Neil Kramer

Pilot study of dietary fatty acid supplementation in the treatment of adult periodontitis

The anti-inflammatory effects of both n-3 and n-6 polyunsaturated fatty acids (PUFA) have been demonstrated in vitro and in many disease states, in particular in the treatment of rheumatoid arthritis. The benefit of n-3 PUFA supplementation has been documented in animal models of periodontal inflammation and a trend towards reduced inflammation has been seen in human experimental gingivitis. The purpose of this study was to examine the potential anti-inflammatory effects of PUFA supplementation, by administration of fish oil as a source of the n-3 PUFA, eicosapentaenoic acid, and borage oil as a source of the n-6 PUFA, gamma-linolenic acid (GLA), to adults with periodontitis. Thirty adult human subjects with periodontitis were administered either fish oil 3000 mg daily; borage oil 3000 mg daily; fish oil 1500 and borage oil 1500 mg daily, or placebo. The modified gingival index, the plaque index (PI), periodontal probing depths and beta-glucuronidase levels in gingival crevicular fluid were measured at baseline and after 12 weeks of treatment. Improvement in gingival inflammation was observed in subjects treated with borage oil (P<0.016), with a trend apparent in subjects treated with fish oil or a combination of PUFA. There was no statistically significant improvement in PI, although a trend was apparent in those receiving borage oil. Improvement in probing depth was seen in those subjects treated with either fish oil alone or borage oil alone, but statistical significance was only seen for the comparison of borage oil and placebo (P<0.044). No change was seen in gingival crevicular fluid (GCF) beta-glucuronidase levels. The use of borage oil supplementation, a source of the n-6 PUFA, GLA, can have beneficial effects on periodontal inflammation. n-6 PUFA supplementation seemed to offer more impressive results than either n-3 PUFA supplementation or the combination of lower doses of the two supplements. Additional studies will be necessary to more fully assess the potential of these agents to favorably affect periodontal inflammation.

Working memory deficits in chronic fatigue syndrome: Differentiating between speed and accuracy of information processing

To examine the relative influence of speed of information processing versus working memory ability, CFS participants with psychiatric comorbidity (CFS-Psych) and CFS without a psychiatric history (CFS-noPsych) were examined on tests of visual and auditory processing speed and visual and auditory working memory. Compared to healthy controls (HC) and a group of participants with rheumatoid arthritis (RA), the CFS-noPsych group displayed significantly reduced performance on tests of information processing speed, but not on tests of working memory. No significant differences were observed between the CFS-Psych group and any other group in the study. The implications of group heterogeneity on the understanding of cognitive impairment in CFS are discussed.

Lyme Disease Misdiagnosed as a Brown Recluse Spider Bite

Excerpt To the editor: Lyme disease is a tick-borne illness caused by the spirocheteBorrelia burgdorferi(1). The condition is usually heralded by the appearance of the characteristic skin lesion, e...

ANCA‐positive vasculitis associated with simvastatin/ezetimibe: expanding the spectrum of statin‐induced autoimmunity?

Although autoimmune syndromes such as systemic lupus erythematosus and dermatomyositis have been previously reported in association with statin use, vasculitis has not been well described. We present a patient with an antineutrophil cytoplasmic antibody‐positive, predominantly cutaneous vasculitis, the temporal course of which was associated with simvastatin/ezetimibe use. The patient’s serologic findings were consistent with drug‐induced disease, with high titer antimyeloperoxidase, in addition to antinuclear and anti‐Ro (SSA) antibodies. The patient demonstrated complete resolution of symptoms simply by withdrawing the drug.

The prevalence of insulin receptor antibodies in patients with systemic lupus erythematosus and related conditions.

Autoantibodies to the insulin receptor have been demonstrated to antagonize the physiologic actions of insulin, most often resulting in hyperglycemia unresponsive to massive doses of insulin (type B insulin resistance). Patients with these anti-insulin receptor antibodies typically have a coexistent autoimmune disorder, most commonly systemic lupus erythematosus (SLE) or undifferentiated autoimmune syndromes. Attempting to determine the prevalence and significance of anti-insulin receptor antibodies, sera from consecutive patients with SLE and early undifferentiated connective tissue disease (UCTD) were tested for the presence of anti-insulin receptor antibodies by radio-immuno assay. Thirty-eight patients participated in the study. Twenty-six had SLE and 12 had UCTD. One patient with SLE (2.6%) was positive for anti-insulin receptor antibodies. None of the patients demonstrated evidence of insulin resistance, hypoglycemia, ovarian hyperandrogenism, or acanthosis nigricans, findings commonly linked with the presence of anti-insulin receptor antibodies.The results presented here indicate that the incidence of anti-insulin receptor antibodies in patients with SLE or UCTD, without associated history of altered glucose metabolism, is quite low. Because in most cases the disturbance of glucose metabolism dominates the clinical picture at presentation and the associated systemic autoimmune syndrome presents either simultaneously with or subsequent to the diagnosis of diabetes, the measurement of anti-insulin receptor antibodies should be reserved for patients with indications of disordered glucose homeostasis.

Hypereosinophilia and Seroconversion of Rheumatoid Arthritis

At the intersection of atopy and autoimmunity, we present a patient with seronegative rheumatoid arthritis (RA) who developed hypereosinophilia, without evidence of other etiologies, as she became rheumatoid factor (RF) positive. Although the magnitude of eosinophilia in patients with RA has been thought to reflect the severity or activity of the RA, in our patient, eosinophilia developed at a time when the patient’s synovitis was well controlled. Although eosinophilia may reflect associated drug hypersensitivity, discontinuation of the medications utilized to control our patient’s disease, adalimumab and methotrexate, did not promote clinical improvement. Probably the most curious aspect of our patient was the concomitant development of rheumatoid factor seropositivity in the setting of previously seronegative RA. The temporal relationship between the development of peripheral eosinophilia and seroconversion suggests a possible connection between these events. We speculate that the T cell cytokine production that can induce eosinophilia may simultaneously activate RF production.

Evolving connective tissue disease influenced by splenectomy: beneath the sword of Dameshek.

In years past, there was concern that splenectomy could lead to dissemination of occult systemic lupus erythematosus. Clinical studies subsequently effectively refuted that concept. However, there remains uncertainty regarding the role of the spleen in autoimmune diseases and the effect of splenectomy on their course. We present a case of a 56-year-old woman with autoimmune hepatitis and rheumatoid arthritis, without clinical or serologic features of lupus, who developed glomerulonephritis and antiphospholipid syndrome subsequent to an elective splenectomy. Literature review was performed to identify examples of the effect of splenectomy on other autoimmune diseases. Splenectomy has been linked with the development of new autoimmune phenomenon, alterations in the clinical course of patients with prior autoimmune disease, such as in our patient, and in a progressive redistribution of memory B cells that may influence autoimmune disease activity and may have been involved in the alteration in our patients clinical course.

Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin

PURPOSE Although aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert inhibitory effects on platelets in vitro and in vivo, there are insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet function. SUBJECTS AND METHODS We enrolled 25 healthy adult volunteers who were administered ketoprofen (extended-release capsules, 200 mg daily) for 1 week, followed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprofen (200 mg daily) alone during the second week. Platelet aggregation, stimulated by epinephrine and arachidonic acid, and cyclooxygenase activity, measured by thromboxane B(2), were measured at baseline, on day 8, and on day 15. RESULTS On day 8, all subjects demonstrated abnormal platelet aggregation (>50% inhibition), which persisted at day 15 in both the aspirin and no aspirin groups. One week of ketoprofen treatment reduced thromboxane B(2) levels by 84% in the aspirin group and by 85% in the no aspirin group (P = 0.8), without any further inhibition measured on day 15. CONCLUSION Extended-release ketoprofen significantly inhibited platelet aggregation and thromboxane B(2) production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patients who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy.

Case Report:Langerhans Cell Histiocytosis Associated With Elevation of Angiotensin-Converting Enzyme Levels

The authors describe a 22-year-old man with osteolytic mandibular and maxillary lesions. Biopsy substantiated the presence of Langerhans cell histiocytosis (eosinophilic granuloma). Levels of serum angiotensin-converting enzyme (ACE) were elevated repeatedly. After definitive therapy with excision and bone grafting, ACE levels returned to normal. The role of histiocytes in ACE production is discussed. Langerhans cell histiocytosis should be considered in the diagnosis of conditions occurring with elevation of serum ACE levels and clinical findings similar to sarcoidosis.

Renal Lymphoma: Unusual Lymphoproliferative Manifestation of Sjögren’s Syndrome

To the Editor: Sjogren’s syndrome (SS) is a chronic autoimmune disease characterized early in its course by lymphocytic infiltration in the salivary and lacrimal glands, resulting in the major manifestations of keratoconjunctivitis sicca and xerostomia. Presumably through a multistep lymphoproliferative process, SS has been associated with the development of non-Hodgkin’s lymphoma (NHL) in 5%–10% of patients1. Mucosa-associated lymphoid tissue (MALT) lymphomas constitute the majority of NHL subtypes seen in SS, followed by nodal marginal zone lymphomas and diffuse large B-cell lymphomas (DLBCL)2. We describe what could be the first case of primary DLBCL of the kidney, a rare extranodal lymphoma, as a lymphoproliferative complication of SS. A 64-year-old woman presented at age 39 with polyarthralgias and morning stiffness attributed to rheumatoid arthritis (RA). She was treated with hydroxychloroquine and nonsteroidal agents. She subsequently developed dry eyes, dry mouth, difficulty swallowing without drinking fluids, and vaginal and nasal dryness, which she treated with topical moisturizing agents. At age 58, she was noted to have mild pancytopenia with leukocytes 3600/mm3, hemoglobin 11.3 g/dl, and platelets 95,000/mm3. Bone marrow examination revealed erythroid hyperplasia, megakaryocytic hyperplasia, and atypical lymphocytosis. Urinalysis showed 20–30 white blood cells/high-powered field (HPF), without red cells, bacteria, nitrite, or proteinuria. Serological testing revealed antinuclear antibody (ANA) 1:640 speckled pattern; absence of antibodies to dsDNA and Sm/RNP; anti-SSA antibody 413 U (strongly positive); anti-SSB 129 U (weakly positive); rheumatoid factor (RF) 32 IU (normal … Address correspondence to Dr. E.D. Rosenstein, Institute for Rheumatic and Autoimmune Diseases, Overlook Medical Center, 33 Overlook Road, Summit, New Jersey 07901, USA., E-mail: elliot.rosenstein{at}atlantichealth.org