Background: With the rising mean age, more patients will be diagnosed with one or more other serious diseases at the time of lung cancer diagnosis. Little is known about the best way to treat elderly patients with comorbidity or the outcome of treatment. This study was undertaken to evaluate the independent effects of age and comorbidity on treatment and prognosis in patients with non-small cell lung cancer (NSCLC). Methods: All patients with NSCLC diagnosed between 1995 and 1999 in the southern part of the Netherlands (n = 4072) were included. Results: The proportion of patients with localised NSCLC who underwent surgery was 92% in patients younger than 60 years and 9% in those aged 80 years or older. In patients aged 60-79 years this proportion also decreased with comorbidity. In patients with non-localised NSCLC the proportion receiving chemotherapy was considerably higher for those aged less than 60 years (24%) than in those aged 80 or older (2%). The number of comorbid conditions had no significant influence on the treatment chosen for patients with non-localised disease. Multivariable survival analyses showed that age, tumour size, and treatment were independent prognostic factors for patients with localised disease, and stage of disease and treatment for those with non-localised disease. Comorbidity had no independent prognostic effect. Conclusions: It is questionable whether the less aggressive treatment of elderly patients with NSCLC is justified.

Laparoscopic fenestration in PCLD patients results in volume reduction of 12.5% and decrease of symptoms.

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Incisional hernia repair without mesh mainly consists of tissue transfer to bridge or close the defect. Bridging includes rotational or free musculocutaneous flaps, rendering acceptable short-term results but a rather disappointing long-term outcome. Abdominal wall closure where there has been significant loss of domain, with intraperitoneal organs residing permanently outside the abdominal cavity, can only be achieved using the patients' own tissue if preoperative expansion of the abdominal cavity is performed using artificial expanders or pneumoperitoneum. From a scientific point of view, however, evidence supporting any treatment option is weak because prospective randomized controlled trials are virtually impossible to conduct owing to the inhomogeneity of the patient population being considered. Treatment of this condition by the above-mentioned means should therefore be proposed on an individual basis utilizing one or more of the many possible techniques described.

Polycystic liver disease (PCLD) is an inherited disorder caused by mutations in either PRKCSH (hepatocystin) or SEC63 (Sec63p). However, expression patterns of the implicated proteins in diseased and normal liver are unknown. We analyzed subcellular and cellular localization of hepatocystin and Sec63p using cell fractionation, immunofluorescence, and immunohistochemical methods. Expression patterns were assessed in fetal liver, PCLD liver, and normal adult liver. We found hepatocystin and Sec63p expression predominantly in the endoplasmic reticulum. In fetal tissue, there was intense expression of hepatocystin in ductal plate, bile ducts, and hepatocytes. However, Sec63p staining was prominent in early hepatocytes only and weak in bile ducts throughout development. In PCLD tissue, hepatocystin was expressed in hepatocytes, bile ducts, and in cyst epithelium of patients negative for PRKCSH mutation. In contrast, the majority of cysts from PRKCSH mutation carriers did not express hepatocystin. Sec63p expression was observed in all cyst epithelia regardless of mutational state. We conclude that hepatocystin is probably required for development of bile ducts and does not interact with Sec63p. The results support the hypothesis that cyst formation in PCLD results from a cellular recessive mechanism involving loss of hepatocystin. Cystogenesis in SEC63-associated PCLD occurs via a different mechanism.