Drug-induced lupus.

Arylamine N-acetyltransferases (NATs) are polymorphic drug-metabolizing enzymes, acetylating arylamine carcinogens and drugs including hydralazine and sulphonamides. The slow NAT phenotype increases susceptibility to hydralazine and isoniazid toxicity and to occupational bladder cancer. The two polymorphic human NAT loci show linkage disequilibrium. All mammalian Nat genes have an intronless open reading frame and non-coding exons. The human gene products NAT1 and NAT2 have distinct substrate specificities: NAT2 acetylates hydralazine and human NAT1 acetylates p-aminosalicylate (p-AS) and the folate catabolite para-aminobenzoylglutamate (p-abaglu). Human NAT2 is mainly in liver and gut. Human NAT1 and its murine homologue are in many adult tissues and in early embryos. Human NAT1 is strongly expressed in oestrogen receptor-positive breast cancer and may contribute to folate and acetyl CoA homeostasis. NAT enzymes act through a catalytic triad of Cys, His and Asp with the architecture of the active site-modulating specificity. Polymorphisms may cause unfolded protein. The C-terminus helps bind acetyl CoA and differs among NATs including prokaryotic homologues. NAT in Salmonella typhimurium supports carcinogen activation and NAT in mycobacteria metabolizes isoniazid with polymorphism a minor factor in isoniazid resistance. Importantly, nat is in a gene cluster essential for Mycobacterium tuberculosis survival inside macrophages. NAT inhibitors are a starting point for novel anti-tuberculosis drugs. Human NAT1-specific inhibitors may act in biomarker detection in breast cancer and in cancer therapy. NAT inhibitors for co-administration with 5-aminosalicylate (5-AS) in inflammatory bowel disease has prompted ongoing investigations of azoreductases in gut bacteria which release 5-AS from prodrugs including balsalazide.

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/bph.12598

Arylamine N-acetyltransferases: from drug metabolism and pharmacogenetics to drug discovery.

https://www.ajkd.org/article/S0272-6386(12)80488-4/pdf

The clearance of immune complexes from the circulation of man and other primates

Adverse side effects to drugs and chemicals in which immune mechanisms may be responsible have been described in drug-related lupus (DRL). The spectrum of drugs that may elicit DRL includes such classes as the hydrazines, arylamines, and chemicals that can be metabolised to amines. The 2 major pathways of metabolism — acetylation and N-hydroxylation — are described in detail.

Drug-Related Lupus

GENERAL Classification, diagnosis, and management of drug-induced respiratory disease Mechanisms of chemically induced respiratory toxicities Imaging of drug-induced lung disease Bronchoalveolar lavage in drug-induced lung disease Pathology of drug-induced respiratory disease Drug allergy in lung disease DRUG-INDUCED RESPIRATORY EMERGENCIES Drug-induced upper airway obstruction Drug-induced bronchospasm Drug-induced pulmonary oedema and acute respiratory distress syndrome Pulmonary complications of blood transfusion Drug-induced alveolar haemorrhage Pulmonary complications of illicit drug use Iatrogenic tracheobronchial and chest injury ONCOLOGY AND ALLIED CONDITIONS Pulmonary reactions to chemotherapeutic agents: The 'chemotherapy lung' Pulmonary reactions to novel chemotherapeutic agents and biomolecules Radiation-induced lung disease Pulmonary complications of bone-marrow and stem-cell transplantation Pulmonary complications of solid-organ transplantation Pulmonary infection induced by drugs Therapy-induced neoplasms NON-ONCOLOGICAL CONDITIONS Pneumonitis induced by non-cytotoxic agents Amiodarone pulmonary toxicity Eosinophilic pneumonia induced by drugs Bronchiolitis obliterans organizing pneumonia induced by drugs or radiotherapy Coughing induced by drugs Pleural disease induced by drugs Lupus erythematosus syndrome induced by drugs Vasculitis induced by drugs Pulmonary hypertension induced by drugs and toxins Respiratory involvement from herbals

Drug-induced and Iatrogenic Respiratory Disease

Family studies were carried out to look at CR1 expression in 24 hydralazine-induced SLE patients (Hz Reactors), who had been off the drug for at least 1 year and were clinically well at the time of the study. Mean expression of CR1 was reduced by 27% in the group of hypertensives who had developed Hz-induced SLE compared with a group of 35 normal individuals. CR1 expression was also slightly reduced in the relatives of the Hz Reactors compared to the normal group. Using a solid-phase Clq binding assay, CIC levels were found to be elevated in the plasma of the Hz reactors and an inverse relationship was found between CR1 levels and CIC levels in this patient group. Both CR1 levels and CIC levels in Hz Reactors and normal individuals were constant over the 36 weeks studied. This study suggests that there is an association between an inability to deal efficiently with CIC and susceptibility to developing Hz-induced SLE.

Erythrocyte complement receptor type 1 (CR1) expression and circulating immune complex (CIC) levels in hydralazine-induced SLE.

The well known HLA/disease associations have often in the past been attributed to the effects of Class 1 or 11 MHC products on an individual’s immune responsiveness. However there are reasons for thinking that more than one mechanism may be responsible for these associations. In this paper, we will outline the evidence which leads us to conclude that the Class 111 genes, encoding polymorphisms for the complement system proteins of C4A, C4B, and C2 govern susceptibility to systemic lupus erythematosus (SLE).

https://link.springer.com/content/pdf/10.1007%2F978-1-4612-5014-2_23.pdf

Class III HLA Genes and Systemic Lupus Erythematosus

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Erythrocyte complement receptor type 1 (CR1) expression and circulating immune complex (CIC) levels in hydralazine-induced SLE.

Class III HLA Genes and Systemic Lupus Erythematosus