Background:In many patients, emotional stress may exacerbate acne. Psychological problems such as social phobias, low self-esteem, or depression may also occur as a result of acne. The presence of acne may have some negative effect on the quality of life, self-esteem, and mood of the affected patients. While some studies have been undertaken about anxiety, depression, and personality patterns in patients with acne, only a few studies have been done to identify specific personality disorders in patients with acne. Furthermore, there is a dearth of data regarding the effect of personality disorder on the psychological states of the patients which prompted us to undertake the present study.Methodology:This was a descriptive cross-sectional study, undertaken in a Tertiary Care Teaching Hospital in Eastern India. Consecutive patients suffering from severe (Grade 3 and 4) acne, attending the Dermatology Outpatient Department, aged above 18 years were included to the study.Results:A total of 65 patients were evaluated with a mean age of 26 years. Personality disorder was present in 29.2% of patients. The diagnosed personality disorders were obsessive compulsive personality disorder (n = 9, 13.8%), anxious (avoidant) personality disorder (n = 6, 9.2%), and borderline personality disorder (n = 2, 3%), mixed personality disorder (n = 2, 3%). All patients with personality disorder had some psychiatric comorbidity. Patients having personality disorder had higher number of anxiety and depressive disorders which were also statistically significant.Conclusion:The present study highlights that personality disorders and other psychiatric comorbidities are common in the setting of severe acne.

We have measured the effect of the presence of food in the gastrointestinal tract on proximal small bowel motility during sleep. Motility was measured in eight healthy ambulant subjects using two strain-gauge microtransducers incorporated in a fine (2.5 mm OD) nasojejunal tube. The subjects ate a 540-cal evening meal (EM) on the first day. On the following day they ate an equicaloric meal (with similar proportion of carbohydrates, proteins, and fats) at lunch time (MM) and then another equicaloric late meal (LM) 15 min before going to bed. All subjects were asleep within 30 min of completing the LM. Postprandial activity was significantly (P less than 0.001) shortened after LM, but there was no difference in the postprandial motor activity after MM and EM. Migrating motor complex (MMC) cycle lengths were similar after MM, EM, and LM. There was no difference in the duration of phase II of the MMC cycle after MM, EM, and LM even though subjects were asleep during the MMC cycles after LM. The MMC propagation velocity after LM and EM was significantly (P less than 0.01, P less than 0.001, respectively) slower than the diurnal MMC propagation velocity after MM. In health, postprandial activity is diminished during sleep, whereas the consumption of a LM restores the phase II activity usually absent during sleep. A LM also abolishes the expected reduction in nocturnal MMC cycle length but maintains the circadian variation in the propagation velocity of the MMC cycle.

The effect of pirenzepine on oesophageal, gastric, and enteric motor function was evaluated in six healthy volunteers. Each subject was studied before and after taking pirenzepine, 100 mg/day, for 3 days. Half and complete gastric emptying times of clear liquid, assessed by epigastric impedance, were significantly delayed by the drug: 6.16 +/- 1.74 min and 13.8 +/- 4.64 min versus 16.65 +/- 3.03 min and 25.1 +/- 8.2 min, respectively (p less than 0.05). Enteric motility was assessed by manometry, and variables studied were the duration of the various phases of the migratory motility complex, the frequency of contractions in phase III, and the amplitude of contractions in phases II, III, and in the postprandial period. Only phase I was affected and was significantly prolonged by the drug: 16.08 +/- 5.94 min versus 31.65 +/- 12.88 min (p less than 0.01). Oesophageal motility was assessed by manometry. Variables studied were amplitude and duration of contractions in the body of the oesophagus, and lower oesophageal sphincter pressure. Results were not significantly changed by the drug. We conclude that pirenzepine, given at a dose used for treatment of peptic ulcer disease, significantly delays the gastric emptying of liquids, has minimal effect on enteric motility, and has no effect on oesophageal motility. The effect on gastric emptying may be therapeutically useful by reducing the acid load on the duodenum in duodenal ulcer disease.

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