Biomedical subjects
Publications and source records attributed to A Rubinow.
We describe a 39-year-old man who suffered from delayed pressure urticaria for 2 years. His severe symptoms did not respond to antihistamine (H1 and H2) treatment and corticosteroid therapy was given despite severe side-effects. A new, nonsedating antihistamine drug, cetirizine, relieved most of his symptoms, enabled him to be weaned from corticosteroid therapy, and restored his former quality of life.
Autoantibodies to SSA/Ro and SSB/La antigens may have a pathogenic role in photosensitive skin disease and congenital complete heart block. Since salivary glands are the major target organ in Sjogren's syndrome (SS) we wondered whether these autoantibodies are present in saliva and may be involved in the sicca syndrome. Whole saliva and serum were collected from 15 patients with SS. Elisa analysis disclosed that 8 of the patients had anti-SSA/Ro antibodies, while 6 of them also had anti-SSB/La antibodies. Studies of immunoglobulin classes showed that the sera contained mainly IgG and IgM anti-SSA/Ro or SSB/La antibodies. One serum also contained IgA antibodies. Analysis of the saliva showed that in all positive samples IgG and IgA classes were present, while none of them contained IgM. Elisa and immunoblot analysis of sera and saliva from SLE patients without the sicca syndrome disclosed that both fluids contained anti-Sm antibodies. These findings suggest that the presence of anti-SSA/Ro and anti-SSB/La antibodies in saliva is not a unique phenomenon, characterizing the sicca syndrome. Therefore, their role in the pathogenicity of the Sjogren's syndrome has to be elucidated.
An unusual case of reversible reactive amyloidosis (AA) is described. A patient in the course of lobar pneumonia developed acute transient nephrotic syndrome and renal failure. Renal and liver biopsy showed amyloidosis and positive immunohistochemistry stains for amyloid A protein. The nephrotic syndrome resolved completely following 6 months of colchicine treatment and the urine is protein free after 6 years of follow-up.
In an attempt to define the role of HLA class II genes in predisposition to primary Sjögren's syndrome, patients of two different ethnic groups (Israeli Jews and Greeks of non-Jewish origin) suffering from this disorder were studied. Oligonucleotide genotyping revealed the majority in both groups to carry either DRB1*1101 or DRB1*1104, alleles that are in linkage disequilibrium with DQB1*0301 and DQA1*0501. The high frequency of the two alleles in these SS patients is in contrast with the accepted association of primary SS with HLA-DR3 in Italian and American individuals. Molecular analysis of DQB1 and DQA1 alleles found in American Caucasian and American black SS (or SLE) patients demonstrated high frequencies of DQB1*0201 and DQA1*0501. The fact that the majority of SS patients, across racial and ethnic boundaries, carry a common allele, DQA1*0501, implies its involvement in the predisposition to primary SS. Based on sequence analysis and the computer imaging of the HLA class II molecule structure, a hypothetical model for the role of the DQ molecule in promoting primary SS is proposed.
Reactive arthritis is associated with several gastrointestinal pathogens, particularly Shigella, Salmonella, Campylobacter, and Yersinia. Another, less well recognized bowel infection leading to reactive arthritis is pseudomembranous colitis, caused by Clostridium difficile. An illustrative case is presented, and the clinical features and characteristics of all reported patients with this association are reviewed. The pathogenesis of the reactive arthritis seems to be related to an immunological response in joints and other tissues against bacterial antigens, which gain access to the systemic circulation through increased intestinal permeability. Therapy with nonspecific antiinflammatory drugs, anticlostridial agents, or a combination of the above is effective. Despite the possibility of persistent articular involvement after gastrointestinal symptoms have subsided, the long-term prognosis seems to be excellent.
Progressive systemic sclerosis sine scleroderma, as well as neurological manifestations of progressive systemic sclerosis are rare in adult-onset cases. Neither have been reported in children with progressive systemic sclerosis, either separately or together. We describe a six-year-old girl with nocturnal seizures and Raynaud's phenomenon of three years' duration. She died of cardiopulmonary sclerosis without ever fitting the required criteria of systemic sclerosis. Nailfold capillaroscopy revealed the specific "scleroderma-pattern" and provided the only clue for a diagnosis of progressive systemic sclerosis, confirmed eventually by skin biopsy.
Idiopathic systemic capillary leak syndrome (Clarkson's disease) is characterized by recurring attacks of increased capillary permeability, resulting in severe hypovolemic shock due to plasma extravasation. Additional laboratory features include association with a monoclonal gammopathy, extreme hemoconcentration, and hypoalbuminemia. Rare manifestations of this syndrome are renal damage and rhabdomyolysis due to increased compartment pressure and ischemic myonecrosis. We present the findings in two patients with capillary leak syndrome complicated by severe rhabdomyolysis, in one case leading to acute renal failure. We review therapeutic aspects of this rare syndrome and emphasize the importance of early diagnosis and of prompt and aggressive fluid replacement.
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Rheumatoid nodulosis is a term used to describe adult patients with rheumatoid arthritis with little or no clinical joint inflammation who have numerous subcutaneous nodules indistinguishable from those of patients with active rheumatoid arthritis. This paper reports the case of a woman with quiescent rheumatoid arthritis who developed palmar nodulosis three weeks after the strenuous activity of painting her apartment. This case illustrates the direct association between the appearance of nodulosis and physical pressure despite inactive disease.
OBJECTIVE: To report two cases of enhanced oral anticoagulant effect induced by doxycycline coadministration. DESIGN: Case report. SETTING: University teaching hospital. PATIENTS: Two patients on chronic oral anticoagulation therapy who presented with severe bleeding and marked impairment in blood coagulation tests shortly after the initiation of doxycycline therapy. DISCUSSION: The literature concerning the possible effects of tetracyclines on hemostasis with or without antecedent anticoagulation therapy is reviewed and the speculated mechanisms for such an interaction are discussed. CONCLUSIONS: The administration of tetracyclines such as doxycycline to patients on chronic oral anticoagulation therapy may be associated with a marked enhancement in anticoagulant effect. In such patients the prothrombin ratio should be closely monitored and the anticoagulant dosage adjusted accordingly.
Ectopic GHRH is a relatively uncommon cause of acromegaly, which should be differentiated from pituitary adenoma, in order to avoid damage to the pituitary gland from unnecessary interventions. We report here on a 66-year-old man with acromegaly due to a GHRH-secreting bronchial carcinoid tumour, who recovered completely following removal of the tumour. His hormonal status was studied before and after the operation. Basal GH, GHRH, IGF-I and PRL levels, as well as plasma GH response to glucose load and TRH administration were abnormal before the operation, and became normal thereafter. The somatostatin analogue SMS 201-995 was found to be a potent inhibitor of the ectopic GHRH and the GH secretion (greater than 500 to 42 ng/l and 15.4 micrograms/l to 0.8 microgram/l, respectively). The effect on GHRH proved to be due to direct effect of somatostatin on the tumour cells, as demonstrated in tissue culture studies. A mixed meal was found immediately to suppress GHRH levels without such an effect on GH secretion. We conclude that the neuroendocrine tests usually practised in acromegaly cannot differentiate between ectopic GHRH secretion and pituitary adenoma. High plasma GHRH levels may serve as a diagnostic test for excessive GHRH production, which is almost always ectopic. These high levels are suppressible by somatostatin and a mixed meal.
A middle-aged woman developed recurrent episodes of severe life-threatening anaphylaxis. All episodes were strikingly associated with the first day of menstrual bleeding. Temporary relief was achieved with indomethacin therapy. The patient fully recovered following abdominal hysterectomy and salpingoophorectomy. The possible role of sex hormones and prostaglandin F2 alpha in the pathogenesis of this problem is discussed.
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We have previously found that there is a considerable variation in the responses of lymphocytes of normal individuals to autologous pokeweed mitogen (PWM)-induced lymphoblasts (PWM.AMLR) under completely autologous conditions. Having proposed that the reaction might measure an innate sensitivity for B cell hyperreactivity, we measured the PWM.AMLR of a normal group (8/18 positives) and a group of patients with rheumatoid arthritis (RA; 24/25 positives). Responses of the RA group were in general an order of magnitude greater than those of normal controls that generated positive responses, and the responding cells could clearly be shown to be both CD4-bearing and CD8-bearing T cells. T cell-independent B cell mitogen-induced (staphylococcus A) lymphoblasts derived from RA patients were capable of strongly stimulating autologous responder cells, while similarly treated cells of normal controls induced small responses. The staphylococcus A responses were smaller in general than those induced by PWM-induced lymphoblasts. These results support previous results that the degree of activation of both T cells and B cells determines the size of response in the autologous PWM.AMLR and that the PWM.AMLR may be used to determine differing degrees of the in vivo priming of these cells and their relation to clinical lymphocyte hyperreactivity.
The concentration of zinc in the skin has been determined noninvasively in patients with varicose vein ulcers. The examinations were performed with the use of diagnostic x-ray spectrometry, a method based on x-ray fluorescence for in vivo noninvasive evaluation of trace elements. Four skin foci were examined: at the periphery of the ulcer and control areas in a nonulcerated area in the diseased leg, in the noninvolved leg, and in the proximal inner surface of the arm. Zinc levels around the ulcer (mean +/- SD, 9.8 +/- 4.0 micrograms of zinc in 1 g of wet tissue) were higher than those in the nonulcerated skin in the diseased leg (6.9 +/- 3.0 micrograms/g, p greater than 0.05) and those in the noninvolved leg (5.4 +/- 2.0 micrograms/g, p less than 0.01). The concentration of zinc in the inner proximal surface of the arm (9.8 +/- 2.8 micrograms/g) was significantly higher than those of a control group (5.3 +/- 1.9 micrograms/g, p less than 0.01). These results suggest a defect of zinc distribution in patients with varicose vein ulcers.
Three patients, 2 with congenital valvular heart disease and 1 with a prosthetic aortic valve developed brucellosis. Brucella melitensis was isolated from blood of all 3 patients. The clinical and microbiological features suggested Brucella endocarditis and following successful antibiotic therapy, no surgery was required. The salient diagnostic features are discussed with emphasis on the management and prognosis of patients with Brucella endocarditis.
A 62-year-old woman with CREST syndrome and isolated pulmonary hypertension (without evidence of interstitial lung disease) underwent right heart catheterization to evaluate the effect of steroid and vasodilator treatment on hemodynamic parameters. During 12 weeks of prednisone treatment in a dosage of 40 mg daily, her condition markedly deteriorated clinically and hemodynamically as manifested by pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), mixed venous O2 saturation, and systemic vascular resistance (SVR). Successive trials with various vasodilators demonstrated ineffectiveness of isosorbide dinitrate and phenoxybenzamine, whereas nifedipine was effective in a 15-mg single dose, and prazosin 1 mg was partially effective in reducing PVR, SVR, and increasing CO and mixed venous O2 saturation. The combination of nifedipine 10 mg and prazosin 0.5 mg given alternately every four hours for 48 hours was the most effective in reducing PVR and PAP. Clinical response was favorable as well until treatment with medications was discontinued due to gastrointestinal side effects one month later.