We report the case of a 53-year-old man who consulted the Department of Oral Medicine with a history of peripheral neuropathy affecting the upper and lower limbs, and Raynaud's disease.
The patient was diagnosed with cleft palate or neurologist for a lip salivary gland biopsy, who suspected Sjögren's syndrome (SS), although the patient did not complain spontaneously of xerosis.
There was no clinical evidence of keratoconjunctivitis sicca: a Schirmer's test (Clement Clarke', Edinburgh UK), detected a subnormal collection of fluid (lower than 5 mm).
The Rose-Bengal test was negative.
In the examination of the oral cavity there was no reduction in saliva secretion and salivary quantification by Saxon test was negative (plus 3g after 5 minutes).
The patient was offered a salivary gammagraphy in order to assess the secretion of saliva, but the patient suffered from xerostomia.
A lip salivary gland biopsy was performed on the left lower lip taking five minor salivary glands.
The characteristics of chronic lymphocytic sialadenitis were identified: a nodular periductal nodule consisting mainly of plasma and plasmatic cells, enlarged ducts and a common lymphoid process.
The pathological examination concluded a focus score of 2 and a level 4 on the Chisholm scale.
Laboratory test results were as follows: leukocytes: 7000/mm3; erythrocytes: 481x104; hemoglobin: 13g/dl; thrombocytes: 255 000; total proteinase SG0.5TP; total gammaglobulin/
Several immunological tests had positive values.
Rheumatoid factor was 85Ui/l; antinuclear antibodies (1:2000 with homogeneous model) and anti-SS-A-Ro antibodies were positive.
A mixed cryoglobulinemia (polyclonal IgG and polyclonal kappa IgM) was demonstrated.
Although the slight increase in HCV transmission could be related to a Sjögren's syndrome, anti-HCV antibody tests were performed using enzyme-linked immunogene, enzyme-linked immunob assay, and recombinant Helot.
The results were positive for both techniques.
HCV RNA reversenchor 2.0 presence and its titulation in serum were determined using a reverse transcriptase-polymerase chain reaction for HCV-RNA carried out with a Rocheburg® HCV® microwell plate-base (Am
The results of tests using laboratory enzyme immunoassay (Roche Diagnostic System, Basel, Switzerland) for hepatitis B infection (human anti-hepatitis virus, surface antigens), and immunisation were negative.
A liver biopsy was performed, whose pathological examination showed persistent low-grade chronic hepatitis without fibrosis.
A second lip biopsy was then performed, performing RNA extraction as previously described(5).
Genomic amplification by PCR for HCV RNA was performed by nested PCR from the 5' non-codating and highly conserved genome region.
The specificity was confirmed by the strips hybridization assay of the laboratory (Inno-Lipa II, Innogenetics®, Zwijndrecht, Belgium) and demonstrated the most frequently unknown HCV genotype 1b in individuals.
Despite the absence of fibrosis, and due to the extrahepatic neuropathic manifestations of HCV infection present in the patient, a single dose of interferon alfa-2b (306 IU/week) was administered for 8 months.
At the end of treatment, HCV RNA was no longer detectable in serum, and an evident improvement was observed in the Schirmer test: 9mm for 5 minutes.
The patient did not notice any change in his buccal state since he had no subjective complaint of salivary deficit or objective reduction of salivary flow before starting treatment.
