Rheumatic disorders associated with hepatitis C.

The hepatitis C virus (HCV) is a common virus of world-wide distribution affecting up to 3% of the world's population. Its genetic diversity, with multiple subtypes, and existence in the form of quasispecies in individual hosts, is, in part, responsible for high rates of chronic infection. Individuals with HCV infection will undoubtedly present to rheumatologists and other health care professionals with rheumatic and other immunological disorders related to what was usually a remote and asymptomatic acute infection. The goals of this review are: (1) to summarize clinical observations regarding rheumatological and immunological diseases linked with HCV infection; (2) to provide relevant information on the molecular biology of HCV; (3) to discuss the state of the art regarding the use of diagnostic studies; (4) to consider the differential diagnosis of liver disease and rheumatic disorders; and (5) to provide a practical guide to the history, physical examination, laboratory work-up, disease monitoring, and therapy of HCV patients with rheumatic disorders.

Hepatitis C infection presenting with rheumatic manifestations: a mimic of rheumatoid arthritis.

OBJECTIVE: To describe the clinical features of a group of patients presenting with rheumatic manifestations who were subsequently determined to have hepatitis C infection. METHODS: A case study of 19 consecutive patients referred to private practitioners in Tacoma and Federal Way, Washington, because of polyarthritis, polyarthralgia, or positive rheumatoid factor (RF) who were subsequently found to have hepatitis C. Patients were tested for hepatitis C when they met the following screening criteria: abnormal liver biochemical studies or history of transfusion, jaundice, or hepatitis. RESULTS: Risk factors for hepatitis C infection were present in 14 patients, including transfusions (8) or intravenous drug use (6). Eight patients gave a history of previous jaundice or hepatitis predating their articular complaints by intervals ranging from 3 mos to 23 yrs. Liver biochemical tests were normal in 6 patients. Serologic evidence of hepatitis B or human T lymphotrophic virus type II was present in 3 of 19 and 2 or 14 patients, respectively. Carpal tunnel syndrome (8 patients), palmar tenosynovitis (7 patients), fibromyalgia (6 patients), and nonerosive, nonprogressive arthritis typified the articular manifestations. Fifteen patients fulfilled diagnostic criteria for rheumatoid arthritis (RA). Three patients had small vessel skin vasculitis. The arthritis responded well to treatment with low dose prednisone and hydroxychloroquine. CONCLUSION: Hepatitis C infection can present with rheumatic manifestations indistinguishable from RA. The predominant clinical findings include palmar tenosynovitis, small joint synovitis, and carpal tunnel syndrome. Risk factors such as transfusions and IV drug abuse or a history of hepatitis or jaundice should be included in the history of present illness of any patient with acute or chronic polyarthritis or unexplained positive RF. In such patients, gammaglutamyl aminotransferase, serologic studies for hepatitis C, and other tests appropriate for chronic liver disease should be performed.

Lower esophageal rings as a cause of dysphagia in progressive systemic sclerosis--coincidence or consequence?

Lower esophageal rings were found in five of 40 consecutive patients seen with progressive systemic sclerosis. Three of these five patients had diffuse skin involvement and two had the CREST variant of progressive systemic sclerosis. All of the patients with lower esophageal rings had intermittent esophageal obstruction (initially attributed to esophageal dysmotility), but so did five of seven patients with esophageal strictures without lower esophageal rings. Esophageal bougienage relieved this symptom in four of the five patients with rings in which it was performed. Persistent relief of these obstructive symptoms (6-36 months) in the patients with rings was in contrast to the recurrent dilatations that have been needed in the group of patients with peptic strictures. In contrast to esophageal aperistalsis and/or stricture formation, the lower esophageal ring, perhaps as a consequence of chronic gastroesophageal reflux, may be a more treatable cause of dysphagia in patients with progressive systemic sclerosis.

Concurrent systemic lupus erythematosus and salmonellosis.

Salmonellosis was diagnosed in 4 patients with systemic lupus erythematosus (SLE). Three patients were taking prednisolone, and 3 had evidence of nephritis. All patients were febrile with clinical evidence of lupus activity at the time of diagnosis. Two patients had evidence of hyposplenism during the infection. Because salmonellosis manifests clinical symptoms like those of active SLE, the diagnosis of the salmonella infection was delayed. In 3 patients, the salmonella infection localized to a site of clinical SLE involvement and in all 4 patients, it occurred simultaneously with other bacterial infections. Multiple factors, including impaired mononuclear phagocytic system function, may predispose SLE patients to bacterial infections, especially intracellular parasites such as salmonella.

The occurrence of nail pitting in Reiter's syndrome.

Some authors have stated that nail pitting never occurs in Reiter's syndrome. The case of a patient with incomplete Reiter's syndrome with nail pitting and HLA-A2, 28; B18, 27 is presented. Patients who have both psoriasis and Reiter's syndrome have demonstrated increased frequency of HLA-A2 and B27 and markedly decreased frequency of HLA loci associated with psoriasis. The particular finding of nail pitting is presented to illustrate that this change may occur in Reiter's syndrome and may reflect a predisposition to the development of psoriasis or psoriasiform lesions conferred by HLA-A2 with B27, as suggested by previously reported HLA typing studies.