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Biomedical subjects

S J Zuberi

Publications and source records attributed to S J Zuberi.

At least 19 recordsLinked to original sources
PubMed2002

Determination of alpha-1 antitrypsin genetic deficiency in duodenal ulcer by polymerase chain reaction.

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.

Adult↗
PubMed2000

Phenotypes of alpha 1 antitrypsin in Karachi, Pakistan.

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.

Adolescent↗
PubMed1997

Genetic markers and duodenal ulcer.

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.

Adolescent↗
PubMed1996

Endoscopic re-evaluation of Visick grading.

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.

Adolescent↗
PubMed1996

Triple therapy in duodenal ulcer healing--a follow up study.

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.

Adult↗
PubMed1996

Serum alpha 1 antitrypsin and pulmonary emphysema.

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.

Adolescent↗
PubMed1995

Healing and relapse rates of duodenal ulcer with omeprazole vs ranitidine.

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).

Adolescent↗
PubMed1995

Helicobacter pylori clearance and eradication with triple therapy in duodenal ulcer patients.

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.

Adult↗