Archive January 2019

SAC Trader 'Corrupted' Doctors, Prosecutor Says

<h1>SAC Trader 'Corrupted' Doctors, Prosecutor Says</h1>

SAC Trader ‘Corrupted’ Doctors, Prosecutor Says

Mathew Martoma sought to gain an “illegal edge” that helped him perpetrate the most lucrative insider trading scheme in history, a federal prosecutor said on Friday.

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Think Like a Doctor: Weaker and Weaker Solved!

<h1>Think Like a Doctor: Weaker and Weaker Solved!</h1>

Think Like a Doctor: Weaker and Weaker Solved!

Readers solve the case of a 19-year-old man who suddenly collapsed at work after months of weakness and fatigue dotted with episodes of nausea and vomiting.

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IgA Nephropathy

IgA Nephropathy

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Immunoglobulin A (IgA) nephropathy is characterized by predominant IgA deposition inthe glomerular mesangium. [ 1 ] It isoneofthemost common causes of glomerulonephritis in the world. [ 2 , 3 ] IgA nephropathy wasfirst described by Berger and Hinglais in 1968, andisalso known as Berger disease. [ 4 ] [ 5 ]
Pathologically, a spectrum of glomerular lesions canbe seen, but mesangial proliferation with prominent IgA deposition is observed inalmostall biopsies. See the images below.
Although IgA nephropathy isa limited nonsystemic renal disease, many systemic illnesses are sporadically associated with mesangial IgA deposition. Henoch-Schönlein purpura ( HSP ), a systemic illness, hasbeen closely linked to IgA nephropathy. Other systemic diseases inwhich mesangial deposits of IgA are regularly observed include systemic lupus erythematosus , hepatitis , dermatitis herpetiformis , and ankylosing spondylitis .
For discussion ofthis disorder in children, see Pediatric IgA Nephropathy .
For further information, see Mayo Clinic – Kidney Transplant Information .
IgA nephropathy appears to result froman ordered sequence of events, starting with galactose-deficient IgA1, which contains less thana full complement of galactose residues onthe O-glycans inthe hinge region ofthe heavy chains. [ 6 ] .These may act as auto-antigens that trigger the production of glycan-specific autoantibodies andthe formation of circulating immune complexes thatare deposited in renal mesangium. These then induce glomerular injury through pro-inflammatory cytokine release, chemokine secretion, andthe resultant migration of macrophages intothe kidney. [ 7 ] Immune complexes formed by IgG or IgA antibodies with galactose-deficient IgA lead to deposition inthe glomerulus.
Deposited IgA is predominantly polymeric IgA1, whichis mainly derived fromthe mucosal immune system. The association ofsome cases of IgA nephropathy with syndromes that affect the respiratory tract or gastrointestinal tract, suchas celiac disease, led tothe suggestion that IgA nephropathy isa disease ofthe mucosal immune system. This concept isalso supported bythe clinical observation that hematuria worsens during orafter upper respiratory tract or gastrointestinal tract infections.
The role ofthe complement systeminthe pathogenesis of IgA nephropathy is controversial. While IgA antibodies cannot activate complement throughthe classic pathway, studies have shown that complement canbe activated bythe alternate pathway.
United States
IgA nephropathy accounts forabout 10% of biopsies performed for glomerular disease inthe United States. Prevalence rates are lower inthe United States thanin Asian countries. These lower rates may be influenced bya conservative approach by nephrologists inthe United States, whoare reluctant to perform renal biopsies in asymptomatic patients withonly mild abnormalities on urinalyses.
International
Distribution of IgA nephropathy varies indifferent geographic regions throughout the world. IgA nephropathy is observed inupto 40% ofall biopsies performed for glomerular disease in Asia, compared with 20% in Europe and 10% in North America. High prevalence rates are observed in Singapore, Japan, Australia, Hong Kong, Finland, and southern Europe, whereas low prevalence rates arethe rule inthe United Kingdom, Canada, andthe United States.
A study from Scotland founda significant twofold increase inthe diagnosis of IgA nephropathy inthe patients residing inthemost socioeconomically deprived areas compared withthe least deprived ones. The variation wasnot explained bythe demographics ofthe underlying population. [ 8 ]
In Asia, routine urinalyses are performed for schoolchildren, and renal biopsies are performed for patients with asymptomatic hematuria, thus raising the reported prevalence ofthe disease. The estimated annual incidence in Japan is 3.9–4.5 per 100,000 population. [ 9 ]
The prevalence of IgA nephropathy is highest in geographic areas with large numbers of endemic helminthic species that infest humans, andmostofthe IgA nephropathy susceptibility loci identified by genome-wide association studies include genes involved inthe maintenance ofthe intestinal epithelial barrier and response to mucosal pathogens, whichwould confer protection against helminthic infestation. Thus, the increased risk of IgA nephropathy inthese populations may bean untoward consequence ofa protective adaptation to helminthic infections. It wouldalso explain the association of mucosal infections asa frequent trigger for IgA nephropathy. [ 10 ]
This disorder is thought to follow a benign courseinmost cases. However, many patients areat risk for slow progression to ESRD, which develops in approximately 15% of patients by 10 years and 20% by 20 years, thoughthese percentages depend onhowthe disease is defined.
IgA nephropathy ismore common in Asians and whites andis rare in blacks, bothinthe United States andin Africa. The condition is frequently observed in Native Americans ofthe Zuni and Navajo tribes.
IgA nephropathy ismore common in males thanin females. Virtually all studies show a male predominance ofat least 2:1, with reported ratios ofupto 6:1. [ 11 ] The higher male predilection is observed inwhite patients in northern Europe andthe United States.
IgA nephropathy can affect all ages butismost common inthe second and third decades of life. Eighty percent of patients are aged 16-35 years atthetimeof diagnosis. The condition is uncommon in children younger than 10 years.
Although IgA nephropathy usually follows a benign course, end-stage renal disease (ESRD) develops in 15-20% of patients within 10 years of onset andinabout 25-30% of patients by 20 years. Efforts havebeenmadeto determine clinical and histological features associated with progression to ESRD. [ 12 , 13 ]
The Oxford classification of IgA nephropathy, or MEST score, published in 2009, comprises four histological features thatare independent predictors of clinical outcome. [ 2 ] The IgA Nephropathy Classification Working Group added crescents tothe Oxford classification, to form the MEST-C score. [ 14 ] The features that determine the MEST-C score areas follows:
The clinical significance ofthe individual MEST-C features isas follows:
Other predictors of poor renal outcomes include the following:
A calculator for estimating the risk of progression to ESRD in patients with IgA nephropathy hasbeen developed by Xie et al, based ona cohort of 619 Chinese patients. [ 16 ] It has yet tobe validated inother ethnic groups. The calculator uses four variables: glomerular filtration rate, hemoglobin level, serum albumin level, and systolic blood pressure.
IgA nephropathy. Nat Rev Dis Primers . 2016 Feb 11. 2:16002. [Medline] .
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Coppo R, Troyanov S, Camilla R, et al. The Oxford IgA nephropathy clinicopathological classification is valid for children aswellas adults. Kidney Int . 2010 Mar 3. [Medline] .
Berger J, Hinglais N. [Intercapillary deposits of IgA-IgG]Les Depots Intercapillaires d”IgA-IgG. J Urol Nephrol (Paris) . 1968 Sep. 74(9):694-5. [Medline] .
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Fabiano RC, Pinheiro SV, Simões E Silva AC. Immunoglobulin A nephropathy: a pathophysiology view. Inflamm Res . 2016 Jun 28. [Medline] .
McQuarrie EP, Mackinnon B, McNeice V, Fox JG, Geddes CC. The incidence of biopsy-proven IgA nephropathy is associated with multiple socioeconomic deprivation. Kidney Int . 2014 Jan. 85(1):198-203. [Medline] .
[Guideline] Yuzawa Y, Yamamoto R, Takahashi K, Katafuchi R, Tomita M, Fujigaki Y, et al. Evidence-based clinical practice guidelines for IgA nephropathy 2014. Clin Exp Nephrol . 2016 Apr 20. 70:S56-62. [Medline] . [Full Text] .
Magistroni R, D’Agati VD, Appel GB, Kiryluk K. New developments inthe genetics, pathogenesis, and therapy of IgA nephropathy. Kidney Int . 2015 Nov. 88 (5):974-89. [Medline] . [Full Text] .
Wyatt RJ, Julian BA, Baehler RW, et al. Epidemiology of IgA nephropathy in central and eastern Kentucky forthe period 1975 through 1994. Central Kentucky Region ofthe Southeastern United States IgA Nephropathy DATABANK Project. J Am Soc Nephrol . 1998 May. 9(5):853-8. [Medline] .
Walsh M, Sar A, Lee D, et al. Histopathologic features aid in predicting risk for progression of IgA nephropathy. Clin J Am Soc Nephrol . 2010 Mar. 5(3):425-30. [Medline] . [Full Text] .
Shen PC, He LQ, Tang Y, et al. Clinicopathological characteristics and prognostic factors of asymptomatic IgA nephropathy. J Investig Med . 2010 Mar. 58(3):560-5. [Medline] .
Haas M, Verhave JC, Liu ZH, Alpers CE, Barratt J, Becker JU, et al. A Multicenter Study ofthe Predictive Value of Crescents in IgA Nephropathy. J Am Soc Nephrol . 2017 Feb. 28 (2):691-701. [Medline] .
Le W, Liang S, Hu Y, Deng K, Bao H, Zeng C, et al. Long-term renal survival and related risk factors in patients with IgA nephropathy: resultsfroma cohort of 1155 cases ina Chinese adult population. Nephrol Dial Transplant . 2012 Apr. 27 (4):1479-85. [Medline] .
Xie J, Kiryluk K, Wang W, Wang Z, Guo S, Shen P, et al. Predicting progression of IgA nephropathy: new clinical progression risk score. PLoS One . 2012. 7 (6):e38904. [Medline] . [Full Text] .
Rollino C, Vischini G, Coppo R. IgA nephropathy and infections. J Nephrol . 2016 Aug. 29 (4):463-8. [Medline] .
Scolari F, Amoroso A, Savoldi S, et al. Familial clustering of IgA nephropathy: further evidence inan Italian population. Am J Kidney Dis . 1999 May. 33(5):857-65. [Medline] .
Ai Z, Li M, Liu W, Foo JN, Mansouri O, Yin P, et al. Low α-defensin gene copy number increases the risk for IgA nephropathy and renal dysfunction. Sci Transl Med . 2016 Jun 29. 8 (345):345ra88. [Medline] .
Hahn WH, Suh JS, Cho BS, Kim SD. The enabled homolog gene polymorphisms are associated with susceptibility and progression of childhood IgA nephropathy. Exp Mol Med . 2009 Nov 30. 41(11):793-801. [Medline] . [Full Text] .
Appel GB, Waldman M. The IgA nephropathy treatment dilemma. Kidney Int . 2006 Jun. 69(11):1939-44. [Medline] .
Gharavi AG, Yan Y, Scolari F, et al. IgA nephropathy, themost common cause of glomerulonephritis, is linked to 6q22-23. Nat Genet . 26(3):354-7. [Medline] .
Shoji T, Nakanishi I, Suzuki A, et al. Early treatment with corticosteroids ameliorates proteinuria, proliferative lesions, and mesangial phenotypic modulation in adult diffuse proliferative IgA nephropathy. Am J Kidney Dis . 35(2):194-201. [Medline] .
Praga M, Gutiérrez E, González E, Morales E, Hernández E. Treatment of IgA nephropathy with ACE inhibitors: a randomized and controlled trial. J Am Soc Nephrol . 2003 Jun. 14 (6):1578-83. [Medline] . [Full Text] .
Manno C, Torres DD, Rossini M, et al. Randomized controlled clinical trial of corticosteroids plus ACE-inhibitors with long-term follow-up in proteinuric IgA nephropathy. Nephrol Dial Transplant . 2009 Jul 23. [Medline] .
[Guideline] Chapter 10: Immunoglobulin A nephropathy. Kidney Int Suppl (2011) . 2012 Jun. 2 (2):209-217. [Medline] . [Full Text] .
Floege J, Feehally J. Treatment of IgA nephropathy and Henoch-Schönlein nephritis. Nat Rev Nephrol . 2013 Jun. 9 (6):320-7. [Medline] .
Pozzi C, Andrulli S, Del Vecchio L, et al. Corticosteroid effectiveness in IgA nephropathy: long-term resultsofa randomized, controlled trial. J Am Soc Nephrol . 2004 Jan. 15(1):157-63. [Medline] .
Lv J, Zhang H, Chen Y, Li G, Jiang L, Singh AK, et al. Combination therapy of prednisone and ACE inhibitor versus ACE-inhibitor therapy alone in patients with IgA nephropathy: a randomized controlled trial. Am J Kidney Dis . 2009 Jan. 53 (1):26-32. [Medline] .
Tesar V, Troyanov S, Bellur S, Verhave JC, Cook HT, Feehally J, et al. Corticosteroids in IgA Nephropathy: A Retrospective Analysis fromthe VALIGA Study. J Am Soc Nephrol . 2015 Sep. 26 (9):2248-58. [Medline] . [Full Text] .
Lv J, et al; TESTING Study Group. Effect of Oral Methylprednisolone on Clinical Outcomes in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA . 2017 Aug 1. 318 (5):432-442. [Medline] .
Tang SC, Tang AW, Wong SS, et al. Long-term study of mycophenolate mofetil treatment in IgA nephropathy. Kidney Int . 2010 Mar. 77(6):543-9. [Medline] .
Rauen T, Eitner F, Fitzner C, Sommerer C, Zeier M, Otte B, et al. Intensive Supportive Care plus Immunosuppression in IgA Nephropathy. N Engl J Med . 2015 Dec 3. 373 (23):2225-36. [Medline] . [Full Text] .
Vecchio M, Bonerba B, Palmer SC, Craig JC, Ruospo M, Samuels JA, et al. Immunosuppressive agents for treating IgA nephropathy. Cochrane Database Syst Rev . 2015 Aug 3. CD003965. [Medline] .
Fellström BC, Barratt J, Cook H, Coppo R, Feehally J, de Fijter JW, et al. Targeted-release budesonide versus placebo in patients with IgA nephropathy (NEFIGAN): a double-blind, randomised, placebo-controlled phase 2b trial. Lancet . 2017 May 27. 389 (10084):2117-2127. [Medline] .
Dillon JJ. Fish oil therapy for IgA nephropathy: efficacy and interstudy variability. J Am Soc Nephrol . 1997 Nov. 8(11):1739-44. [Medline] .
Liu LJ, Lv JC, Shi SF, et al. Oral calcitriol for reduction of proteinuria in patients with IgA nephropathy: a randomized controlled trial. Am J Kidney Dis . 2012 Jan. 59(1):67-74. [Medline] .
Lafayette RA, Canetta PA, Rovin BH, Appel GB, Novak J, Nath KA, et al. A Randomized, Controlled Trial of Rituximab in IgA Nephropathy with Proteinuria and Renal Dysfunction. J Am Soc Nephrol . 2017 Apr. 28 (4):1306-1313. [Medline] .
Klahr S, Levey AS, Beck GJ, et al. The effects of dietary protein restriction and blood-pressure controlonthe progression of chronic renal disease. Modification of Diet in Renal Disease Study Group. N Engl J Med . 1994 Mar 31. 330(13):877-84. [Medline] .
Levey AS, Adler S, Caggiula AW, et al. Effects of dietary protein restriction onthe progression of advanced renal disease inthe Modification of Diet in Renal Disease Study. Am J Kidney Dis . 1996 May. 27(5):652-63. [Medline] .
Vergano L, Loiacono E, Albera R, Coppo R, Camilla R, Peruzzi L, et al. Can tonsillectomy modify the innate and adaptive immunity pathways involved in IgA nephropathy?. J Nephrol . 2014 Apr 23. [Medline] .
Kovács T, Vas T, Kövesdy CP, Degrell P, Nagy G, Rékási Z, et al. Effect of tonsillectomy and its timing on renal outcomes in Caucasian IgA nephropathy patients. Int Urol Nephrol . 2014 Sep 3. [Medline] .
Maeda I, Hayashi T, Sato KK, Shibata MO, Hamada M, Kishida M, et al. Tonsillectomy has beneficial effects on remission and progression of IgA nephropathy independent of steroid therapy. Nephrol Dial Transplant . 2012 Jul. 27(7):2806-13. [Medline] .
Watanabe H, Goto S, Kondo D, Takata T, Yamazaki H, Hosojima M, et al. Comparison of methods of steroid administration combined with tonsillectomy for IgA nephropathy patients. Clin Exp Nephrol . 2016 May 23. [Medline] .
Yu L, Jiang L, Zhou XJ, et al. Common genetic variants inthe chromogranin a promoter are associated with renal injury in IgA nephropathy patients with malignant hypertension. Ren Fail . 2010 Jan. 32(1):41-6. [Medline] .
Clayton P, McDonald S, Chadban S. Steroids and recurrent IgA nephropathy after kidney transplantation. Am J Transplant . 2011 Aug. 11 (8):1645-9. [Medline] . [Full Text] .
Baek CH, Lee JG, Park JH, Kim H, Yang WS, Kim YS, et al. The clinical outcomes of second kidney transplantation in IgA nephropathy: a multicenter retrospective study. Clin Nephrol . 2016 Aug. 86 (2):87-93. [Medline] .
Trimarchi H, Barratt J, Cattran DC, Cook HT, Coppo R, Haas M, et al. Oxford Classification of IgA nephropathy 2016: an update fromthe IgA Nephropathy Classification Working Group. Kidney Int . 2017 May. 91 (5):1014-1021. [Medline] .
Gutiérrez E, Zamora I, Ballarín JA, Arce Y, Jiménez S, Quereda C, et al. Long-Term Outcomes of IgA Nephropathy Presenting with Minimal or No Proteinuria. J Am Soc Nephrol . 2012 Oct. 23(10):1753-1760. [Medline] . [Full Text] .
Le W, Liang S, Chen H, Wang S, Zhang W, Wang X, et al. Long-term outcome of IgA nephropathy patients with recurrent macroscopic hematuria. Am J Nephrol . 2014. 40(1):43-50. [Medline] .
Sohail Abdul Salim, MD, FASN, FACP Consultant Physician, Central Nephrology; Affiliate Faculty, Department of Internal Medicine, Division of Nephrology, University of Mississippi Medical Center
Sohail Abdul Salim, MD, FASN, FACP isa member ofthe following medical societies: American College of Physicians , American Society of Nephrology , Mississippi State Medical Association , Renal Physicians Association
Disclosure: Nothing to disclose.
Tibor Fulop, MD, PhD, FACP, FASN Professor of Medicine, Department of Medicine, Division of Nephrology, Medical University of South Carolina College of Medicine; Attending Physician; Medical Services, Ralph H Johnson VA Medical Center
Tibor Fulop, MD, PhD, FACP, FASN isa member ofthe following medical societies: American Academy of Urgent Care Medicine, American College of Physicians , American Society of Diagnostic and Interventional Nephrology , American Society of Hypertension , American Society of Nephrology , International Society for Apheresis, International Society for Hemodialysis, Magyar Orvosi Kamara (Hungarian Chamber of Medicine), Southern Society for Clinical Investigation
Disclosure: Serve(d) asa director, officer, partner, employee, advisor, consultant or trustee for: Fresenius Medical Care, Hungary; Dialysis Clinic Inc., USA.
Luis A Juncos, MD, FASN, FAHA Chief of Nephrology, Central Arkansas Veterans Healthcare System, John L McClellan Memorial Veterans Hospital; Professor of Medicine, University of Arkansas for Medical Sciences College of Medicine
Luis A Juncos, MD, FASN, FAHA isa member ofthe following medical societies: American College of Sports Medicine , American Federation for Clinical Research , American Federation for Medical Research , American Heart Association , American Physiological Society , American Society of Nephrology , Inter-American Society of Hypertension, International Society for Peritoneal Dialysis , International Society of Nephrology , Minnesota Medical Association , National Kidney Foundation , Society of Critical Care Medicine , Southern Society for Clinical Investigation , Zumbro Valley Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics
Christie P Thomas, MBBS, FRCP, FASN, FAHA isa member ofthe following medical societies: American College of Physicians , American Heart Association , American Society of Nephrology , Royal College of Physicians
Disclosure: Nothing to disclose.
Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FASN isa member ofthe following medical societies: American College of Physicians , American Society of Hypertension , American Society of Nephrology , International Society of Nephrology , Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
James H Sondheimer, MD, FACP, FASN Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)
James H Sondheimer, MD, FACP, FASN isa member ofthe following medical societies: American College of Physicians , American Society of Nephrology
Disclosure: Nothing to disclose.
Mona Brake, MD Assistant Professor, Department of Internal Medicine, Kansas University School of Medicine
Mona Brake, MD isa member ofthe following medical societies: American College of Physicians , American Society of Nephrology
Disclosure: Nothing to disclose.
Douglas Somers, MD Assistant Professor, Department of Internal Medicine, Division of Nephrology, University of Iowa Medical Center
Douglas Somers, MD isa member ofthe following medical societies: American Society of Nephrology
Disclosure: Nothing to disclose.
The authors thank Dr. Tim Timmerman, pathologist, for his invaluable help withthe pathology slides. IgA Nephropathy

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Case Report: Lymphocytic Vasculitis of the Central Nervous System

<h1>Case Report: Lymphocytic Vasculitis of the Central Nervous System</h1>

Case Report: Lymphocytic Vasculitis of the Central Nervous System

Print-Friendly Version / Save PDF V a sculitis is a group of chronic inflammatory diseases in which the blood vessel is the target of an immune reaction. They can be secondary to connective tissue disease, idiopathic or due to infection, neoplasm or drugs. 1 Primary angiitis of the central nervous system (PACNS) is a rare syndrome characterized by inflammatory cell infiltration and necrosis of small- and medium-sized blood vessels of the brain parenchyma, spinal cord and leptomeninges. 2 It was reported in 1922 by Harbitz as an unusual type of arteritis associated with multinucleate giant cell arteritis of the small meninges and cerebrum and was first reported as a distinct clinical-pathologic entity in an article by Cravioto and Feigin in 1959. 3,4 Explore this issue January 2019 The estimated annual incidence rate of PACNS is 2.4 cases per 1 million person-years. Middle-aged men are most often affected by PACNS, with a median age at onset of approximately 50 years and a male-to-female ratio of approximately 2:1. 5 We describe the clinical, imaging and histopathological findings in a patient with PACNS. Case Presentation A 37-year-old woman presented at the emergency department with altered mental status, bilateral vision loss and weakness. She had a past medical history significant for multiple sclerosis on interferon beta, type 1 diabetes, hypertension, stage 4 chronic kidney disease and vitamin D deficiency. The patient was in her usual state of health on the morning of presentation. Around 7:30 a.m. she held a phone conversation with her father who had traveled to her home to transport her to a previously scheduled doctor’s appointment. She did not answer the door, but her father could hear her fumbling with the lock. He contacted the property manager and gained access to the home at approximately 8:45 a.m. At that time, he found her standing at the doorway, confused. When he questioned his daughter, she replied in streams of unintelligible, mumbled speech. Her father helped her to a couch and noted she had a poorly coordinated gait. Based on her symptoms, her father took her to the emergency department for evaluation. The patient had no recollection of the morning’s events and reported regaining her orientation and awareness on the way to the hospital. On arrival at the emergency department, she was afebrile and tachycardic (HR 100 beats per minute), with a blood pressure of 125/75 mmHG. She was breathing normally, with oxygen saturation of 99% on room air. When the patient was admitted to the medical ward, her vision loss had resolved. The physical exam was notable for normal mental status, right upper extremity mild dysmetria, with 4/5 strength in the right upper extremity and right lower extremity, with normal sensation and tone. There was no evidence of meningitis or focal neurologic signs. Imaging was obtained and included a computed tomography (CT) of her head, which showed several lesions suspicious for acute or subacute infarction. Magnetic resonance imaging (MRI) of her brain showed widespread foci of restricted diffusion with corresponding low apparent diffusion coefficient (ADC) signal throughout both cerebral and cerebellar hemispheres, most suggestive of acute infarcts. The distribution was atypical for multiple sclerosis, so they were not thought to be demyelinating plaques, despite her past history. Scattered T2/FLAIR signal hyperintensities noted within the left cerebellum and right cerebral peduncle were suggestive of remote infarcts (see Figures 1 and 2). Figure 1A A magnetic resonance angiogram (MRA) of the head/neck showed no high-grade stenosis, focal occlusion or aneurysm. A 2D echocardiogram showed a normal ejection fraction at 60–65% with diastolic dysfunction and no evidence of masses, thrombi or vegetations. Figure 1B An ultrasound of the carotid arteries showed 1–39% stenosis of the right and left internal carotid artery, with mild homogeneous plaque. The patient was started on dual antiplatelet therapy and a statin, and her care was then transferred to the stroke team for continued workup. The patient’s mental status deteriorated during admission. She became disoriented to questioning and eventually lost the ability to speak, swallow and walk. Laboratory tests revealed: erythrocyte sedimentation rate of 102 mm/hour (normal: 0–20 mm/hour), C-reactive protein of 1.7 mg/L (normal: 60 mL/min/1.73 m 2 ). She had a Glasgow Coma score (GCS) of 9 (eye opening, 4; verbal response, 1; motor response, 4) and global aphasia with no usable speech or auditory comprehension. Decerebrate posturing was noted during the exam. Figure 2: An MRI of the brain without contrast. Further tests were performed, including an electroencephalogram (EEG), which was abnormal with generalized slowing indicative of a marked, diffuse, nonfocal and nonspecific encephalopathy. An interventional radiology cerebral angiogram was conducted and showed multifocal areas of distal intracranial artery narrowing, suggestive of vasculitis (see Figures 3 and 4). A rheumatologist was consulted to evaluate the patient for central nervous system (CNS) vasculitis. The patient developed acute hypoxic respiratory failure and experienced a febrile episode. She was subsequently in­tubated and started on broad-spectrum antibiotics (vancomycin and piperacillin/tazobactam). A sputum culture grew Citrobacter werkmanii , which was treated with a seven-day course of piperacillin/tazobactam. Further lab test results: ANCA was normal (<1:20); MPO-ANCA was 2 units (normal: ≤20 units); PR3-ANCA was <0.2 units (normal: <0.4 (negative) units); ANA was negative (<1:160); anti-NMO antibody was negative; serum cryoglobulins were absent; anti-CCP antibody was 0.5 units/mL (normal: <5.0 units/mL); anti-beta 2 glycoprotein antibody was <9 SGU (normal: ≤20 SGU); DRVVT was negative; anticardiolipin antibodies were <9.40 (normal: 0.00–12.49 MPL); HIV was negative; RPR was non-reactive; a hepatitis panel was negative, as were a TB test and a test for Strongyloides antibodies. Cerebrospinal fluid was colorless, and demonstrated the following: The white blood cell count was 2/mm3 (normal: 0–5/mm 3 ), and 100% of these cells were lymphocytes. The red blood cell count was 60/mm 3 (normal: 0/cu mm), and all studies for infectious etiologies were negative, including EBV <2.6 log copies/mL (normal 2.6–7.6 log copies/mL), HSV, CMV PCR <2.30 log IU/mL (normal: <2.30 log IU/mL), Lyme antibody, Aspergillus antibody of <1:8 and Cryptosporidium Ag CSF. Figure 3 and Figure 4An interventional radiology angiogram shows multifocal areas of distal intracranial artery narrowing. Her rheumatoid factor was 22 IU/mL (normal: 0.0–15.0 IU/mL). Her C4 was elevated at 61 mg/dL (normal: 11–44 mg/dL). Her protein/creatinine ratio was 11.07 mg/mmol (normal: 0.00– 0.20 mg/mmol).
Several diseases can mimic PACNS, including reversible cerebral vasoconstriction syndrome, premature intracranial atherosclerosis, fibromuscular dysplasia, secondary cerebral vasculitis, malignancy, infections … Her renal function worsened after the angiogram, and she eventually required dialysis. A nephrologist was consulted and attributed her proteinuria and worsened renal dysfu nction to underlying diabetes and contrast-induced nephropathy. A renal ultrasound was unremarkable. The patient was initially started on 70 mg of prednisone daily. She was switched to pulse-dose steroids (1,000 mg methyl­prednisolone daily for three days) due to worsening neurologic status. Despite the pulse-dose steroids, the patient’s clinical progression continued to worsen. Repeat imaging showed evolving subacute infarcts. After the patient was cleared by an infectious disease specialist and after discussion with the neurologist, the decision was made to administer renally dosed cyclophosphamide (415 mg/m 2 ). About one week after the cyclo­phosphamide infusion, the patient was able to follow commands and was attempting to state her name. She self-extubated and had an improved GCS of 15. A brain biopsy showed lymphocytic vasculitis of uncertain etiology and remote cortical microinfarcts, with the affected vessels showing a modest number of intramural lymphocytes and foci of chronic inflammatory cells within the adventitia, which were primarily positive for CD3 (see Figures 5–10, right). There was no evidence of granulomatous inflammation, fibrinoid necrosis of the vessel walls or infectious organisms. The patient was tapered to 15 mg methylprednisolone for eight days and eventually discharged to an inpatient rehab facility for follow-up with the rheumatologist, neurologist and nephrologist. Figure 5: The leptomenigeal artery has significant narrowing due to cholesterol accumulation, and intramural and perivascular inflammatory infiltrates. Figure 6: The image at higher magnification is highlighted to show the cholesterol accumulation, and intramural and perivascular inflammatory infiltrates. Figure 7: The image at even higher magnification shows the cholesterol accumulation, and intramural and perivascular inflammatory infiltrates. Figure 9: Subacute cortical microinfarct displaying loss of parenchyma and reactive gliosis. Figure 8: Immunostaining for CD3 highlights the inflammatory T cell population permeating the vascular wall. CD20 was mostly negative.
Courtesy of Maria-Beatriz Lopes, MD, University of Virginia Pathology Discussion PACNS is a poorly understood entity, and significant challenges remain for diagnosis and treatment. The pathogenesis is not well understood, and to date no evidence has been found to suggest a genetic predisposition. Various viral infections have been proposed as factors, such as varicella zoster virus, West Nile virus, Mycoplasma gallisepticum and HIV. 6-14 In 1988, Calebrese and Mallek proposed diagnostic criteria for PACNS combining clinical, imaging and histology, which includes 1) acquired neurological deficit unexplained after complete evaluation, 2) diagnostic cerebral angiogram with narrowing of vessels suggestive of vasculitis, and 3) no evidence of systemic vasculitis or any other condition that could mimic the angiogram findings. 15 These criteria were revised in 2009 by Birnbaum and Hellmann to either a definite or probable diagnosis of PACNS, with the main difference being confirmation of vasculitis on biopsy specimen to prevent patients with reversible vasoconstriction syndromes (RVCS) from being treated with cytotoxic therapy. 16 Our patient fulfilled all three criteria for diagnosis of PACNS and had lymphocytic perivascular infiltrates on brain biopsy. The characteristic histopathologic findings consist of inflammatory infiltration of vessel walls by T lymphocytes and activated macrophages, which undergo granulomatous differentiation with giant cell formation. Different clinical subsets of PACNS include granulomatous angiitis of the central nervous system (GACNS), a rare subset of PACNS characterized by granulomatous angiitis confined to the brain. Patients present clinically with chronic insidious headaches, along with diffuse and focal neurologic deficits, often bilateral infarcts, as well as high-intensity T2-weighted fluid attenuation inversion recovery (FLAIR) lesions on MRI in the subcortical white matter and deep gray matter. Atypical CNS vasculitis, another subset of PACNS, comprises multiple manifestations of PACNS that are clinically, radiologically or pathologically distinct from GACNS. The most frequent and heterogeneous subset of PACNS included in this subset are patients with specific presentations, such as lesions, or patients with pathologic findings of lymphocytic infiltration or necrotizing vasculitis with transmural fibrinoid necrosis rather than granulomatous angiitis. 17 Benign angiopathy of the central nervous system (BACNS), which is now referred to as reversible cerebral vasoconstriction syndrome, was considered to be the third mimic of PACNS although not a true vasculitis. 2 The median age of onset is 50 years, but PACNS may affect patients of all ages. The neurological manifestations are diverse, ranging from hyperacute to chronic and insidious. In a study of 101 patients, Salvarani et al. found patients who presented with subacute manifestations of diffuse CNS dysfunction and acute presentation were highly unusual. 18 The most common init ial symptoms are headache (63%) and cognitive impairment (50%). Focal symptoms usually appear later in the course of the disease and include hemiparesis (44%), stroke (40%), aphasia (28%), transient ischemic attack (28%), ataxia (19%), seizures (16%), dysarthria (15%) and blurred vision or decreased visual acuity (11%). Infrequent manifestations, occurring in less than 10% of patients, include intracranial hemorrhage; amnesic syndrome; and spinal cord manifestations, such as paraparesis, quadriparesis, Parkinsonism, vertigo, dizziness or cranial nerve palsy; and most patients have multiple manifestations. No definite laboratory abnormality is diagnostic. The diagnosis of PACNS is challenging because of the nonspecific clinical presentation, the lack of highly specific laboratory and radiologic tests, and the difficulty of obtaining pathologic material. In the majority of published case series of PACNS, abnormal cerebrospinal fluid (CSF) findings have been reported; both CSF pleocytosis and protein elevation are frequent. 19 Obtaining appropriate CSF cultures, microbiologic stains, cytology and flow cytometry is crucial to rule out infectious and neoplastic disease. MRI is the neuroimaging modality of choice for patients with suspected PACNS, and MRI findings are abnormal in 90–100% of patients. MRI may demonstrate ischemic and hemorrhagic lesions of different ages, leukencephalopathies, tumor-like lesions or gadolinium enhancement of the meninges. 20 Infarcts may be seen in approximately 50% of cases; when present, infarcts are usually seen bilaterally in multiple-vessel tributaries affecting the cortex, as well as the subcortex. Gadolinium enhancement may occur in as many as one-third of cases; leptomeningeal enhancement may occur in 10–15% of cases, and when present in the nondominant lobe, may represent an ideal site for biopsy. 21 Angiography sometimes demonstrates bilateral vessel stenoses or occlusions consistent with an angiitis. In some cases, patients with histologically proved PACNS have an entirely normal angiogram. The angiographic pattern considered diagnostic of vasculitis is often caused by reversible vasoconstriction syndromes associated with drugs, migraine, hypertension, eclampsia or the postpartum period. 19,22 Patients must be evaluated for systemic vasculitis, which is characterized by the presence of constitutional symptoms and serological markers indicating systemic inflammation. The inflammatory process in PACNS is limited to the CNS. Several diseases can mimic PACNS, including reversible cerebral vasoconstriction syndrome, premature intracranial atherosclerosis, fibromuscular dysplasia, secondary cerebral vasculitis, malignancy, infections (e.g., VZV, HIV, hepatitis C, tuberculosis), other multi-system inflammatory disorders, such as sarcoidosis, moya­moya disease, genetic conditions (e.g., CADASIL), posterior reversible encephalopathy syndrome (PRES), chronic hypertension (microvascular cerebral ischemia), demyelinating diseases and others with multifocal cerebral thromboembolism. Other rare syndromes resembling cerebral vasculitis include reversible posterior leukoencephalopathy syndrome, MELAS (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes), ma­lignant intravascular lymphomatosis, Degos disease, amyloid angiopathy, Fabry’s disease, pseudoxanthoma elasticum, lipohyalinosis and storage diseases. 2,20 Brain biopsy is the gold standard for diagnosis to confirm and exclude other etiologies. In a study done by Alrawi et al., out of 61 patients referred for biopsy to test for suspected PACNS, alternative diagnoses were established in 24 cases (39%); 12 patients had infections, including three patients with brain abscesses, and eight patients had malignant neoplasms, including six with primary CNS lymphoma. 23 CNS vasculitis is a patchy disease that affects vessels in a skipped and segmental pattern, which limits the sensitivity of the procedure, and as many as 25% of the biopsies were falsely negative. 23 To improve the diagnostic yield, targeted biopsies should be performed with inclusion of leptomeninges. 17,24 Unfortunately, no randomized studies of PACNS have been done, and thus, all information on treatment is based on retrospective observational data and clinical experience. Treatment recommendations are derived from the protocols for systemic vasculitides with severe organ involvement in which a combination of steroids with cyclophosphamide is recommended. 20 The majority of case series suggest a high degree of good outcomes when patients are treated with glucocorticoids or glucocorticoids and cyclophosphamide. After remission is achieved, maintenance therapy with azathioprine or mycophenolate mofetil—and, rarely, methotrexate, given its low CNS penetration—is initiated. 2 Some reports indicate that combining mycophenolate mofetil and steroids allows disease control with disappearance of the neurological abnormalities, restoration of normal daily activities and dramatic improvement in brain MRI abnormalities. 25 Some case reports used rituximab as the initial treatment for CNS vasculitis, and TNF alpha inhibitors are being used for treatment of CNS vasculitis resistant to immunosuppressive treatment. 18,26,27 Figure 10: Immunohistochemistry for GFAP (glial fibrillary acidic protein) highlights the reactive gliosis of the subacute infarct. The disease is considered in remission when the patient is stable and improved clinical and radiologic features are observed. Serial MRIs should be obtained to help in the assessment of disease activity, and clinicians may consider repeat CSF analysis. 2 Efforts to limit accelerated atherosclerosis through aggressive control of diabetes, hypertension and dyslipidemia, as well as smoking cessation, is important. Routine vaccinations, osteoporosis prevention and prophylaxis for opportunistic infections should be included in treatment plan. 2 The estimated mortality rate of PACNS varies between 10% and 17%. Hajj-Ali et al. found that survival correlated with the initial findings of infarcts and gadolinium-enhanced lesions on MRI. 28 In the study analysis of 101 patients, Salvarani et al. reported 20% of patients with PACNS had moderate to severe disability, as assessed by the modified Rankin disability scores and the Barthel index, respectively. 5 A literature review shows a Marburg variant of multiple sclerosis that presents with vasculitis and extensive demyelination; however, our patient did not have any areas of demyelination on pathological specimens, which makes this diagnosis less likely. 29 A case of stroke occurring after initiation of interferon beta treatment for relapsing-remitting white matter disease has been reported. 30 This case is similar to our patient, who had met criteria for multiple sclerosis and developed progression of neurological symptoms after initiation of the interferon-beta treatment. The question remains if her diagnosis of multiple sclerosis was accurate or if her symptoms at that time were related to undiagnosed CNS vasculitis. Some evidence suggests autoimmune disease, especially vasculitis, worsens with interferon treatment. Thus, another concern is whether the interferon beta treatment was inappropriate and contributed to the severe cerebrovascular insufficiency. 30 Conclusion Diagnosis of PACNS remains a challenge and requires a high index of clinical suspicion, with appropriate workup to exclude other conditions. Further research needs to be done to improve our understanding of the etiology and pathogenesis of this disease, as well as our diagnosis and treatment approaches. Gbemisola Olayemi, MD , is a graduate of the University of Pretoria, South Africa, and obtained her medical degree at the Medical University of the Americas, Charlestown, Nevis, West Indies. Her internal medicine residency was at Leonard J. Chabert Medical Center, Houma, La., and she is currently engaged in a rheumatology fellowship at Ochsner Clinic Foundation, New Orleans. Eve Scopelitis, MD , joined the Department of Rheumatology at Ochsner Clinic in 2006. Prior to that she was professor of medicine and director of the Rheumatology Clinics at the Louisiana State University Health Sciences Center, New Orleans. Her medical degree was obtained at SUNY Upstate Medical Center in Syracuse, N.Y. She completed an internal medicine residency at Nassau County Medical Center, East Meadow, N.Y., and a fellowship in Rheumatology at the LSU Health Sciences Center, New Orleans. Jerald M. Zakem, MD , joined the Department of Rheumatology at Ochsner Clinic in 2000. He is currently an Instructor for the University of Queensland at Ochsner Clinical School. Prior to that, he was a clinical assistant professor of medicine at the University of South Florida in Tampa. His medical degree was obtained at University of Louisville, Ky. He completed an internal medicine residency and a rheumatology fellowship at the University of South Florida. References Carolei A, Sacco S. Central nervous system vasculitis . Neurol Sci. 2003 May;24(suppl 1):S8–S10. Firestein G, Budd R, Gabriel SE, et al. (2012). Kelley’s Textbook of Rheumatology , 9th ed . Philadelphia: Saunders, an imprint of Elsevier.

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Drugs, Safe and Not Safe, in Pregnancy

Drugs, Safe and Not Safe, in Pregnancy

The thalidomide tragedy of the 1960’s touched off intense concern and a vast amount of research about the safety of drugs taken during pregnancy. Many drugs (and druglike substances, including coffee, alcohol and tobacco) were tested in laboratory…

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Osteopenia Treatment Market to Garner Brimming Revenues by 2018 to 2026

Osteopenia Treatment Market to Garner Brimming Revenues by 2018 to 2026

Osteopenia Treatment Market to Garner Brimming Revenues by 2018 to 2026
Rockville, MD Thinning of bone mass is known as Osteopenia. Osteopenia is considered to be a serious risk factor for osteoporosis. Osteopenia is commonly observed in people aged above 50 who do not have osteoporosis but have average bone density. Smoking and drinking can affect the calcium level in the body, leading to weakening of bones. High salt, caffeine and soda consumption can also lead to osteopenia. Osteopenia treatment is a must for people above the age of 50. Healthy lifestyle plays a very important role in strengthening of bones. Regular exercise and healthy diet improve bone density. Developing healthy habits and osteopenia treatment methods can slow osteopenia and strengthen bones and prevent osteoporosis. Osteopenia treatment includes medications, which include bisphosphonate medications, such as ibandronate (Boniva), alendronate (Fosamax), risedronate (Actonel), zoledronate (Reclast) and raloxifene (Evista). Calcium and vitamin D supplements are also a part of osteopenia treatment. According to the National Osteoporosis Foundation, women aged 65 years and above & men aged 70 years and above should be tested for osteopenia. Also, adults aged 50 and above with a fractured bone, postmenopausal women, adults taking medication, such as prednisone or other steroids, and prone to medical conditions associated with bone loss, such as rheumatoid arthritis, should be tested for osteopenia. These group of people are at a high risk of developing osteopenia and osteoporosis. All these factors will act as driving factors for the growth of the osteopenia treatment market. Claim Sample Report For FREE: https://www.factmr.com/connectus/sample?flag=S&rep_id=2579 Osteopenia Treatment Market: Drivers and Restraints The growing aging population is one of the key factors responsible for the growth of osteopenia treatment market. Aging population is always at a high risk of osteopenia as aging causes loss of bone density. Moreover, increasing alcohol consumption is another factor that will drive the growth of the osteopenia treatment market. However, lack of awareness about osteopenia treatment may restraint the growth of the market. Additionally, the high cost of treatment and unavailability of treatments options in developing countries will also hamper the growth of the osteopenia treatment market. The global osteopenia treatment market can be segmented on the basis of test, method, end user and geography. Based on test, the global Osteopenia Treatment market is segmented as: Quantitative Computed Tomography (QCT) Peripheral Quantitative Computed Tomography (pQCT) Dual Energy X-ray Absorption (DEXA) Peripheral Dual Energy X-ray Absorption (pDXA) Others Based on method, the global osteopenia treatment market is segmented as: Invasive Based on end user, the global Osteopenia Treatment market is segmented as: Hospitals

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What is Prednisone for Cats? And What About Prednisolone for Cats?

<h1>What is Prednisone for Cats? And What About Prednisolone for Cats?</h1>

What is Prednisone for Cats? And What About Prednisolone for Cats?

Next on The Scoop: Is Cat Snoring Normal? Catster Tips What is Prednisone for Cats? And What About Prednisolone for Cats? What is prednisone and why would someone use prednisone for cats? And what’s the difference between prednisone and prednisolone for cats?
Melvin Pena | Jan 16th 2019 Also:
Prednisone and prednisolone for cats are steroids typically used to reduce inflammation and swelling; they have potentially dangerous side effects. Let’s review some other important facts about prednisone and prednisolone for cats here: Why is prednisone for cats used? Photography by Anna Dudko/Thinkstock. What is prednisone? What is prednisolone?
Nestled closely by the kidneys, a cat’s adrenal glands produce a hormone called cortisol. Cortisol serves a number of functions, not only breaking down glucose for use as energy, but also aiding with the immune system’s response to swelling and inflammation. Prednisone for cats and its metabolized form, prednisolone, are steroids, powerful synthetic versions of cortisol. Because of their potentially dangerous side effects, neither prednisone nor prednisolone should be prescribed for use in kittens or pregnant cats .
Why are there two versions of this catabolic steroid? First of all, if the thought of steroids and cats causes you to picture your cat gaining muscle mass and getting ripped, those performance-enhancing drugs are anabolic steroids, which build up. Catabolic steroids do the opposite; they break down. A cat’s liver processes prednisone, turning it into prednisolone. Prednisolone for cats is prescribed to kitties with weak or compromised livers. Why would someone use prednisone or prednisolone for cats?
Prednisone and prednisolone for cats tend to be prescribed as short-term anti-inflammatory medications. Because it reduces inflammation, prednisone for cats can be usefully deployed in kitties who suffer from swelling caused by allergies . These include relieving skin irritation from flea bites as well as anaphylatic shock responses to bee stings . Prednisone for cats is also used to treat all kinds of internal swelling, whether the source of the problem is an upper respiratory infection , pancreatitis or irritable bowel syndrome.
Though the most common uses are to reduce or inhibit swelling in cats, prednisone and prednisolone for cats are also used occasionally as a long-term steroid therapy for cats who suffer from more extreme health conditions. As a long-term treatment option, prednisone for cats is prescribed as an immune system suppressant to felines being treated for cancers such as lymphoma , giving other treatment methods a chance to work. Prednisone for cats is also given with brain swelling brought on by head trauma, or long-term joint pain and mobility issues associated with osteoarthritis. Is there a standard dosage when it comes to prednisone and prednisolone for cats?
Prednisone and prednisolone for cats are most frequently used to provide short-term relief. The standard dosages, at least for humans, are 5mg, 10mg, and 20mg. Cats are different and much smaller creatures, though. With great medicinal power comes great risk of side effects and withdrawal, so veterinarians might begin a short-term course of prednisone for cats at a high dosage initially, which is then rapidly tapered off until treatment is complete and symptoms or swelling have subsided.
Is prednisone for cats safe? Not especially, which is why it should be administered only under veterinary supervision while following all dosage instructions. A veterinarian will take all of a cat’s health information into account to determine proper dosage. Aside from the state of a cat’s kidneys, which guides the choice of prednisolone over prednisone, these major factors for dosage include: Weight Overall health and fitness How is prednisone for cats administered?
Prednisone for cats can be administered in a variety of formats, including tablets, oral liquid, syrup, eye drops or by direct injection. The format and dosage of prednisone for cats all depend on context, and veterinarians determine treatment cat by cat. Because prednisone and prednisolone for cats can damage the digestive tract, as we’ll see below, your veterinarian might recommend that the medication be given along with the cat’s food at mealtime. Side effects of prednisone and prednisolone for cats
Prednisone and prednisolone are extremely powerful steroids that are best and most effectively prescribed to cats as part of a short-term treatment plan. Unlike the commercials you see for any number of medications on television or while streaming online content, the side effects are generally not mild. Even a short-term treatment handled poorly can lead to severe withdrawal symptoms, and that’s just the start. The longer a cat takes prednisone or prednisolone, the more severe the side effects become. Mood/behavioral changes: including depression and lethargy as well as anxiety and aggression Trouble breathing: increased panting , rapid fatigue Impaired healing: minor injuries take longer to resolve Susceptibility to infection: a cat may be more apt to develop bacterial and viral infections

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MLK Hours

<h1>MLK Hours</h1>

MLK Hours

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