Biomedical subjects
Publications and source records attributed to M G Moshal.
Gastric (GP) and lower oesophageal sphincter pressures (LOSP) were measured in non-pregnant female volunteers (group I) and pregnant women with (group III) or without (group II) heartburn. Patients in early pregnancy had greater gastric pressures than group I. Mean barrier pressure (LOSP-GP) was significantly decreased in pregnant patients complaining of heartburn (group III) compared with groups I and II.
From 1972 to 1979, a total of 3392 patients with endoscopically proven ulcers were seen, in six ethnic groups. The distribution was as follows: Africans 456 males, 182 females; Muslim Gujerati Indians 206 males, 60 females; Hindu Hindi 433 males; total North Indians 639 males, 195 females; Hindu Tamils 593 males, 184 females; Hindu Telegu 179 males, 46 females; total South Indians 872 males, 230 females, and Whites 465 males, 303 females. In the continent of India, it is predominantly the South Indians who suffer from duodenal ulcer. In Durban, the number of North Indians with duodenal ulcers approximates that of those from the South (North: South ratio 0.83). The first question raised by this study is that the protective factors in North Indians in India are not genetic, and are lost when they emigrate to Natal. This may be due to changes in diet. A seasonal analysis indicates that, for females, there is a striking Autumn and Winter predominance in all Indian groups, reaching 80% in Muslims and Telegus but not in African females (52.7%). The second question raised by this study is that protective factors must be sought which operate in Indian females in the Spring and Summer months. The third question emanating from this study is that duodenal ulcers (and ischaemic heart disease) appear to increase in times of dietary and social change. This occurred in the West from 1890 to 1960, and is still occurring in the Third World. The restoration of dietary fibre and unsaturated fat, and the possible adjustment to stress in the West since 1960, has been accompanied by a fall in the incidence of these diseases. A 'changing factors' theory of duodenal ulcers and ischaemic heart disease is proposed. These conditions fall when a 'plateau situation' is reached.
Forty-five patients with endoscopically proven uncomplicated active duodenal ulcers were placed in a randomised double-blind trial. Six patients were lost to follow-up. Twenty patients received 50 mg trimipramine (Surmontil) at night, and 19 patients received placebo. Complete healing was defined as disappearance of the ulcer, with or without a scar; partial healing was defined as a reduction of ulcer size to 25% of its size, or a large deep ulcer that became flat, if erosions were present even if the ulcer had gone. After 4 weeks of trimipramine treatment 35% had completely healed and 50% had partly healed, compared with 21% completely and 21% partly healed with placebo (chi-square 7.9; p less than 0.025 in favour of trimipramine). There were no side effects. Trimipramine, 50 mg at night, is a safe and effective treatment for active duodenal ulceration.
Fifty patients with endoscopically diagnosed uncomplicated duodenal ulcers were given ranitidine 150 mg twice daily, or placebo for 4 weeks in a randomised double-blind study. After 4 weeks, 76% of patients on ranitidine showed healing. Fifteen (60%) were completely healed, 5 (20%) were partly healed, and 5 had active unchanged ulcers. On placebo, 6 (27%) were completely healed, 6 (27%) were partly healed, 10 had active unchanged ulcers and 3 had absconded. Grouping partly healed with active ulcers, a Z value of 2.23 was obtained in the Mantel-Haenszel Test; p = 0.013 in favour in ranitidine over placebo. Of ten patients who were partly healed or active after ranitidine in Stage 1, 7 healed on one further course in an open study, and 3 were active after 2 further courses. Of 16 patients who were partly healed or active after placebo, 3 healed on one course of ranitidine, 6 healed on 2 courses of ranitidine, 6 remained active after 2 courses, and 1 absconded. No side-effects were noted. Ranitidine is a safe and effective therapy for active duodenal ulceration.
We undertook a series of double-blind studies test the efficacy of sucralfate in the treatment of active duodenal ulcers and the prevention of relapse. In addition, we undertook studies to test the hypothesis that there is a fundamental localized weakness in the duodenum, where ulcers tend to recur. In the short-term study, 80% of patients on sucralfate and 52% on placebo healed their ulcer in 6 weeks (chi 2 = 6.3672; p less than 0.025). The long-term (1-year) study is still underway, but preliminary results show that 37% on maintenance sucralfate and 78% on placebo have had a relapse of duodenal ulcer (Fisher's exact p = 0.0176). A prospective study to ascertain the site of recurrence of duodenal ulcers revealed that 58% recur at the same site in the same quadrant, and a further 31% recur in a adjacent quadrant; thus, a total of 89% recurred in the same hemisphere. We believe this indicates that a weakness in the duodenal cap at a specific site leads to relapse in that area.
In a double-blind endoscopic study of 55 patients with uncomplicated duodenal ulcers, treatment with the mucosal-protective agent, bicitropeptide (BCP-Compound), was superior to that with cimetidine (Tagamet) after 6 weeks. After the administration of bicitropeptide, 77% of ulcers had completely healed and 25% had partially healed, and after treatment with cimetidine 38% had completely healed and 38% had partially healed (chi 2 = 6,316; P < 0,025). There was no difference between the results of treatment with either drug at 12 weeks. Patients were followed up 3 months after the ulcers healed, and 44% who had been on bicitropeptide and 72% on cimetidine had active ulcers (no significant difference). Blood and urine bismuth levels were estimated before therapy, after 6 weeks of therapy, and after 3 months without therapy. Results showed that in patients taking bicitropeptide, urine bismuth levels rose significantly between 0 and 6 weeks, but decreased to pretreatment levels after 3 months without therapy. Blood bismuth levels did not change.
Ten samples of jejunal fluid from patients with tropical sprue and 11 from controls without this disease were examined bacteriologically, using techniques designed to obtain the optimal yield of aerobic and anaerobic bacteria. Total colony counts did not differ significantly in the two groups studied. The organisms isolated comprised a wide range of aerobic and anaerobic bacteria. With the exception of Haemophilus species, no bacterial group was isolated in significantly greater numbers in sprue patients than in controls. The pathogenesis of tropical sprue in Natal is discussed in the light of these findings.
This trend was maintained at 12 weeks (on sulcralfate 77% complete healing and 7% partial healing, on placebo 44% complete healing and 15% partial healing; chi 2 score 4,9402; P < 0,05). No statistically significant difference was achieved at 6 or 12 weeks for small ulcers. At 6 weeks, 73% of large ulcers were completely healed and 18% were partially healed compared with 21% on placebo completely and 43% partially healed (Fisher's exact P value of 0,092 in favour of sucralfate). No differences were found at 12 weeks. No side-effects were noted. Measurement of kaolin partial thromboplastin time and single-stage prothrombin time as measurement of heparin-like activity showed no differences before and after therapy. It is concluded that sucralfate is a safe and effective therapy for duodenal ulceration.
A previously undescribed explanation for the development of duodenal ulcer is advanced. Stressful situations and avoidance-avoidance conflicts in individuals with a dependant compliant personality incapable of appropriate "stimulus-seeking behaviour" lead to an immobilised state. This predicament is denied. Helplessness develops. This state is associated with an autonomic imbalance in which a central monoamine depletion results in uncompensated parasympathetic overactivity which facilitates the development of duodenal ulceration. Denial often invalidates superficial psychological investigations into the aetiology of duodenal ulceration and may explain the contradictory findings in the literature.
Increasing the resting lower esophageal sphincter (LES) tone is a useful method of preventing gastroesophageal reflux. The effects of a new antiemetic, domperidone, on LES were studied in 28 subjects. Group I included eight normal nonpregnant control subjects. The remaining 20 pregnant women were divided into two groups, Group II and III--ten parturients without and ten with symptoms of heartburn. Domperidone increased LES pressure by 19, 11 and 10 cm H2O in Groups I, II and III, respectively (P less than 0.05). Domperidone may be a valuable premedicant in some patients to decrease the chance of gastro-esophageal reflux.
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A case is discussed of a 30-year-old Black woman who developed a massive pseudocyst of the pancreas while under investigation in hospital for a left pleural effusion. An internal pancreatic fistula to the pleural space was demonstrated at endoscopic retrograde cholangiopancreatography. The patient recovered completely after distal pancreatectomy with splenectomy.
The effect of long-term cimetidine therapy on the ultrastructure of human parietal cells was investigated in 2 subjects. It was found that after cimetidine therapy for 1 year: (i) the ultrastructural appearance of the parietal cells was normal, and (ii) the parietal cells responded normally to stimulation by pentagastrin. Evidence in favour of a membrane flow mechanism involved in acid secretion is presented.
Although heartburn, thought to indicate reflux of gastric contents into the oesophagus, occurs frequently in pregnant women during the last trimester, its aetiology is not clear. Prolactin blood concentrations rise progressively during pregnancy and heartburn is known to disappear spontaneously during the last weeks of pregnancy. In view of this and other factors, motility studies and estimation of serum prolactin levels were carried out on 20 pregnant Black women. Results show that patients with prolactin levels over 3,000 microunits/ml had significantly higher mean barrier presures (sphincter pressure-gastric pressure) than the patients with hormone levels of less than 3,000 microunits/ml (P less than 0,02). No direct correlation could, however, be demonstrated between barrier pressures and prolactin levels (r = 0,3494). It is concluded that further studies would seem to be indicated on an animal model to establish the importance of prolactin in the regulation of the lower oesophageal sphincter tone.
Duodenal ulceration among Black and Indian patients admitted to King Edward VIII Hospital, Durban, over a 26-year period (1950-1976) was studied. Analysis was made over a series of time intervals within this period, and expressed as the number of admissions for duodenal ulcer per 1,000 total admissions (excluding obstetric and gynaecological patients). Admissions for duodenal ulceration increased 2,4-fold among the Indians and 11,9-fold among the Blacks from 1950 to 1976. The disease appears to have become commoner among women in both race groups. The peak age for Indian men is the 3rd decade, but for Indian women the peak age incidence has changed from the 4th to the 6th decade. There is now a peak in the 3rd decade for Black men, compared with the 4th decade, as reported 20 years ago. The pattern is similar in Black women. The clinical presentation is similar in the two groups, although it is significant that haemorrhage occurs more frequently among the Black patients.
The effect of intravenous ergometrine 0.5 mg during general anaesthesia for Caesarean section on lower oesophageal sphincter (LOS) function was investigated in eight patients. Ergometrine increased the LOS pressure markedly (p less than 0.005).
Twenty adult Indian patients suffering from the spastic form of irritable colon, i.e. abdominal pain and constipation, were given trimebutine (Mebutin), 2-phenyl, 2-dimethylamino-n-butyl 3, 4, 5-trimethoxybenzoate. Patients were given treatment with 200 mg trimebutine three times daily, or placebo for 4 weeks, and then crossed over. In addition, stool transit times were assessed by the single stool transit time (SST) method of Cummings. Results showed a statistical improvement in abdominal pain and constipation with both trimebutine and placebo after 4 weeks, but only with trimebutine after 8 weeks. Single stool transit time was significantly reduced after trimebutine.
Five hundred and twenty-two African and Indian patients were studied, including 206 with duodenal ulcers, 25 with irritable colon, 51 with oesophagitis, 31 with pancreatitis, 14 with ulcerative colitis or Crohn's disease, 71 miscellaneous gastrointestinal diagnoses and 124 controls. The mean ages were similar in each group. Every patient underwent endoscopy and a detailed psychosocial questionnaire was applied. Comparison of occupations of patients and their patients was investigated on 3 scales, for Status/Prestige (9 levels), Responsibility (5 levels) and Control over Others (10 levels). Significantly more patients with duodenal ulcers were in the lowest group in terms of occupational authority compared to other diagnoses and controls. Similar number of all groups had been urban for their entire life. Stress was present in the 10 days preceding an attack in significantly more Indian males with duodenal ulcers compared to controls. Upward shifts in prestige had not occurred in African male patients with duodenal ulcers when compared to their parents but had occurred among Indian men. More duodenal ulcer patients were in the very lowest occupational authority category compared to other groups. It may thus not be occupational prestige as such that is important, but factors associated with it, such as lack of control over others and, among Indian men, stresses associated with social disruption following upon occupation mobility.