ADMIRAL RECOGNIZES EB WORKERS - Electric Boat Corporation

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Bob Hurley, MDMedical DirectorHEALTHMATTERSPodagra. It sounds like some SouthAmerican fruit, yet individuals whoexperience the purple red, hot, swollenand excruciatingly painful joint will tellyou otherwise. Acute gout with its associatedarthritis sends millions of patientsto doctors’ offices for treatment everyyear. And the numbers are increasing.Recent data indicates that U.S. caseshave increased two cases per 1,000 personsbetween 1990 and 1999. Many studiessuggest a correlation with increasingrates of obesity and hypertension. Moreimportantly, there is recent evidence thatgout increases your risk for heart attack.GoutGout is caused by altered purinemetabolism leading to increased bloodlevels of uric acid (hyperuricemia). If youremember your high school chemistry,when a substance supersaturates thesolution, it falls out and deposits a crystalin the bottom of the test tube. In thehuman body, when monosodium uratesupersaturates the blood, it falls out ofsolution and into your soft tissue. Thistypically occurs near an area of slow orpoorly moving blood flow such as in thelower extemities near the great toe, ankleor knee. Crystals deposited in soft tissuescreate maladies such as arthritis of thejoints, and kidney problems such asstones or filtration difficulties.In most mammals, the urate oxidase(uricase) enzyme converts uric acid toallantoin, leading to very low serum uricacid levels. Somewhere in our evolutionarypast, humans and great apes developedmutated genes for uricase and themanifestation of this genetic dysfunctionis gout. When the serum uric acidexceeds 6.5 mg per dL, one is at high riskfor a gouty attack.There are many individuals who don’thave symptoms of increased uric acid inthe bloodstream. In fact, only one halfof 1 percent of people with uric acid levelsbetween 7 and 8.9 ever experiences agouty attack. When that number goesover nine, a little less than 5 percent ofthe population experiences a gout attack.Risk FactorsThe deposition of urate crystals intotissue that is cool or dehydrated leads toan attack. Variables such as a highpurinediet, alcohol use, obesity, anddiuretic therapy increase one’s chances ofan attack. Consumption of red meat andseafood increases your chances whereasconsumption of dairy products appearsto be protective. Other known triggersfor acute gout are infection; intravenousdye; acidosis; and rapid fluctuations inserum uric acid concentrations such aswith trauma, surgery, psoriasis flare-ups,initiation of chemotherapy, diuretic therapy,and stopping or starting the antigoutmedication allopurinol.Clinical PresentationAcute gouty arthritis most commonlybegins with involvement of a single jointor multiple joints in the lower extremities,most commonly the great toe (i.e.,podagra), midfoot, ankle, or knee joints.Pain, redness and swelling often begin inthe early morning and increase and peakwithin 24 to 48 hours. The pain can bequite severe, with individuals unable tobear the slightest touch to the area. Evenwithout treatment, the attacks typicallysubside within five to seven days.Acute gout sometimes resembles askin infection and can cause the overlyingskin to slough off after the acuteinflammatory phase has receded. Goutcan also cause inflammation to nearbybursa (lubricating fluid filled sacks) tendonsor structures near joints. Sometimesgout can cause a high fever withincreased white blood cell counts mimickingan infection of the joint. Oftenyour doctor will need to obtain bacteriologiccultures of blood or the fluidwithin the joint (synovial fluid) if infectionis considered.Frequent, recurrent acute attacksoften cause chronic tophaceous gout.Tophi are deposits of monosodium uratecrystals in soft tissue that may occur inthe helix of the ear and over the joints ofthe fingers. Tophaceous gout may lead tojoint erosion and destruction. Occasionally,tophaceous gout over many jointscan mimic rheumatoid arthritis.DiagnosisBesides infection, the other entity toconsider is pseudogout. In pseudogout,calcium pyrophosphate is deposited inthe tissues. Clinically, if a patient hasinflammation of the great toe joint withor without tophi it strongly points togout as a diagnosis. To confirm this,your doctor may attempt to obtain asample of fluid from within the joint.The reason for the joint sample is to differentiateit from pseudogout as the presenceof monosodium urate crystals inthe fluid acquired by a needle andsyringe can differentiate between the twoconditions. In many cases of gout, by thetime you see your doctor, your blooduric acid levels have returned to normal.TreatmentThe goals of gout treatment are tocontrol the painful symptoms, to explainways to reduce risk factors, and to prescribedrugs to prevent recurrence andchronic damage to joint and surroundingtissue. First-line therapy for pain, feverand swelling of acute gout are nonsteroidalanti-inflammatory drugs such asmotrin or naprosyn. Alternatively, pred-8 I SEPTEMBER 2007 I ELECTRIC BOAT NEWS
nisone may be given. The second linetherapy is the old medication colchicine.Occasionally, these therapies may need tobe supplemented by short-acting opioidssuch as hydrocodone and oxycodone forpain control. After the first gout attack,individuals should reduce risk factors,which include purine in their diets, alcoholuse, obesity and diuretic therapy.Urate-lowering therapy (allopurinol) maybe initiated after multiple attacks or afterthe development of tophi or kidneystones.Chronic GoutAbout 60 percent of people who experiencea gout attack will have anotherattack within 12 months. Therefore, nonpharmacologictreatment of hyperuricemiashould begin with the first goutattack and should initially focus on modifyingthe risk factors mentioned above.Changing the type of diuretic or treatmentof your hypertension may reducethe hyperuricemia in many cases.There are two classes of medicationsfor the treatment of chronic gout. Theyare the xanthine oxidase inhibitors anduricosuric agents. They are employedwhen patients have tophi, or x-raydemonstrated joint damage. With eitherof these classes of medications, a targetserum uric acid level of less than 6 mgper dL is the goal. This requires adjustmentupwards in order to reach this level.Allopurinol is the first-line urate-loweringtherapy. Between 2 to 5 percent ofpatients taking allopurinol have minorrashes and other adverse effects. Rarely,individuals suffer a severe hypersensitivitysyndrome, which your doctor will discusswith you. Those intolerant of allopurinolmay undergo desensitization ormay take oxypurinol (the active metaboliteof allopurinol), if available.Uricosuric agents are second-line therapyfor patients who are intolerant ofallopurinol, or they may be used in combinationwith allopurinol in patients withdifficult to treat hyperuricemia.Probenecid is the uricosuric agentmost often used in the U.S. Uricosurictherapy is contraindicated in patientswith a history of kidney stones and doesn’twork well in those with failing kidneys.In addition to probenecid, there aretwo drugs – losartan (cozaar) and fenofibrate(tricor) – that have uricosuric propertiesand may be useful adjunctive therapiesfor patients with gout, hypertension,and hyperlipidemia.Remember, gout is a chronic conditionassociated with joint and soft tissue damageif left untreated. If you have hadepisodes in the past, now is an excellenttime to speak with your doctor todevelop a long-term preventive strategy.Your can find more information onGout at the resources below:American College of RheumatologyTelephone: 1-404-633-3777Web site:http://www.rheumatology.org/public/factsheets/gout_new.aspArthritis FoundationTelephone: 1-800-283-7800Web site:http://www.arthritis.org/conditions/diseasecenter/gout.aspNational Institute of Arthritis andMusculoskeletal and Skin DiseasesTelephone: 1-877-226-4267Web site:http://www.niams.nih.gov/hi/topics/gout/ffgout.htmMedline PlusWeb site:http://www.nlm.nih.gov/medlineplus/goutandpseudogout.htmlUpToDate Patient InformationWeb site:http://www.patients.uptodate.com (clickon Arthritis and Rheumatism, then onGout)Retirees241 Walter E. Asendorf39 yearsO S <strong>Electric</strong>ian W/L241 Chester B. Stedman III31 yearsForeman242 James J. Chinigo31 yearsO S Machinist 1/C242 Joseph F. Czajka Jr.31 yearsO S Machinist 1/C243 Herbert G. Chappell38 yearsPipefitter 1/C355 Charles J. Wall II33 yearsPlanning Spec Sr403 Jon D. Morosini33 yearsEng Project Spec431 John E. Bass42 yearsEngineer Senior449 Richard A. Boyd23 yearsMgr of Engineering452 Lucy P. Sullivan23 yearsP/C Tech Aide453 Donald A. Varno12 yearsMech Sr Designer458 Juliette P. Thornton33 yearsA/A Administrative Aidecontinued on page 11ELECTRIC BOAT NEWS I SEPTEMBER 2007 I 9
Page 1 and 2: SEPTEMBER 2007INSIDEWelcome To Elec
Page 3 and 4: Dan Barrett,EditorBob Gallo,Gary Sl
Page 5 and 6: MARINE GROUP UPDATEElectric Boat Aw
Page 7: Electric Boat Employees Volunteer T
Page 11 and 12: Service AwardsRetirees45551 Paul E.

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