulty in chewing and swallowing solid foods for almost six months. Biopsies were performed and secondary amyloidosis was diagnosed based upon histological and immunohistochemical findings. Our patient presented with typical signs of periodontal disease that include gingival tenderness, bleeding, recession, alveolar bone loss, tooth mobility, and tooth loss. In addition, several inflammation markers, such as erythrocyte sedimentation rate (ESR), white blood cell count (WBC), fibrinogen and high sensitive C-reactive protein (hs-CRP) were all elevated.

    It has been shown that chronic infection or inflammatory diseases may cause secondary amyloidosis even without obvious infection or inflammation [ 14. 15 ]. Patients with chronic periodontal diseases had higher levels of SAA, the precursor protein of amyloid fiber in secondary amyloidosis, than patients without periodontal disease [ 22 ]. To date, only a few reports address the interaction between periodontal disease and secondary amyloidosis [ 20. 23 ]. One study showed the prevalence of moderate to severe periodontitis was greater in FMF patients with amyloidosis than without amyloidosis [ 20 ]. The other study was a case report that illustrated an interaction between systemic amyloidosis and severe periodontitis in a patient with rheumatoid arthritis [ 23 ]. Our case results were in line with findings reported in the literature.

    The definitive method of diagnosing amyloidosis is tissue biopsy. Although biopsies can be obtained from compromised organs, blood vessel fragility associated with amyloid deposition carries a risk of bleeding. Biopsy of oral tissues has been advocated as an adjunctive or alternate method of detecting amyloid deposition. Gingival, tongue, buccal mucosa and minor salivary gland tissue have all been reported as potential sites for biopsy; however, there are inconsistent results with regard to the sensitivity of amyloid detection in each of these tissues [ 24 ]. As a result, it has been reported that the anatomic location of the amyloid deposition within the tissue was consistent regardless of the location of the biopsy. This may have important implications for the biopsy technique used for the detection of amyloid [ 24 ]. If intra-oral biopsies are used more commonly for patients with chronic periodontal disease, amyloid may be found more frequently than expected.

    Our patient's differential diagnosis include pulmonary X-ray, pulmonary function tests, sputum cytology, fasting gastric juice and tuberculin skin testing, they were all negative for tuberculosis and bronchiectasis. His history, physical examination and laboratory findings were negative for rheumatoid arthritis and FMF patients (rheumatoid factor and MEFV gene mutation were negative, respectively). There was no evidence for chronic infection or inflammation such as rheumatoid arthritis, sarcoidosis, Crohn's disease, ulcerative colitis and tuberculosis except chronic periodontitis. In addition, smoking is a strong risk factor for periodontitis [ 25 ] and it certainly contributed to our patient's problems since he is a heavy smoker (more than 1-1.5 packs/day).

    Secondary amyloidosis is also associated with malignant diseases such as Hodgkin's disease and mesothelioma. Clinical examination, abdominal and chest computed tomography were negative for any malignant disorders or airflow obstruction. With the decline of tuberculosis in the developed countries, rheumatoid arthritis and inflammatory bowel disease remain the leading cause of secondary amyloidosis [ 12 ]. However, in the developing countries, chronic infectious diseases such as tuberculosis and leprosy are major causes [ 12 ]. There was no clinical evidence for inflammatory bowel diseases or leprosy in our patient.

    Although, our patient did not have any pulmonary system complaints, due to his habit of smoking, his pulmonary system was investigated extensively for disease that might trigger the secondary amyloidosis. All pulmonary function tests were normal except a mild emphysematous appearance on chest computed tomography. No bronchiectasis or obstruction was noted. So far, no secondary amyloidosis or increased inflammatory markers in patients with mild or moderate emphysema has been reported [ 26 ].

    A thorough investigation for the etiology that may cause secondary amyloidosis was carried out. None was identified except chronic periodontitis. Our patient developed reactive amyloidosis (AA-type), most likely secondary to his long-standing periodontitis. This could be attributed to the increase in the levels of systemic inflammatory mediators due to chronic periodontal disease/infection that led to the secondary amyloidosis. Indeed, patients with chronic periodontal diseases have higher levels of SAA protein in secondary amyloidosis than patients without periodontal disease [ 22 ]. Chronic periodontal disease could exaggerate secondary amyloidosis via increased levels of systemic inflammatory mediators. In addition, our report highlights the possibility that amyloid deposition in patients with systemic amyloidosis causes accelerated periodontal destruction and bone loss of affected teeth. Amyloid deposition within the periodontium elicited an inflammatory reaction similar to that of foreign body material. Accelerated destruction of periodontium and associated supporting bone apparently is caused by this foreign-body-type giant cell reaction. Therefore, elimination of local infection associated with periodontal diseases will aid in the reduction of levels of systemic inflammatory mediators, which may slow the progression of secondary amyloidosis.

    Sustained overproduction of SAA is a prerequisite for the development of AA amyloidosis, although the reasons for these remain unknown. Robbins [ 27 ] proposed two possible explanations for this. First, SAA-protein is normally degraded to soluble end products via monocyte-derived enzymes. Conceivably, individuals who develop amyloid have an enzyme defect that cannot breakdown SAA-protein completely hence insoluble AA molecules were produced. Second, a genetically determined structural abnormality in the SAA-protein molecule itself renders it resistant to degradation by monocytes. Evidence has suggested that individual genetic susceptibility to amyloidosis may influence the host's response to infection. Nibali et al. [ 28 ] have found the link between polymorphisms of genes encoding for neutrofil receptors and pro-inflammatory cytokines and the presence of pathogenic bacteria in patients with aggressive periodontits. The authors then speculated that complex interactions between the microbiota and host genome may be at the basis of a patient's susceptibility to aggressive periodontitis. Currently many investigators are trying to define the genotype-phenotype correlations and risk factors for the development of secondary amyloidosis.


    To our knowledge, this is the first case report that documents secondary amyloidosis supported by the tongue, buccal mucosa and retromolar trigon biopsies, while ruling out all possible known etiologic factors as a cause for secondary amyloidosis. In addition, this study has demonstrated that secondary amyloidosis can be slowed down if periodontal condition can be improved. Further studies in a larger population will provide insight of this rare but destructive systemic disease.


    Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

    Competing interests

    The authors declare that they have no competing interests.

    Authors' contributions

    MİC and HW analyzed and interpreted our patient data. They were also major contributors in writing the manuscript. LY performed the histological examination of the tissue biopsies. All the authors read and approved the final manuscript

    Authors’ Affiliations

    Faculty of Dentistry, Department of Periodontology, Zonguldak Karaelmas University

    Department of Periodontics & Oral Medicine, School of Dentistry, University of Michigan

    Faculty of Medicine, Department of Pathology, Ondokuz Mayıs University

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