Search

Background: Frequency of gallbladder cancer in Karachi has been reported to be 8% and that from other parts of Pakistan varies between 6-7%. This is very high as compared with the Western studies. With this in mind a case control study was designed to identity risk factors responsible for gallbladder cancer., Methods: This case control study included 107 histologically proven cases of gall bladder cancer from Jinnah Postgraduate Medical Center, Civil Hospital and two private hospitals of Karachi. Age and sex matched controls were of two types. Those with and without cholelithiasis screened sonographically. Demographic, socio-economic factors, life-style, dietary habits and dietary intake were recorded on a proforma. The cases and controls were compared for various factors using odds Ratio., Results: Among 107 cancer cases 27 were males and 80 females (M:F = 1:3). Mean age of males was 59 years (range 35-82 years) and females 53 years (range 31-70 years). One hundred and five (98%) had associated choleliathiasis. Important risk factors appeared to be gallstones, high parity, young age at first delivery, low fiber and Vitamin A intake (p < 0.01), high fat intake (p < 0.01), prolonged fasting hours/habit of missing dinner (OR:6.8), using repeatedly boiled or improperly stored ghee or oil (OR:2.6)., Conclusions: According to this case-control study major risk factors for gall bladder cancer were gallstones, dietary malpractices and poorly balanced diet. Poorly stored/processed food acts as a promoter in the presence of gall stones and may favour cancer development.

Objective: To confirm alpha-1-AT deficiency status in duodenal ulcer using a combination of PCR and restricted enzyme digestion., Methods: Fifty patients with endoscopically proven duodenal ulcer and hundred controls with no signs of the disease were included. Alpha-1-AT phenotypes were confirmed by polymerase chain reaction followed by restriction enzyme digestion., Results: Alpha-1-AT concentration in duodenal ulcer patients showed a mean value of 2.12 +/- 0.11 g/l (range: 0.52-3.95 g/l, p < 0.05). In controls this was 2.47 +/- 0.08 g/l (range: 0.52-5.0 g/l). Among the controls 70% had the MM phenotype, 28% M1 M2 and 2% FM. In duodenal ulcer, MM predominates (70%), followed by M1 M2 (18%), SS (4%), SZ (4%), ZZ (2%) and MZ (2%)., Conclusion: Alpha-1 AT deficiency was found in 10% of duodenal ulcer patients. DNA analysis more accurately resolved the phenotypes as S and Z mutations.

Albendazole and metronidazole were compared in 68 patients diagnosed positive for giardiasis. Albendazole 1200 mg, one dose was given to 24 patients, albendazole 400 mg twice a day for 3 days was given to 23 patients, and metronidazole 400 mg 3 times a day for 5 days to 21 patients. Response to therapy was monitored by clinical examination and analysis of fresh faecal samples on days 0, 3, 7 and 10. Response to the single dose of albendazole was 55%, to the divided dose of albendazole 70%, and to metronidazole 84%. The results show that albendazole, originally recommended for helminthic infection, can also be used in patients with mixed protozoal infection or for infections resistant to metronidazole.

Objective: To determine serum level of the protease inhibitor, to identify phenotypes and determine their frequencies., Study Design: A prospective study., Setting: PMRC, Research Centre, JPMC and the Aga Khan University Hospital, Karachi., Subjects: Healthy adults without history of peptic ulcer disease and a normal endoscopy., Methodology: Quantitative measurement of serum alpha 1 AT was carried out by radial immunodiffusion, phenotyping by iso-electric focusing and confirmation of phenotypes by immuno-fixation and DNA analysis technique., Results: Serum alpha 1 AT was low in 13.4% of the subjects. MM phenotype predominated followed by SZ, SS,MZ and ZZ. DNA diagnosis accurately resolved the phenotypes as S and Z., Conclusion: Frequency of phenotype associated with total and intermediate deficiency is less in the population.

Serum pepsinogen, alpha 1-antitrypsin (alpha 1-AT) and blood groups were studied as genetic markers in 32 patients with endoscopically proven duodenal ulcer and 44 control subjects with no family history of ulcer disease. Serum pepsinogen was determined by the modified method of Edward et al, alpha 1-AT by single radial immunodiffusion (RID) and phenotyping was carried out by isoelectric focusing (IEF). Duodenal ulcer patients with hyper- pepsinogenemia (28%) and low serum alpha 1-AT (35%) had a dominant blood group O, lower mean age, an early onset of disease, a higher frequency of gastrointestinal (GI) bleeding and ulcer perforation. These parameters were found considerably different in patients with normal serum pepsinogen and alpha 1-AT. Phenotype analysis of alpha 1-AT revealed that four duodenal ulcer patients had partial deficiency of the protease inhibitor and none of the normal exhibited the deficiency pattern. The etiology of the disease appears to be genetic anomaly in 28% of patients while the rest (72%) had ulcers as a result of neuroendocrinological or environmental factors.

The comparative efficacy of roxatidine and ranitidine in the treatment of patients with acute duodenal ulcer was assessed at 4 and 6 weeks in this multicenter study. Ninety-four of 192 patients were given roxatidine in a single nightly dose of 150 mg, and 98 patients were given ranitidine in a single nightly dose of 300 mg. All the patients had endoscopically proven duodenal ulcer. Of the 171 assessable patients, ulcers were healed in 88% of the roxatidine group (73 of 83) and in 84% of the ranitidine group (74 of 88). No serious adverse events were reported in either group. We conclude that roxatidine 150 mg once daily is as effective and safe for the treatment of acute duodenal ulcer as ranitidine 300 mg once daily.

Thirty-nine Helicobacter pylori (HP) positive chronic duodenal ulcer patients completed the 4 weeks treatment of triple therapy (Denol, Metronidazole and Amoxil). Of these 29 showed healed duodenal ulcer and negative CLO test at 8 weeks (eradication). They were followed at 3,6 and 12 months and at each follow-up, endoscopy and CLO testing were repeated. At 12 weeks, 54% showed a healed ulcer and negative CLO and these figures reached to 69 and 66% at 6 and 12 months respectively. Thirty percent relapsed within 1 year. The present study indicates a prolonged remission of duodenal ulcer following HP eradication.

Correlation of Visick grading was done with serial endoscopies in 19 patients operated for duodenal ulceration. Deeper mucosal lesions like ulceration showed good association with Visick grading (100%), while superficial mucosal lesions were mostly asymptomatic and therefore, caused disparity in grading. Moreover, as symptoms and endoscopic findings changed with passage of time, it was concluded that in the light of endoscopic findings the grading need re-evaluation.

Using isoelectric focusing (IEF) and radial immunodiffusion (RID) techniques, serum samples from 100 normal healthy adults and 21 patients with pulmonary emphysema were analysed to identify various alpha 1 antitrypsin phenotypes and the serum concentrations. Ten percent of the patients had low serum values. The normal or most common genetic form, MM, is the predominant phenotype in both controls and patients.

To assess the efficacy of famotidine in the healing of reflux oesophagitis, 25 endoscopically proven cases were treated with famotidine 40 mg B.I.D. for 6 to 12 weeks. Six patients were lost to follow-up, of the 19 cases analysed, 16 (84.2%) healed at 6 weeks and 17 (89.5%) at 12 weeks. Twelve cases (63%) became asymptomatic within six weeks of treatment. In conclusion famotidine 40 mg B.I.D. is effective in the healing of reflux oesophagitis.

Complete absence of data on alpha 1 antitrypsin in this country prompted us to determine serum levels using radial immunodiffusion (RID) and phenotypes by isoelectric focusing (IEF) in 100 healthy adults (52 males and 48 females). Mean serum alpha 1 antitrypsin concentration in healthy subjects was 2.47 +/- 0.08 g/l and the main phenotypes MM (70%), M1 M2 (28%) and FM 3 (2%) are infrequent in our population.

The efficacy of omeprazole 20 mg a day was assessed against ranitidine 150 mg twice a day in the healing and relapse of duodenal ulcer. Forty three endoscopically verified cases were allocated to 2 weeks of treatment, which was extended to 4 weeks, if the ulcer persisted on day 15. Two cases were excluded due to deviation from the protocol. Of 41 evaluable cases, 21 received omeprazole and 20 ranitidine. Healing rates with omeprazole and ranitidine at 2 weeks were 71% and 70% respectively which rose to 100% and 90% at 4 weeks (N.S). There was no significant difference in pain relief in two groups. Follow-up endoscopies, in 33 healed cases revealed 100% relapse at 3 months in omeprazole and 79% in ranitidine treated cases (P < 0.05).

Triple therapy was given to 49 chronic helicobacter pylori positive chronic duodenal ulcer cases to see its efficacy in H. pylori clearance, eradication and ulcer healing. H. pylori clearance and eradication rates at week 5 and 8 were 87.8% and 81.5% while ulcer healing rates 68.2% and 81.5% respectively. Seven (18%) cases failed to clear H. pylori and were classified as non-responders. Histologically 60% showed post-treatment regression of gastritis. Tolerance to drugs was excellent with a good compliance rate.

Evaluation of serum alpha 1-antitrypsin levels in the South Asian population and its possible involvement in disease conditions such as duodenal ulcer has not been given due consideration. This is mainly because reports from European and North American countries indicate that the genetic deficiency of this protease inhibitor is rare among Asians of the subcontinent. Using isoelectric focusing (IEF) and radial immunodiffusion (RID) techniques, we analysed serum samples from 100 normal, healthy adults and 50 patients with endoscopically proven duodenal ulcers to determine if there is a possible relationship between alpha 1-antitrypsin phenotype and this disease. Five duodenal ulcer patients had low alpha 1-antitrypsin levels as well as SZ and S phenotype. None of the controls showed presence of S or SZ phenotypes. The normal or most common genetic form, MM, is the predominant phenotype in both controls and patients.

The association of upper gastrointestinal (G.I.) lesions with various addictions was studied in 383 consecutive patients endoscoped over a year. Of the total, 179 (47%) had no addictions and 204 (53%) were addicted to either cigarette smoking (70%), tobacco chewing with pan (23%), pan alone (5%) or alcohol (2%). Overall, 78% cases with and 59% without addictions had an upper G.I. lesion on endoscopy (P < 0.001). Duodenal ulcer was commonest lesion in all types of addiction.

To assess the comparative efficacy of omeprazole 20 mg in the morning versus ranitidine 150 mg twice a day, in the healing of duodenal ulcer, 43 endoscopically verified cases were randomly allocated to 2 or 4 weeks (if ulcer did not heal at 2 weeks) treatment. Two cases were excluded due to deviation from the protocol. Of 21 cases treated with omeprazole 15 (71%) healed at two weeks and all (100%) at 4 weeks. Similarly of 20 cases treated with ranitidine, 14 (70%) healed at 2 and 18 (90%) at 4 weeks (P = NS). Two patients who did not heal with ranitidine, when crossed over to omeprazole healed at 4 weeks. No significant difference in the rate of pain relief, clinical or laboratory parameters or adverse effects were noted in either group. Both the drugs were well tolerated and were potent healer of duodenal ulcer; but omeprazole appears to be superior in the healing of resistent ulcers.