Biomedical subjects
L Bielory
Publications and source records attributed to L Bielory.
Keratoconjunctivitis sicca in male patients infected with human immunodeficiency virus type 1.
Keratoconjunctivitis sicca (KCS) has not been reported as occurring as a single entity in the acquired immune deficiency syndrome (AIDS) population. In a survey of human immunodeficiency virus type 1 (HIV-1) infected male patients, the authors found that 21% (9/42) had signs and symptoms compatible with KCS with positive Schirmer test results. Tear osmolarity determinations were obtained from this group and from an age- and sex-matched group of HIV-infected patients without symptoms of KCS and with negative Schirmer test results. Eighty-nine percent of the suspect group had increased tear osmolarity, whereas none of the control patients had a hyperosmolar tear film (P less than 0.0001). Results strongly suggest that KCS occurs at a significantly greater rate in male individuals infected with HIV-1 than in the general population.
Serum sickness from iron-dextran administration.
Hypersensitivity vasculitis occurs in response to various exogenous agents. A case of a serum sickness syndrome with cutaneous vasculitis is described in a patient given an intravenous iron-dextran infusion.
Rapid oral desensitization to isoniazid and rifampin.
A 45-year-old black woman, sputum positive for acid-fast bacilli, developed hypersensitivity to both isoniazid and rifampin. She was admitted to the hospital and desensitized to both medications using modified penicillin protocols. Skin testing was negative to both drugs. Desensitization to isoniazid was complicated by a drug fever that was controlled by prednisone. The patient was able to maintain once-a-day dosing without incident even with steroid taper. To our knowledge, this is the first reported case of dual isoniazid and rifampin hypersensitivity with rapid oral desensitization.
Migraines, spontaneous abortions, central nervous system involvement and a positive VDRL in a 36-year-old white female.
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Administration of egg-derived vaccines in patients with history of egg sensitivity.
A history of a prior hypersensitivity reaction to egg has precluded patients from receiving egg-derived vaccines. We present three cases of successful administration of egg-derived vaccines; specifically influenza and measles, mumps, and rubella (MMR) to patients with egg hypersensitivity. Two were given influenza vaccine without incident and one was successfully desensitized to MMR. Skin testing and desensitization protocols are described. Desensitization to all three components of MMR has not been reported previously.
Clinical decision making. Conference on therapeutic and diagnostic options.
Clinical decision-making conference will be a new quarterly feature. Suggestions or contributions should be addressed to the authors. The authors discuss a 67-year-old male with coronary heart disease and renal failure.
Temporal arteritis in blacks.
Clinicians should be aware that temporal arteritis in blacks has a clinical presentation similar to that found in the white population. Heightened clinical awareness of the possibility of temporal arteritis in black patients should lead to earlier diagnosis and initiation of immunosuppressive therapy, thus helping prevent the severe sequela of blindness that has been documented in about half of the cases of untreated temporal arteritis.
Antithymocyte globulin hypersensitivity in bone marrow failure patients.
We evaluated the predictive value of immediate epicutaneous (prick) skin testing in 36 patients receiving a heterologous protein of equine origin, antithymocyte globulin (ATG), for bone marrow failure. Three of the 36 patients had positive epicutaneous test results. Two of these three received ATG treatment; one died of anaphylaxis while the other was desensitized successfully. Intradermal skin tests revealed positive wheal-flare reactions to progressively increasing dilutions of ATG in 96% of patients tested. None of these patients suffered any anaphylactic symptoms during treatment. Nine patients who had received ATG were evaluated subsequently for the possible development of immediate epicutaneous reactions three to 12 months after treatment; one of the nine patients developed a positive epicutaneous skin test reaction. We recommend that all patients who are to be treated or re-treated with heterologous antisera should be tested using the epicutaneous technique and that patients with positive reactions should be desensitized.
Allergic bronchopulmonary aspergillosis: report of three cases.
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Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure.
We have prospectively evaluated the clinical and immunological features of serum sickness in 35 patients treated for bone marrow failure with anti-thymocyte globulin (ATG 15 mg/kg/day) and methylprednisolone (1 to 1.5 mg/kg/day). Twenty-one patients were treated for 10 days and 14 were treated for 28 days. Clinical evidence of serum sickness developed in 30 patients (86%) and included fever and malaise (100%), cutaneous eruptions (93%), arthralgias (67%), gastrointestinal complaints (67%), cephalgia (57%), blurring of vision (37%), arthritis, (30%) and lymphadenopathy (13%). Clinical serum sickness began on day 7 +/- 1 (X +/- S.E.M.) and lasted for 10 +/- 2 days in the 18 affected patients receiving the shorter course of ATG. In the 12 affected patients receiving the longer course of ATG, serum sickness began on day 9 +/- 1. The earliest manifestations of serum sickness were fever, malaise, and cutaneous eruptions. Cutaneous findings consisted of morbilliform eruptions (n = 19) and urticaria (n = 1) or a combination (n = 8) that lasted 10 to 14 days. Twenty-one patients (75%) developed a highly characteristic serpiginous band of erythema and purpura along the sides of the fingers, toes, palms and soles 12 to 48 hours before other symptoms of serum sickness. Biopsies of lesional skin during the course of serum sickness revealed immune deposits (IgM, IgE, IgA and C3) in dermal vasculature in 7 of 9 patients. Immunological changes that occurred during the course of serum sickness included increased serum levels of IgG, IgM, IgA, and IgE. Circulating immune complexes, as measured by the C1q-binding assay, increased from a mean value of 12% to 45% on day 13 +/- 1. Complement levels (C3, C4, and CH50) decreased 50 to 80% from their baseline levels on day 10 +/- 2. Acute phase reactants increased: erythrocyte sedimentation rate, C-reactive protein and beta-2 microglobulin. Abnormal urinalysis developed in 17 patients (57%) over the course of serum sickness and included proteinuria, hematuria and hemoglobinuria on day 10 +/- 3. Hematopoietic response occurred in 43%. All 5 patients who did not develop serum sickness recovered from bone marrow failure. Our data document the clinical and immunopathological findings in human serum sickness and suggest that the principles of antigen-antibody interaction, complement activation, and resultant inflammatory response as seen in the previous animal studies are directly applicable to studies of patients with serum sickness.
Uveitis, cutaneous and neurosarcoid: treatment with low-dose cyclosporine A.
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Aeroallergen prevalence in New Jersey.
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Acute posterior multifocal placoid pigment epitheliopathy with unilateral retinal lesions and bilateral disk edema.
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Patients with bone marrow failure demonstrate decreased cutaneous reactivity to human C5a.
In vivo studies have shown that human C5a, a potent complement-derived anaphylatoxin and chemoattractant, produces immediate inflammatory reactions following intradermal injection in human skin. At concentrations within its potential physiologic range, intradermal injection of C5a elicits immediate wheal and flare reactions, increased vascular permeability, mast cell degranulation, and neutrophil-rich infiltrates. To assess the relative contribution of interacting cellular elements to C5a-induced inflammation in normal human skin, purified human C5a was tested intradermally in 8 patients with bone marrow failure (BMF). Reactions to C5a in patients with BMF were compared with responses at identical test sites in healthy volunteers and other patients with cutaneous disorders. Patients with BMF demonstrated significantly less wheal and flare reactivity following intradermal injection of C5a than controls (p less than 0.05 and less than 0.02, respectively). In these studies, patients with the greatest cytopenia generally showed the least cutaneous reactivity to human C5a. Biopsies of C5a test sites in patients with BMF revealed an absence of leukocytes in marked contrast to neutrophil-rich infiltrates observed at test sites in healthy volunteers. Avidin-fluorescent and/or Giemsa staining of skin biopsies revealed no difference between the number of dermal mast cells in patients with BMF and samples of normal human skin. In addition, skin test studies with histamine (2 micrograms) and morphine (5 micrograms) performed to assess cutaneous vascular and mast cell responsiveness in patients with BMF, normal volunteers and controls with rhinitis revealed no significant differences in cutaneous reactivity to these pharmacologic agents. These in vivo studies demonstrate that patients with BMF specifically exhibit decreased cutaneous reactivity to human C5a and suggest that neutrophils make an important and an immediate contribution to inflammatory responses elicited by this anaphylatoxin.
Lymphocyte phenotype and lymphokines following anti-thymocyte globulin therapy in patients with aplastic anaemia.
Twenty-two patients with adult onset aplastic anaemia were analysed before and after therapy with anti-thymocyte globulin (ATG). Lymphocyte phenotype, lymphokine levels or production, and haematopoietic progenitor cell number were measured 3 months after therapy; clinical response was determined 1 year post-therapy. By flow cytometry there was a significant reduction in both the proportion and absolute number of peripheral blood lymphocytes expressing activation antigen Tac (IL-2 receptor) and in the proportion of HLA-DR+ lymphocytes. For T cells bearing HLA-DR, there were proportional decreases in both activated helper and suppressor cells. There was no statistically significant difference pre-ATG to post-ATG in the absolute numbers of total, helper and suppressor lymphocytes. In all 10 haematologic responders the number of Tac bearing lymphocytes after ATG therapy was in the normal range, but half of 12 non-responding patients continued to have abnormally elevated numbers of Tac+ T cells. The proportion of Tac+ cells were not related to transfusion history. Gamma-interferon levels in serum by radioimmunoassay were elevated in almost half the aplastic patients; post-ATG, gamma-interferon was detectable in only three patients. Haematologic response to ATG therapy was associated with increased numbers of haematopoietic progenitors post-treatment, but pre-treatment values were not predictive of a response. These results are consistent with a pathogenic role for activated T-cells and their lymphokine products and suggest that the target of ATG therapy may be a Tac+ lymphocyte.
Serum sickness and haematopoietic recovery with antithymocyte globulin in bone marrow failure patients.
We have evaluated 33 patients with various bone marrow dyscrasias treated with horse antithymocyte globulin (ATG) (Upjohn) to determine the relationship of haematopoietic response to the occurrence of serum sickness. Patients received ATG intravenously over 10 or 28 d at a dose of 15 mg/kg/d. Total or partial haematological responses were noted in 12 of 33 patients. Twenty-eight patients developed clinical signs of serum sickness 6-14 d after the first infusion of ATG, while five patients did not. Twenty-five of these patients were evaluated by immunochemical assays for circulating immune complexes (C1q-binding assay) and 21 patients for serum complement (C3, C4 and CH50 assay) levels. There was a direct correlation between increases in immune complex levels, decreases in serum complement levels, and the development of the clinical signs and symptoms and serum sickness. Twenty-one of 28 patients who developed serum sickness failed to show haematological improvement. However, haematopoietic recovery occurred in all five patients who did not manifest serum sickness (P less than 0.05) and in four patients who failed to develop immune complexes. These findings indicate that the development of serum sickness is not required for a haematopoietic response with ATG and may indeed impair recovery.
Bone marrow failure: immunologic implications and treatment modalities.
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