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PubMed1986

[A rare cause of 2 unclear fatalities: undiagnosed acute and chronic amebiasis].

Two cases are reported of unexpected and unclarified death caused by an infection with Entamoeba histolytica. The first case concerned a German whose disease was not diagnosed during the asymptomatic phase (2 years' duration) or in the acute phase during the last 3 weeks before death. This is typical of the disease. In the final phase, he developed a hepatic abscess. Death occurred as a consequence of bilateral apoplexia in the adrenal glands. In the second case a Turk fell ill with gastralgia and diarrhea. Developing hepatic insufficiency with comsumptive coagulopathy, he died after 6 days. Intoxication and/or intolerance of fructose were assumed as tentative diagnoses. These two cases show clearly that even outside an endemic area, one has to reckon with the possibility of amebiasis.

Adrenal Glands↗
PubMed1986

Fructose-induced hyperlactemia in hyperosmolar syndromes.

Severe hyperlactemia of 8.7, 8.6 and 7.9 mmol/l, respectively, developed in three patients with hyperosmolar syndromes (two hypernatremic, 417 and 415 mosmol/kg H2O; one hyperglycemic 437 mosmol/kg H2O) during rehydration treatment with 5% fructose in water (fructose dosage 0.5 g/kg body wt. per hour). After resolution of the electrolyte disturbances, the infusion of fructose at the same dosage increased the plasma lactate concentration in two of the patients to 4.9 and 4.0 mmol/l, indicating near normalization of hepatic lactate utilization. Thus, in addition to peripheral insulin resistance and decreased muscular glucose utilization, the hyperosmolar state is associated with a reduced tolerance to fructose. This is most likely due to an osmolality-dependent impairment of hepatic gluconeogenesis. In rehydration therapy for hyperosmolar syndromes, fructose-containing infusion solutions should no longer be used.

Acidosis↗
PubMed1997

Measurement of glucose turnover--implications for the study of inborn errors of metabolism.

Aspects of glucose metabolism have been investigated quantitatively employing stable isotopes for 20 year. Use of non-recycling [6,6-2H2] or [U-13C] glucose labels provides a value for total hepatic glucose production (glycogenolysis plus gluconeogenesis). Quantitation of gluconeogenesis with isotopic tracers has itself recently been revisited employing protocols and analytical options that purport to overcome the isotope exchanges (dilution) experienced at the level of oxaloacetate when the rate of incorporation of label into glucose from infused alanine, lactate or pyruvate is monitored. Labelled glucose has been employed to investigate metabolic disturbances of glycogen storage disease type I (GSD-I) and type III (GSD-III). Endogenous glucose production and glucose recycling have been studied in both these storage diseases employing a primed-continuous infusion of D-[U-13C] glucose and quantitation of isotope enrichments and isotopomer distribution observed in plasma glucose either by mass spectrometry or nuclear magnetic resonance spectroscopy. General aspects of glucose metabolism as investigated with stable isotopes are presented.

Fructose Intolerance↗
PubMed2000

Fecal bacterial activity in symptomatic carbohydrate malabsorption: effect on the fecal short-chain fatty acid ratio.

BACKGROUND: It is still not clear why only some patients with carbohydrate malabsorption experience symptoms. In a previous study on healthy fructose malabsorbers an increased degradation of fructose in anaerobic fecal cultures from symptomatic malabsorbers was found, indicating increased bacterial activity. In the present study, the same investigation was repeated in patients with nonspecific abdominal complaints and fructose malabsorption. Moreover fecal short-chain fatty acids (SCFA), products of colonic bacterial fermentation of carbohydrates were measured. PATIENTS AND METHODS: A standard quantity of fructose (500 mg) was added to anaerobic fecal cultures from 25 patients (nine men, 16 women; median of age 53 years, range 36-69 years). The fructose degradation rate was assessed using photometry, and interpreted as representing bacterial activity in the colon. In 14 of the patients, SCFA levels were also measured using chromatography on a capillary column. RESULTS: 10 of the 25 patients had a history of symptoms after ingesting fructose-containing foods, and also showed symptoms during the test; 6 patients had symptoms either in their history or during the test; and the remaining 9 were free of symptoms. There were no differences in the H2 increase. The fructose degradation rate was higher in symptomatic malabsorbers (255 mg vs. 217 mg), but the difference was not significant. However, there was a strong inverse correlation between this bacterial activity and the acetate level, with r = -0.822 (P = 0.000) and r = -0.868 (P = 0.000) in the rank correlation. The correlation for propionate was r = 0.479 (P = 0.083), and that for butyrate was r = 0.599 (P = 0.024). CONCLUSIONS: This study failed to confirm a significant correlation between fecal bacterial activity and the occurrence of symptoms in patients with fructose malabsorption. However, the interesting correlation with the SCFA raises questions regarding possible connections between colonic bacteria, carbohydrate malabsorption, and the beneficial effect of this pattern of SCFA in several colonic diseases.

Adult↗
PubMed2000

Fructose- and sorbitol-reduced diet improves mood and gastrointestinal disturbances in fructose malabsorbers.

BACKGROUND: Fructose malabsorption is characterized by the inability to absorb fructose efficiently. As a consequence fructose reaches the colon where it is broken down by bacteria to short fatty acids, CO2 and H2. Bloating, cramps, osmotic diarrhea and other symptoms of irritable bowel syndrome are the consequences and can be seen in about 50% of fructose malabsorbers. We have previously shown that fructose malabsorption is associated with early signs of mental depression and low serum tryptophan concentrations. It was therefore of interest whether a fructose-reduced diet could not only improve gastrointestinal complaints but also depressive signs seen in fructose malabsorbers. METHODS: Fifty-three adults (12 males, 41 females), who were identified as fructose malabsorbers according to their breath-H2 concentrations, filled out a Beck's depression inventory-questionnaire, and a questionnaire with arbitrary scales for measurement of meteorism, stool frequency and quality of life for a 4-week period before dietary intervention and 4 weeks after dietary change as for fructose- and sorbitol-reduced diet. RESULTS: Depression scores were reduced by 65.2% after 4 weeks of diet (P < 0.0001), and there was a significant reduction of meteorism (P < 0.0001) and stool frequency (P < 0.01). Improvement of signs of depression and of meteorism was more pronounced in females than in males. CONCLUSION: Fructose- and sorbitol-reduced diet in subjects with fructose malabsorption does not only reduce gastrointestinal symptoms but also improves mood and early signs of depression.

Adolescent↗
PubMed1978

Four cases of long-standing diarrhoea and colic pains cured by fructose-free diet--a pathogenetic discussion.

Four patients with a long history of abdominal swelling, colic pains and diarrhoea were cured by a fructose-free diet. They were all given an oral load of (14C) fructose and their expiratory excretion of 14CO2 was found to be significantly lower than that of control patients with similar symptoms. It is concluded taht the patients cured by a fructose-free diet might have a partial fructose malabsorption.

Adult↗
PubMed1980

Type III glycogenosis with deposition of urate and amyloid.

A case of a 44-year-old man with hepatic form of glycogenosis was presented. The patient had abdominal distension and muscular weakness. The glucose tolerance test showed a diabetic pattern, though he had hypoglycemia in fasting state. The fructose tolerance test showed an ability of conversion from fructose to glucose. The double glucagon test showed no rise of blood glucose in fasting state but a rise 2 hours after meal. These symptoms and laboratory data supported the clinical diagnosis of type III glycogenosis. At autopsy, glycogen was markedly deposited in the liver, and slightly in the kidneys and heart. The glycogen pooled in the hepatic cells histochemically showed a normal reaction to several glycogen stainings. Electron microscopy by using Thiéry's method revealed that the pooled glycogen particles were clearly arranged as rosettes measuring 1,000A in largest diameter composed of clustered monoparticulates. There were marked hyalinization of the islets of Langerhans containing amyloid. As to its pathogenesis, this change can be interpreted as a morphological expression of the hypofunction of beta-cells ascribed to long-standing hypoglycemia.

Adult↗