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Biomedical subjects

A Weinstein

Publications and source records attributed to A Weinstein.

At least 109 records · Page 6Linked to original sources
PubMed1982

Partial H (beta 1H) deficiency and glomerulonephritis in two families.

H (beta 1H) controls the C3b amplification loop by its ability to displace Bb from the alternative pathway convertase, C3b,Bb, and acts as a cofactor with I (C3b inactivator) to produce inactive C3b. Serum C3 levels are dependent to a large extent on the levels of H and I. Partial H deficiency was found in two families. The index case in Family 1 had vasculitis, thrombocytopenia, proteinuria, and depressed serum H and C3 levels. The index case in Family 2 had depressed serum H and B (Factor B) levels and IgA nephropathy which progressed to renal failure. His sister also had IgA nephropathy and depressed serum H and C3 levels. The depressed serum C3 level, B level, and H level could be responsible for the development of the immune diseases found in some members of these families.

Adolescent↗
PubMed1980

Familial discoid lupus erythematosus associated with heterozygote C2 deficiency.

Two siblings with chronic discoid lupus erythematosus and several family members were found with heterozygous C2 deficiency. An association with histocompatibility markers HLA-B18 and HLA-Dw2 was demonstrated, and the slow allotype of factor B was present. Linkage studies in this family suggested a close linkage between the C2 deficiency gene and genes coding for B18, Dw2, and BfS antigens. One HLA-ACB/DBf recombinant was observed showing closer linkage between HLA-D and Bf than between HLA-B and Bf.

Adolescent↗
PubMed1980

Familial partial deficiency of the third component of complement (C3) and the hypocomplementemic cutaneous vasculitis syndrome.

Familial hypocomplementemia of the third component of complement (C3) was found in four members of a family. The prospositus had cutaneous vasculitis, hypocomplementemia, arthralgia, proteinuria and thrombocytopenia. The combination of clinical, laboratory and pathologic findings resembled the "hypocomplementemic cutaneous vasculitis syndrome" (HCVS) or the "SLE-like syndrome" but serum C3 concentration was 35 to 57 per cent of normal in the propositus and in three relatives. Results of Clq precipitins, cryoglobulins and serologic tests for systemic lupus erythematosus were negative. Proteinuria (815 mg/day) but no hematuria was present. Analysis of the C3 phenotypes in this family showed that three hypocomplementemic members were apparent homozygous C3 slow but one was heterozygous C3 fast-slow. Metabolic studies with 125-Iodinated C3 in the clinically normal mother showed a 50 per cent reduction in C3 synthesis which was consistent with hypocomplementemia documented by serum protein assay. The occurrence of an immune complex-like disease (with characteristics of the HCVS) in a patient with a familial deficiency of C3 suggests that the preexisting C3 deficiency may predispose such persons to certain diseases.

Adolescent↗
PubMed1980

Drug-induced systemic lupus erythematosus.

Despite some confusion in the literature, drug-induced SLE is a well defined reversible clinical entity. The lupus syndromes induced by procainamide, hydralazine, and isoniazid have been well studied and the data obtained have been convincing. Other drugs may also induce a lupus syndrome, but adequate prospective studies have not been done. Furthermore, many other drugs previously incriminated appear to activate spontaneous SLE rather than induce the de novo lupus syndrome. The mechanism by which procainamide, hydralazine, and isoniazid exert their effect is not known, and animal studies have been unrewarding. However, hydralazine and procainamide are capable of complexing with nuclear antigens in vitro and possibly in vivo and may evoke antinuclear antibody responses in this way. A number of defined factors influence the development of the clinical syndrome, including the cumulative drug dosage, the acetylator phenotype of the individual, and the biochemical nature of the drug. Studies to date have not revealed how these drugs induce the clinical disease. While these agents may induce antinuclear antibodies in many individuals, genetic influences may be important in determining which patients will develop clinical symptoms. Further study of drug-induced systemic lupus erythematosus is necessary in order to resolve these problems regarding pathogenesis. The resolution of these problems may shed light on the pathogenesis of spontaneous SLE.

Antibodies, Antinuclear↗
PubMed1980

Familial late complement component (C6, C7) deficiency with chronic meningococcemia.

Two patients with chronic meningococcemia were found to lack hemolytic complement, one because of C6 deficiency, the other because of C7 deficiency. In both cases family studies were consistent with inheritance of the deficiencies as non-HLA-linked, autosomal co-dominant traits. Functional studies showed the deficient sera to support monocyte chemotaxis but not phagocytosis or lysis of meningococci. Both patients have remained well following antibiotic treatment.

Adolescent↗
PubMed1979

Changes in the pathogenesis and detection of intrahepatic abscess.

A comparison of two distinct 11 year time periods at our institution demonstrated a change not only in the cause of intrahepatic abscess but also in the procedures used to diagnose this condition. Significant improvement in the methods of detection of intrahepatic abscess permits earlier diagnosis and therapy and thus a significantly improved prognosis.

Adult↗
PubMed1978

Hypomorphic variant of C3, arthritis, and chronic glomerulonephritis.

Decreased synthesis (hypomorphism) of the fast variant of the third component of complement was detected in three generations of a family in which the propositus has an immune complex-type glomerulonephritis, arthritis, and a false positive test for syphilis. An affected sibling has bursitis, hematuria, and proteinuria. Decreased serum C3 protein was detected in three of four and decreased C3H50 in four of four family members with this hypomorphic variant (C3f). This is the first association between C3f and immune complex-type disease.

Adolescent↗
PubMed1978

CT detection of infected synthetic grafts: preliminary report of a new sign.

The diagnosis of infected synthetic grafts is difficult using traditional radiographic techniques. In four cases, computed tomography demonstrated small pockets of gas in the clot around the grafts, a distinctive finding for an infected prosthesis. Further experience is required to determine whether this will prove to be a reliable diagnostic sign. The gas collections in infected grafts differ from normal gas in their multiplicity and occurrence more than 10 days after surgery.

Aged↗
PubMed1978

Connective tissue disease and hyperviscosity syndrome with cryoprotein and immune complexes. Report of a case with autopsy findings and review of the literature.

A case is reported of chronic polyarthritis, hepatitis and hyperviscosity syndrome associated with the presence of intermediate and high molecular weight plasma complexes, a mixed cryoprotein and widespread endarteritis obliterans of small muscular arteries. The features of this case are compared with those of other reported cases of connective tissue disease associated with hyperviscosity syndrome.

Antigen-Antibody Complex↗
PubMed1977

Skin immunofluorescence in infective endocarditis.

Immunofluorescent microscopy was performed on the clinically normal skin of 3 patients with infective endocarditis, 3 patients with bacteremia, and 6 normal subjects. Perivascular deposition of immunoglobulin and complement was demonstrated in two of the three patients with infective endocarditis and in none of the bacteremic or control subjects.

Adult↗
PubMed1977

Treatment of rheumatoid arthritis with gold.

There have been three important double-blind studies evaluating the use of gold therapy in rheumatoid arthritis. Patients treated with gold have decreased number of joints with synovitis, decreased ring size, increased grip strength, and roentgenographic evidence of arrest or decrease in the progression of skeletal lesions. If a patient with active synovitis does not respond to nonsteroidal anti-inflammatory drugs after four months of treatment, he is a candidate for gold therapy. Maintenance gold therapy has been shown to sustain clinical improvement. Patients must be monitored with appropiate laboratory tests.

Arthritis, Rheumatoid↗