Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenobarbital and phenytoin have good antiepileptic effect, but clinically significant untoward effects occur during their long-term use. Phenobarbital may cause hyperactivity, behavioral problems, sedation, and even dementia; these effects are dose related to some extent. Side effects of phenytoin include sedation, a cerebellar syndrome, phenytoin encephalopathy, psychosis, locomotor dysfunction, hyperkinesia, megaloblastic anemia, decreased serum folate level, decreased bone mineral content, liver disease, IgA deficiency, gingival hyperplasia, and a lupus-like hypersensitivity syndrome. Especially susceptible to the neurotoxic effects of phenytoin are epileptic children with severe brain damage who are on multiple drugs. In those children, balance disturbance may develop and be followed by gradual loss of locomotion. Among 131 mentally retarded epileptic patients, phenytoin intoxication occurred in 73 (56%), of whom 18 experienced persistent loss of locomotion. There is experimental evidence that the toxic action of phenytoin lies at the cellular level, predominantly in the cerebellum. Many experts avoid the long-term use of phenytoin because of its insidious and potentially dangerous side effects.
 ...
PMID:Side effects of phenobarbital and phenytoin during long-term treatment of epilepsy. 642 97

Recurrent bacteremia and enteritis due to a specific serotype of Campylobacter jejuni occurred over a 12-month period in a patient on hemodialysis with systemic lupus erythematosus who was also deficient in serum IgA and IgM. A bactericidal defect in the patient's sera for C. jejuni was shown. A role for immunoglobulins in the host response to C. jejuni is suggested, in that the IgA deficiency may have predisposed the patient to chronic gastrointestinal carriage and because the resolution of the bacteremia corresponded with the delayed appearance in the blood of IgG specific for the infecting strain.
 ...
PMID:Persistent Campylobacter jejuni infection in an immunocompromised patient. 672 Dec 98

A survey of 138 patients with systemic lupus erythematosus (SLE) (113 with nephritis) was carried out following the finding of a patient with membranous nephropathy and IgA deficiency who later developed SLE. Two hundred random hospital patients and 143 patients with idiopathic glomerulonephritis were also studied. One patient with minimal change nephrotic syndrome had IgA deficiency, but the other 342 patients had normal IgA concentrations. In the SLE group, in contrast, 4 patients had IgA deficiency and another patient prolonged IgA deficiency following phenytoin treatment. These and other published data suggest that the association of IgA deficiency is about 20 times more common in patients with SLE and nephritis than in the general population. This association may be a manifestation of defective T-cell regulation, a failure to eliminate immune complexes in the absence of IgA, or both.
 ...
PMID:Systemic lupus erythematosus and IgA deficiency. 682 88

The case of a 23 year-old female with a diagnosis of systemic lupus erythematosus associated to selective IgA deficiency is reported. The patient persistently had serum IgA levels below 0.05 mg/dl, while the remaining serum immunoglobulins were normal. No salivary IgA was detected, and the karyotype disclosed no abnormalities of the chromosome 18. In the in vitro immunological study a normal number of B and T lymphocytes was found, and decreased production of all surface immunoglobulins was observed.
 ...
PMID:[Selective IgA deficiency in systemic lupus erythematosus (author's transl)]. 732 32

In 1974 and 1975 7000 patients' sera were tested for levels of IgG, IgA and IgM. In 330 patients at least one of the three Ig classes was low. In most instances secondary immunodeficiency was present in association with myeloma, etc. However, 81 patients above 8 years of age fulfilled the criteria of idiopathic late onset Ig deficiency. In 44 of these patients clinical follow-up and repeated measurements of Ig levels were possible 1--8 years after the initial diagnosis. Selective IgA deficiency was present initially (15 patients) most frequently and persisted most often (14 patients). 4 patients had initially low IgG and 6 patients low IgM, findings which were only rarely confirmed later on. In 19 patients 2 or 3 Ig classes were initially low, with persistence of Ig deficiency in 12 individuals. In no instance had clinical symptoms appeared in the first two years of life. The following diseases were documented in the 44 patients studied (28 individuals with persistent and 16 with transitory Ig deficiency): recurrent infections (16 patients), atopic disease (8 times), rheumatoid arthritis (6 times), epilepsy (4 times), SLE (3 times) and enteropathies (twice). Seven patients also had a malignancy, 4 diabetes, and 2 hyperthyroidism.
 ...
PMID:[Idiopathic immunoglobulin deficiency in juveniles and adults. Catamnestic studies]. 739 75

We report three cases of selective immunoglobulin A (IgA) deficiency in which lack of direct immunofluorescent staining for IgA on renal biopsy specimens contributed to the diagnosis. In two patients, one with systemic lupus erythematosus and the other having asthma with nephrotic syndrome, the diagnosis of IgA deficiency was suggested by the complete absence of IgA on the renal biopsy. In the third patient, a renal transplant recipient, initial biopsies demonstrated donor-derived IgA, which disappeared on subsequent biopsies. The diagnosis of IgA deficiency was confirmed in all three patients by serologic quantification of IgA.
 ...
PMID:Identification of selective immunoglobulin a deficiency by renal biopsy. 764 63

A 58 year old woman developed systemic symptoms, interstitial lung disease, splenomegaly, leukopenia and anti-histone and anti-nuclear antibodies (ANA), while treated with hydralazine for hypertension. Five months after presentation she was admitted with high fever, skin rash and atypical lymphocytosis due to acute cytomegalovirus (CMV) infection. Worsening leukopenia and increased ANA were found, and high titres of anti-DNA antibodies, anti-cardiolipin antibodies and rheumatoid factors appeared. Hydralazine was stopped and the patient gradually became asymptomatic. All autoantibodies spontaneously disappeared (over 16 weeks), and the white cell count and spleen size became normal. The patient was found to be a slow acetylator and to have both HLA-DR4 and selective IgA deficiency. Thus, a multifactorial genetic susceptibility to develop drug-induced lupus was brought out in stages first by hydralazine and then by CMV, yet all manifestations and autoantibodies resolved spontaneously, demonstrating the complex interplay of varied environmental factors with a genetic predisposition in the pathogenesis of autoimmunity.
 ...
PMID:Effect of acute cytomegalovirus infection on drug-induced SLE. 783 Nov 73

The association of IgA deficiency with SLE is clearly established but occurs in only a small percentage of patients. Several hypotheses address the relationship between the two disease processes but the common link remains undetermined. It is important to investigate the diagnosis of IgA deficiency in patients presenting with SLE in order to provide the most appropriate treatment. This patient not only represents a rare presentation of SLE but highlights the uncommon occurrence with IgA deficiency and brings forth valuable teaching points of both diseases.
 ...
PMID:Cardiac tamponade and recurrent upper respiratory tract infections in a 22-year-old woman. 799 58

A young woman presented with high fever and edema in January, 1984, and was diagnosed as having systemic lupus erythematosus. Prednisolone administration failed to improve her symptoms. In May she was admitted to hospital because of elevated erythrocyte sedimentation rate (ESR), hypoproteinemia, hypogammaglobulinemia, hypocomplementemia, positive antinuclear antibody, elevated immune complex level, and diarrhea. Edema disappeared following administration of diuretics and albumin, although the pathogenesis was still undetermined. In September, she was referred to our institution because of severe watery diarrhea and hypoproteinemia. Endoscopic examination showed a diffuse inflammatory lesion in the duodenum and the colon. Radioisotopic 51Cr-albumin study results were compatible with protein-losing enteropathy. Hypoproteinemia and inflammatory changes of the intestine were improved by antibiotics, suggesting that the inflammatory lesion was caused by bacterial infection. Despite the improvements in clinical symptoms and laboratory findings, the serum IgA level was still low and the thrombocytopenia remained. The morphological characteristics of the megakaryocytes were consistent with idiopathic thrombocytopenic purpura. In May, 1986, the thrombocytopenia deteriorated, causing purpura. Prednisolone was administered again, and this resulted in normalization of the platelet count, although the IgA level remained low. Finally the prednisolone was stopped, and the IgA level gradually recovered, with the improvement of the enterocolitis. The exact pathogenesis of the whole picture in this case is unclear, but an 8-year-long clinical course suggests that the protein-losing was caused by an infectious enterocolitis superimposed on IgA deficiency.
 ...
PMID:A case of protein-losing enteropathy in idiopathic thrombocytopenic purpura with decreased IgA. 806 5

Approximately 10% of patients with systemic lupus erythematosus (SLE) develop epileptic seizures. When occurring before the onset of generalized SLE, the seizures are mainly primary generalized. Accordingly, long-term treatment with anti-epileptic drugs may precipitate SLE, or epilepsy and SLE may both occur as manifestations of a genetically determined predisposition. Some patients develop IgA deficiency during phenytoin treatment. This condition is reversible and IgA becomes normalized when phenytoin is withdrawn (drug-induced IgA deficiency). Some epileptic patients have a drug-independent IgA deficiency. Patients with drug-induced IgA deficiency are usually HLA-A2, while those with drug-independent IgA deficiency are HLA-A1,B8. The gene coding for IgA deficiency seems to be located in the HLA complex on chromosome 6. The gene locus for juvenile myoclonus epilepsy and related disorders is also on chromosome 6 and in close relation to the gene locus for the HLA system. Juvenile myoclonic epilepsy may be accompanied by drug-induced IgA deficiency, but there are also cases with other sometimes less-defined epilepsies, associated with this anomaly. It is possible that the relationship between epilepsy and immune disturbances is related to a common genetically determined susceptibility.
 ...
PMID:Immunological aspects of epilepsy. 833 10


<< Previous 1 2 3 4 5 6 Next >>