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Biomedical subjects

R O Bailey

Publications and source records attributed to R O Bailey.

9 recordsLinked to original sources
PubMed1988

Myasthenia gravis with thymoma and pure red blood cell aplasia.

A case of myasthenia gravis with histopathologic confirmation of spindle cell thymoma and pure red blood cell aplasia is reported. This is the twelfth case in the literature in which a simultaneous occurrence of all three disorders, with documented thymic pathology, is noted. Immunologic observations in this patient include an elevated acetylcholine receptor antibody and antinuclear antibody titer, agglutination of mouse red blood cells when combined with the patient's serum, and lack of inhibition of binding of radioactive erythropoietin to mouse red cell receptors when combined with the patient's serum. Although both myasthenia with thymoma and pure red blood cell aplasia may have a common immunologic denominator, our findings in this case indicate that inhibition of erythropoiesis is unrelated to erythropoietin receptor blockade. An alternative hypothesis is offered based on defective T-cell function.

Aged↗
PubMed1988

Sensory motor neuropathy associated with AIDS.

Clinical, laboratory, and pathologic observations in six patients with sensory motor peripheral neuropathy associated with the acquired immunodeficiency syndrome (AIDS) are presented. Blood and urine testing failed to reveal other causes for peripheral neuropathy. Distinctive CSF findings included elevated human immunodeficiency virus-specific indices. Peripheral nerve pathology confirmed the results of electrodiagnostic studies and revealed axonal loss and demyelination. Epineurial and endoneurial mononuclear infiltrates were present in three patients, and in one with early neuropathy, retroviral-like particles were present in peripheral nerve axoplasm. The findings indicate that in some patients with AIDS, neuropathy may be the direct result of a viral insult, although the causes are likely multifactorial.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Static spinal muscular atrophy causing temporomandibular joint dysfunction.

A case of static spinal muscular atrophy is described. The patient presented with temporomandibular joint dysfunction. This case is unusual, not only from the perspective of clinical disease progression, but also that markedly elevated creatine kinase levels were demonstrated. Despite an obvious association of neuromuscular disorders and TMJ disease, reports of primary disorders of muscle and nerve which may predispose to this condition are rare. This case emphasizes the need for careful neuromuscular evaluation in all patients with TMJ dysfunction of nonarticular origin.

Adult↗
PubMed1987

Myositis and acquired immunodeficiency syndrome.

Clinical and pathologic observations made in a patient with inflammatory myopathy associated with the acquired immunodeficiency syndrome (AIDS) are presented. Multinucleated giant cells were a prominent histopathologic feature in the muscle biopsy samples. The findings indicate that in some patients with AIDS myositis, inflammatory myopathy may be the direct result of infection with the human immunodeficiency virus.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Benign muscular dystrophy with contractures: a new syndrome?

Three patients are described with muscular dystrophy and contractures. Although this disorder bears similarities to Emery-Dreifuss disease and variants previously described, absence of cardiomyopathy is a distinguishing feature. Electrodiagnostic testing and muscle biopsy are consistent with a myopathy. An autosomal dominant pattern of inheritance is suspected, but the possibility of a Y-to-Y transmission cannot be completely excluded.

Adult↗
PubMed1986

Benign monoclonal IgAK gammopathy associated with polyneuropathy and dysautonomia.

The first case of benign IgAK monoclonal gammopathy associated with peripheral neuropathy is described. Dysautonomia is an unusual, yet prominent, manifestation of neuropathy in this patient. Electrodiagnostic testing and nerve biopsy were compatible with demyelination and axonal loss. Myelin sheath, perineural, and endoneural interstitial tissue fixation of anti-IgA and anti-kappa light chains was demonstrated by direct immunofluorescence microscopy. Absorption studies utilizing human peripheral nerve myelin resulted in complete removal of the paraprotein band. Analytic procedures with myelin-associated glycoprotein and gangliosides, however, were negative. Based on these findings, an alternative etiology for this neuropathy is hypothesized.

Aged↗
PubMed1986

Infantile facioscapulohumeral muscular dystrophy: new observations.

Clinical, electrodiagnostic, and biopsy findings in a family with infantile facioscapulohumeral muscular dystrophy are reported. Four of eight family members having the disorder, all with onset in infancy, developed severe weakness leading to death in adolescence. The clinical course and prognosis of infantile facioscapulohumeral muscular dystrophy may, therefore, be as devastating as that of Duchenne muscular dystrophy. The unusual infantile presentation and high mortality in our affected family members suggest that the gene coding for this disorder may be different from that responsible for conventional facioscapulohumeral muscular dystrophy.

Adolescent↗
PubMedDate not supplied

Familial amyloid polyneuropathy.

Amyloid fibrils were isolated from the myocardium of two patients with familial amyloid polyneuropathy. The solubilized amyloid fibril whole protein shared immunologic determinants with normal human serum prealbumin (transthyretin), but revealed subtle differences on immunoelectrophoresis and radial immunodiffusion. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, amyloid fibril whole protein was resolved into numerous bands that reacted with antitransthyretin on immunoblots. The whole protein also contained peptide fragments of fibronectin, but was devoid of amyloid P protein. An antiserum raised against the whole protein was suitable for immunocytochemistry of amyloid in paraffin sections. In contrast, commercial antitransthyretin, raised against the intact tetrameric protein failed to react with tissue amyloid. Immunochemical and immunocytochemical results support the concept that familial amyloid polyneuropathy with cardiomyopathy is due to infiltration of susceptible tissues by an anomalous transthyretin.

Aged↗