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OBJECTIVE: To explore the experience of diabetes in British Bangladeshis, since successful management of diabetes requires attention not just to observable behaviour but to the underlying attitudes and belief systems which drive that behaviour. DESIGN: Qualitative study of subjects' experience of diabetes using narratives, semi-structured interviews, focus groups, and pile sorting exercises. A new qualitative method, the structured vignette, was developed for validating researchers' understanding of primary level culture. SUBJECTS: 40 British Bangladeshi patients with diabetes, and 10 non-Bangladeshi controls, recruited from primary care. RESULT: Several constructs were detected in relation to body image, cause and nature of diabetes, food classification, and knowledge of complications. In some areas, the similarities between Bangladeshi and non-Bangladeshi subjects were as striking as their differences. There was little evidence of a fatalistic or deterministic attitude to prognosis, and most informants seemed highly motivated to alter their diet and comply with treatment. Structural and material barriers to behaviour change were at least as important as "cultural" ones. CONCLUSION: Bangladeshi culture is neither seamless nor static, but some widely held beliefs and behaviours have been identified. Some of these have a potentially beneficial effect on health and should be used as the starting point for culturally sensitive diabetes education.

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Patient education in chronic diseases should always take into account the many maps--individual, cultural and medical--that patients have of their own bodies, in both health and disease. Physicians should become explorers, working in co-operation with patients and their families to understand their perceptions of body and self--and whether or not these are compatible with medical interventions.

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Each family can be regarded as a unique small-scale society, with its own internal organization and view of the world or family culture. A crucial aspect of each family culture are those beliefs, behaviors, habits, and life-styles that are either protective of health or pathogenic, depending on the context. For family physicians, the insights of medical anthropology are useful in understanding the role of family culture in health, illness, and medical care.

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A 48-yr-old man with chronic myelogenous leukemia and basophilia developed a duodenal ulcer and hemorrhage. Gastric analysis revealed basal hyper-secretion of acid (33.1 mEq/h) and pepsin (44.5 x 10(-4) peptic units/h). Blood, serum, and urine histamine was elevated and serum gastrin was normal. Although acid output was markedly suppressed with ranitidine (50 mg i.v.), pepsin secretion was only inhibited 63% and had returned to basal levels by the sixth hour. Maximal acid output does not suggest a trophic effect of histamine in this patient. The previously reported cases of basophilic leukemia and gastric hypersecretion or duodenal ulcer disease are reviewed.

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Modified sham feeding-stimulated gastric secretion is a recognized means of testing vagal integrity. The chew-and-spit technique is esthetically distasteful and difficult to perform without some of the food being swallowed. Simple chewing of an inert substance does not stimulate acid secretion. We thus tested to determine whether chewing gum, a potent cholinergic stimulant of salivary secretion, also stimulates the stomach. We compared the gastric acid output stimulated by the chew-and-spit method, using a cheeseburger chewed for 15 min, with gastric acid output stimulated by chewing seven sticks of chewing gum over 15 min, in 12 patients with duodenal ulcer disease. Acid output stimulated by chewing gum was 36% +/- 5%, and by cheeseburger was 39% +/- 6% of pentagastrin maximum acid output (r = 0.97). We conclude that chewing gum is a simple, cheap, convenient method for testing vagally mediated gastric acid secretion.

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We studied gastric emptying of solid food, using a radionuclide technique, in 18 patients with chronic renal failure patients on hemodialysis: nine with nausea and vomiting or postprandial bloating and nine without. Both groups were compared with a group of normal subjects. Gastric emptying was consistent with a linear elimination in all groups. The regression coefficients of the symptomatic, asymptomatic, and control groups were -0.48 +/- 0.1%, -0.5 +/- 0.14%, and -0.58 +/- 0.15% min, respectively. These were not statistically different. Half-emptying times were 116.4 +/- 7.1 min, 97.8 +/- 13.7 min, and 98.7 +/- 5.6 min, respectively. These also were not statistically different. Values of percentage retention at 2.5 hours for the same groups were 31.6 +/- 5, 24.8 +/- 6.4, and 18.6 +/- 4.4, respectively, again with no statistical difference. Patients with chronic renal failure on hemodialysis, symptomatic or asymptomatic, have no obvious impairment of gastric emptying of solids.

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To further investigate differences in the responses of normals and patients with duodenal ulcer with respect to gastrin release and acid and pepsin secretion, we infused bombesin (1 microgram/kg X h) or bethanechol (40 micrograms/kg X h) during the middle hour of a 3-h infusion of pentagastrin and compared the results with a pentagastrin infusion without added drug. Pentagastrin dosage (0.1 microgram/kg X h) was set to give about half-maximal response, to detect either inhibition or further stimulation of gastric secretion, whereas the dose of bombesin was chosen to give maximal gastrin but less than maximal acid secretion. Serum gastrin and somatostatin were also measured. In all subjects tested, bethanechol produced no effects on acid, gastrin, or somatostatin release but increased pepsin output. By contrast, bombesin inhibited pentagastrin-stimulated acid output in all 6 normal men by an average of 55%, whereas it inhibited acid output in only 2 of the 9 men with duodenal ulcer. Serum gastrin increases after bombesin in duodenal ulcer were three to four times greater than in normals. Although bombesin stimulates acid only by releasing gastrin, we postulate that bombesin may also simultaneously limit acid and pepsin secretion and speculate that this effect could be mediated by bombesin-induced somatostatin release. The cause for differences between duodenal ulcer and normal remain speculative.

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For over 20 years, the image of the coronary-prone 'type A' individual, ambitious, competitive, hostile, and time-obsessed has been a familiar feature of cardiology literature, and of popular discourse on health. A closer examination of the moral content of this model, suggests that it is based on a binary classification of social values type A (bad) and type B (good). But the type A individual is also a figure of moral ambiguity, embodying many of the inherent contradictions of Western industrial society. In particular, his anti-social behaviour is rewarded in money, or status by that same society. The paper proposes a model of symbolic inversion, whereby these social contradictions are resolved for both victim, and society by his development of coronary heart disease. The type A behaviour pattern can be regarded as a 'culture-bound syndrome', particularly of middle-aged, middle-class men, and one which condenses key concerns and behavioural norms of the society. As a diagnostic category, it can only be understood in the social context of the industrialized world and against the background of the unique social and symbolic characteristics of Western time.

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Gastric acid and pepsin secretion and serum gastrin concentrations were measured in nine patients with uncomplicated duodenal ulcer (DU) and 10 normal controls in the fasting state and in response to graded doses of bombesin, a tetradecapeptide gastrin releaser, and, for reference, synthetic gastrin G-17. Serum gastrin with bombesin stimulation was significantly greater in duodenal ulcer (maximum 467 pg/ml) than in controls (153 pg/ml), while in seven of the DU group tested gastrin levels after a meal were not different from that seen in five of the normal controls. Gastric acid concentrations and outputs were greater in duodenal ulcer with both stimuli. Secretory responses were then related to serum gastrin levels; despite increasing gastrin levels with bombesin stimulation, peak outputs achieved with bombesin were only 50% of G-17 maximum in normals and up to 90% of maximum in duodenal ulcer. Up to the point of peak response to bombesin, acid and pepsin outputs were the same with exogenous and endogenous gastrin, ie, bombesin acted only via G-17. Furthermore, in direct comparison of duodenal ulcer and normals with G-17 infusion, acid and pepsin outputs related to serum gastrin were congruent up to 75% of duodenal ulcer maximum, at which point normals reached their maximum level. These data have shown that duodenal ulcer patients are not more sensitive to either exogenous or endogenous gastrin; we have also shown regulatory defects in duodenal ulcer patients not previously described: an exaggerated release of gastrin with bombesin stimulation, and a defective inhibition of acid and pepsin secretion with higher doses of bombesin.

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Electrocardiographic assessment of the R/Q wave ratio (lead 2) of patients with a first acute inferior wall myocardial infarction (IWMI) offers important indirect quantitative information regarding the severity and extent of the myocardial damage. Eighty-eight consecutive patients with IWMI were investigated by echocardiography and radionuclear angiography. After measuring the R/Q ratio in lead 2 during the ST-wave stabilized stage of myocardial infarction, patients were separated into three groups--group 1 with an R/Q ratio greater than 2; group 2 with an R/Q ratio between 1 to 2; and group 3 with an R/Q ratio less than 1. Utilizing the information thus gathered from the electrocardiogram (ECG) offers a simple and efficient method for early prognosis which merits further investigation.

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This pilot-study examines the self-perceptions, and explanatory models, of 42 patients with either respiratory or gastrointestinal psychosomatic disorders. For several reasons, these disorders comprise an anomalous category within the biomedical model. It is suggested that clinicians explain their chronic, unpredictable course by 'psychologization'--shifting responsibility for etiology, exacerbations or therapeutic failure to patients' emotions, personality, or lifestyle. Evidence is presented that psychologization is socially constructed, in clinical encounters over time. Patients respond to this process by reifying pathogenic emotions, personality traits, or malfunctioning body parts, and thus separating them from an idealized concept of the social self. It is also suggested that patients with gastrointestinal or respiratory conditions differ in their self-perceptions and explanatory models: a proportion of patients in each group organize their experiences around a central natural symbol--respiration or digestion/excretion. These 2 images link physiological experiences to concepts of pathogenic emotions or personality, physical weakness, and types of social relationships.

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A patient with pneumatosis coli presenting as an abdominal mass is reported. A review of the pathogenesis and treatment is also covered.

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KIE: A pilot study was conducted to explore the nature of communication among clinicians and patients in primary care. Data were gathered from 12 primary care physicians, 6 nurse practitioners, and 42 patients with psychosomatic disorders of the respiratory or gastrointestinal systems. Questions focused on the clinician's view of the patient's health problem, the clinician's view of the patient's view of the problem, and the patient's view of his or her health problem. The degree of agreement or disagreement among the three perspectives was analyzed as a model for measuring the extent of communication between clinician and patient.^ieng

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All doctor-patient interactions take place in a specific context-a particular physical, social or cultural setting. The important role of these contexts in doctor-patient communication, diagnosis and treatment is discussed, with reference to both hospital medicine and general practice.

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Muscarinic mechanisms in basal acid and pepsin secretion in man were quantitated by graded intravenous doses of atropine (1-16 micrograms/kg). Secretion was dose-responsively inhibited in six healthy controls. For the mean dose response, maximum inhibition (Imax) was 100%, and D50 (dose inhibiting 50%) was 0.31 +/- 0.06 and 0.93 +/- 0.13 micrograms/kg, respectively, for acid and pepsin. In 24 patients with duodenal ulcer (DU), calculated Imax was also 100%, and D50S were 1.2 +/- 0.27 and 1.7 +/- 0.3 micrograms/kg, respectively. The low D50 values and the 100% calculated maximum inhibition indicated that in both groups basal secretion was largely or completely cholinergic dependent. We also found that atropine raised heart rate in controls by 44 +/- 1 beats per min (bpm) (D50 = 6 +/- 1.1 micrograms/kg), while the mean maximum increase in DU was only 23 +/- 2 bpm (P less than 0.01) with (D50 = 5.3 +/- 1.0 micrograms/kg (NS)). In DU atropine increased fasting serum gastrin from 62 to 82 pg/ml (P less than 0.05); the increase in normals from 32 to 38 pg/ml was not significant. Thus, while both normals and DU exhibited the same qualitative responses to muscarinic receptor antagonism by atropine with respect to gastric secretion, gastrin levels, and heart rate, there were quantitative differences in all three parameters.

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