Vaccine immune response and side effects with the use of acetaminophen with influenza vaccine.

The purpose of this study was to determine whether acetaminophen impairs the immune response to influenza vaccine. Influenza vaccine is an under-utilized preventive measure, partly because of the unfounded perception that fever and myalgias frequently follow vaccination. While acetaminophen may decrease these infrequent side effects, it may also alter the immune response to vaccination. We compare the effect of acetaminophen with placebo on the humoral immune response to the 1991-1992 commercially available influenza vaccine. We studied 60 healthy, elderly subjects from a geriatric clinic and 20 infirm, elderly subjects from a nursing home. The subjects were randomly assigned to receive placebo or acetaminophen (1,000 mg every 6 h) for 2 days. Acetaminophen did not depress or enhance the immune development of serum hemagglutination inhibition antibody to the three vaccine antigens. The systemic side effects of fever and myalgia were uncommon in both groups. The healthy elderly subjects mounted a significantly better immune response to the influenza virus A/Taiwan/1/86 (H1N1) vaccine strain than did the infirm elderly subjects (geometric mean titer, 115 versus 51; P = 0.003). The functional activity score obtained by using the chronic healthy evaluation component of the Acute Physiology and Chronic Health Evaluation system could be used to distinguish the healthy from the infirm elderly (scores of 1.27 versus 3.75, P < 0.001). Acetaminophen neither depressed nor enhanced the serum antibody response to the vaccine in the healthy and infirm elderly subjects studied.     

Re: Re: Did King Herod suffer from a rheumatic disease? doi: 10.1007/s10067-017-3583-z

Clinical Rheumatology -     

Food induced ("allergic") arthritis: clinical and serologic studies

These studies sought to confirm our recent report of a patient with rheumatoid-like arthritis (RA) with clinical and immunologic milk sensitivity, to assess the prevalence of food related rheumatic symptoms, and to identify clinical and serological features of these patients. Thirty percent of our patients with RA alleged food related ("allergic") arthritis. Sixteen patients have now completed 19 double blind, controlled food challenge studies: 3 demonstrated subjective and objective rheumatic symptoms after double blind, encapsulated food challenges. The 3 were virtually asymptomatic when receiving elemental nutrition or not taking the offending foods. One was our milk sensitive patient who had increased IgG4 anti-alpha-lactalbumin, IgG-milk complexes, and delayed skin and cellular reactivity to milk; one developed inflammatory synovitis after shrimp ingestion and had increased IgG antishrimp; and another was a cardiac care unit (CCU) nurse who experienced rheumatic symptoms after exposure to nitrates. All were seronegative with palindromic symptoms and nonerosive disease. IgG, G4, A, M, and E antifood, Ig-food immune complexes, and in vitro cellular reactivity to foods were not otherwise distinctively abnormal in these or other patients with rheumatic diseases. Thus most patients alleging food induced rheumatic symptoms did not show these on blinded challenge, but some did. Probably not more than 5% of rheumatic disease patients have immunologic sensitivity to food(s). Such patients have been identified only by controlled challenge studies. These observations suggest a role for food allergy in at least some patients with rheumatic disease.     

Challenging issues in rheumatology: thoughts and perspectives

Clinical Rheumatology -     

Coincident Kikuchi-Fujimoto’s disease and adult-onset Still’s disease: report of a patient from an uncommonly affected population and case-directed systematic review

Clinical Rheumatology - Kikuchi-Fujimoto's disease (KFD) and adult-onset Still’s disease (AOSD) are rare idiopathic inflammatory conditions of unknown etiology. Ten prior instances of KFD...     

Unrecognized staphylococcal pyarthrosis with rheumatoid arthritis

Four patients whose rheumatoid arthritis (RA) was complicated by staphylococcal arthritis were identified. All patients had active, long-standing disease with destructive changes. Affected joints included hip (two patients), knee (one patient), and shoulder (one patient). Pain and loss of motion in the affected joint were prominent, but toxic features of pyogenic infections--hectic fever, chills, sweats, local warmth, or erythema--were conspicuously absent. Two patients had moderate fever and three patients had mild leukocytosis. No patient was leukopenic. When present, fever was attributed to infected decubiti or urinary tract infection and treated with antibiotics. Therapy with corticosteroids and nonsteroidal antiinflammatory drugs (NSAIDs) probably masked symptoms and delayed the correct diagnosis. Purulent synovial effusions were discovered serendipitously--during arthrography (knee), attempted Girdlestone procedure (hip), and aspiration prior to steroid injection (shoulder). Sepsis was included in the preoperative diagnoses only once (hip). Prior instrumentation (aspiration or injection) of the affected joint was not a feature in any patients, although one patient had undergone insertion of a knee prosthesis one year prior to sepsis. Infectious organisms were Staphylococcus aureus in three patients and Staphylococcus epidermidis in one. Severe sequelae ensued in three of four patients: death from recurrent sepsis (one patient), loss of prosthesis leading to knee arthrodesis (one patient), and protracted sepsis with additional pyarthrosis (one patient). The only patient to regain preseptic joint function (shoulder) had not been on long-standing corticosteroids. Pyarthrosis must be considered in RA patients with unusually painful or stiff joints even in the absence of toxic symptoms.     

Epilogue: How Will We Care for Patients with Early Arthritis?

This article draws conclusions about pinpointing the actual onset of disease and when interventions should start to occur. The identification of necessary biomarkers will be discussed. We will also examine the incremental consequences of delaying therapy, particularly for 'preclinical' disease. Medical economic analyses can help us balance benefits and avoid some adverse outcomes for patients. To conclude, we will discuss the new roles that need developing for primary care physicians and non-physican providers.