A 73-year-old woman with idiopathic pulmonary fibrosis (IPF) had an elevated serum CA19-9 level, but not KL-6. Her condition worsened and she subsequently died and this was associated with a rise in the serum KL-6 level. At autopsy, the lung showed a honeycomb appearance macroscopically and, microscopically, hyaline membrane formation was seen. Immunohistochemical staining revealed partial colocalization of KL-6 and CA19-9 to dilated bronchiolar cells. These features suggest that the mechanisms that cause the synthesis and release of CA19-9 and KL-6 from damaged lung tissue in IPF are likely to differ from those in diffuse alveolar damage. In addition, serum KL-6 levels may reflect the severity of disease more sensitively than CA19-9 levels.

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Systemic sclerosis (SSc) is a generalized disorder characterized by fibrosis and vascular obliteration in the skin, lung, gastrointestinal tract, and kidney. One of its two subsets is a stable, limited cutaneous group (lSSc). Pulmonary involvement in scleroderma is common, and several types of pulmonary disorders are associated with SSc. Bronchiolitis obliterans organizing pneumonia (BOOP) is a rare finding in lung disorders associated with SSc. We describe a case of lSSc with BOOP that was responsive to steroid therapy. Of interest is that the lung disorders appeared in different periods and areas. It might be important to diagnose abnormal shadows in lung fields before treatment of patients with SSc.

SynopsisThe effect of chronic administration of sulpiride on serum human growth hormone (hGH), prolactin and thyroid stimulating hormone (TSH) was examined in 6 normal subjects. Sulpiride was given orally at a dose of 300 mg (t. i. d.) for 30 days. Sulpiride raised serum prolactin levels in all subjects examined.In addition, sulpiride suppressed hGH release induced by L-dopa, although the basal hGH level was not changed.Sulpiride treatment appeared to antagonize partially the inhibitory effect of L-dopa on prolactin release.Following thyrotropin-releasing hormone (TRH) injection, the percent increment in prolactin levels from the baseline in sulpiridetreated subjects was less than in controls without sulpiride. In contrast, both the basal and TRH-stimulated TSH levels were not influenced by sulpiride.These observations suggest that sulpiride suppressses L-dopa-induced hGH release and stimulates prolactin release, presumably by acting against the dopaminergic mechanism, either on the hypothalamus or on the pituitary.The decreased prolactin response to TRH after sulpiride treatment may indicate a diminished reserve capacity in pituitary prolactin release.

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