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Biomedical subjects

M Ledochowski

Publications and source records attributed to M Ledochowski.

29 records · Page 2Linked to original sources
PubMed1998

Fructose malabsorption is associated with early signs of mental depression.

Fructose malabsorption is characterized by the inability to absorb fructose efficiently. As a consequence fructose reaches the colon were 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 consequence and can be seen in about 50% of fructose malabsorbers. Having made the observation that persons with fructose malabsorption very often seem to present not only with signs of irritable bowel syndrome but also with signs of pre-menstrual syndrome and mental depression, it was of interest to establish whether such an association could be demonstrated in patients. Fifty-five adults with gastrointestinal complaints of unknown origin (12 males, 43 females) were analyzed by measuring breath hydrogen concentrations after an oral dose of 50 g fructose and were classified as normals or fructose malabsorbers according to their breath H2 concentrations. All patients filled out a Beck s depression inventory - questionnaire. Fructose malabsorption was detected in 36 of 55 individuals (65.5%). Subjects with fructose malabsorption (DeltaH2 concentrations >10 p.p.m. after fructose load) showed a significantly higher score in the Beck s depression inventory than normal fructose absorbers. This was true especially for females. Fructose malabsorption may play a role in the development of depressed mood. Fructose malabsorption should be considered in patients with symptoms of major depression or pre-menstrual syndrome. Further studies are needed to clarify the background of this association.

Adult↗
PubMed1998

Lactose malabsorption is associated with early signs of mental depression in females: a preliminary report.

Lactose malabsorption is characterized by a deficiency of mucosal lactase. As a consequence, lactose reaches the colon where it is broken down by bacteria to short-chain fatty acids, CO2, and H2. Bloating, cramps, osmotic diarrhea, and other symptoms of irritable bowel syndrome are the consequence and can be seen in about 50% of lactose malabsorbers. Having made the observation that females with lactose malabsorption not only showed signs of irritable bowel syndrome but also signs of premenstrual syndrome and mental depression, it was of interest to establish whether a statistical correlation existed between lactose malabsorption and mental depression. Thirty female volunteers were analyzed by measuring breath H2 concentrations after an oral dose of 50 g lactose and were classified as normals or lactose malabsorbers according to their breath H2 concentrations. All patients filled out a Beck's depression inventory questionnaire. Of the 30 female volunteers, six were lactose intolerant (20%) and 24 were normal lactose absorbers (80%). Subjects with lactose malabsorption showed a significantly higher score in the Beck's depression inventory than normal lactose absorbers did. The data thus suggest that lactose malabsorption may play a role in the development of mental depression. In lactose malabsorption high intestinal lactose concentrations may interfere with L-tryptophan metabolism and 5-hydroxytryptamine (serotonin) availability. Lactose malabsorption should be considered in patients with signs of mental depression.

Adolescent↗
PubMed1995

Colonoscopic diagnosis and treatment of acute appendicitis.

An atypical case of acute appendicitis is reported, in which the initial presentation was not suggestive of this diagnosis. A routine work-up revealed elevated levels of inflammatory markers, an ultrasonographically normal abdomen and normal endoscopic findings in the upper gastrointestinal tract. During colonoscopy, performed 3 days after admission, the inflamed appendiceal orifice was localized and intubated using an endoscopic retrograde cholangio-pancreatography (ERCP) catheter; pus was aspirated. Elective appendectomy was carried out 5 months later on the asymptomatic patient. Histological analysis revealed fibrous thickening of the appendiceal wall, correlating with an old inflammatory process, along with changes typical for acute ulcerophlegmonous appendicitis. To the best of our knowledge, this is the first case of an endoscopically diagnosed and treated acute ulcero-phlegmonous appendicitis. We draw the following conclusions: (1) Acute appendicitis may present atypically, leading to an extensive clinical work-up including gastroscopy and colonoscopy. (2) This condition may be effectively treated, at least temporarily, by colonoscopic suction of appendiceal pus, provided that clinical urgency for laparotomy is absent. (3) Histological changes typically associated with acute ulcero-phlegmonous appendicitis may be present in asymptomatic patients and in patients without fever and with normal erythrocyte sedimentation rates and blood leucocyte counts. (4) Elective appendectomy should be considered in patients with conservatively healed acute appendicitis or periappendiceal abscess.

Acute Disease↗
PubMed1986

Water intoxication in the course of an acute schizophrenic episode.

In the course of a schizophrenic episode a woman drank a large amount of tap water. She was found nearly unconscious in her room and was admitted to the clinic. Very low sodium and potassium values in the serum were indicative of water intoxication. During hospitalization she also suffered from several convulsive seizures. After replacement of electrolytes she recovered within 12 to 17 h. This case report demonstrates that water intoxication should also be considered in cases of suspected poisoning with other substances such as drugs. In all these cases an electrolyte status is indicated.

Acute Disease↗
PubMed1985

Salt sensitivity in normotensives with family history of hypertension: studies of membrane transport, intracellular electrolytes and alpha 2-adrenergic receptors.

Using long-term automatic blood pressure recording it has previously been shown that subjects with family history of hypertension show a minute fall of blood pressure during sodium restriction, which is reversible by high sodium intake. Thus normotensives with hypertensive antecedents as a group are salt-sensitive, whereas normotensives without heredity of hypertension as a group are salt-resistant. The present study compares intracellular sodium, potassium and calcium, sodium pump activity, NaK-cotransport of red blood cells and density and affinity of alpha 2-adrenergic receptors of platelets in normotensive subjects classified according to family history of hypertension and according to 'salt sensitivity' and 'salt resistance'. Neither the family history of hypertension nor salt sensitivity correlated with intracellular sodium, potassium, calcium, Na-pump activity and NaK-cotransport. Alpha 2-adrenergic density was higher in salt-sensitive than in salt-resistant subjects (P < 0.05) but similar in subjects with a positive and negative family history of hypertension. However, alpha 2-adrenergic receptor density decreased significantly during 2 weeks of moderate salt restriction from 169.6 +/- 34.2 to 142.6 +/- 30.8 (P < 0.01, paired t-test), which may explain the decreased pressor response to infused noradrenaline observed in a previous study during moderate salt restriction. It is concluded that in humans there is no association of genetic predisposition of hypertension or of salt sensitivity to an alteration of sodium pump activity, NaK-cotransport, intracellular sodium and calcium. Alpha 2-receptor density of platelets deserves further study as a possible predictor of salt sensitivity in normotensives.

Adult↗
PubMed1984

Inherited salt sensitivity in normotensive humans as a cause of essential hypertension: a new concept.

The following concept of the pathogenesis of essential hypertension is proposed: there may be a continuous spectrum of noradrenergic sensitivity in normal subjects which is not only inherited but also modified later by different levels of psychological stress or by different types of behavior. The higher the noradrenergic sensitivity in a given subject, the greater the salt sensitivity and the greater the likelihood that hypertension will develop in later life if the usual high sodium-low potassium diet is consumed. Noradrenergic hypersensitivity may be linked to salt sensitivity in that it causes enhanced proximal tubular sodium reabsorption which is compensated for by pressure natriuresis. Enhanced pressure natriuresis requires persistently elevated blood pressure which leads to hypertension if maintained for many years. The phenomenon of salt sensitivity does not become apparent with a sodium intake of less than 50 mmol/day. Although enhanced noradrenergic sensitivity also persists with this low-sodium intake, salt-sensitive subjects are able to compensate for the enhanced rate of proximal tubular sodium reabsorption by reabsorbing less sodium at the distal tubules as compared with that reabsorbed by salt-resistant subjects. Enhanced noradrenergic sensitivity and enhanced proximal tubular sodium reabsorption, however, cannot be compensated for by fine-tuning aldosterone secretion while on the usual high sodium diet containing greater than 100 mmol/day. Under these conditions aldosterone secretion is already suppressed to its basal rate and cannot be suppressed more in salt-sensitive than in salt-resistant subjects. Therefore with the usual high sodium diet the enhanced rate of proximal tubular sodium reabsorption in salt-sensitive subjects is compensated for by enhanced pressure natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Salt sensitivity in humans is linked to enhanced sympathetic responsiveness and to enhanced proximal tubular reabsorption.

If high sodium intake is involved in the pathogenesis of essential hypertension, the effects of changing the sodium intake should be demonstrable in the susceptible part of the normotensive population. Therefore, we have investigated the effects of moderate salt restriction in 52 young normotensive subjects with and without a family history of hypertension; 22 (42%) responded to moderate salt restriction (200 to 50 mmol/day) over 2 weeks, with a significant fall in blood pressure shown by continuous automatic blood pressure recordings. Accordingly, these subjects were classified as salt-sensitive, and the remainder as salt-resistant. Compared to salt-resistant subjects, salt-sensitive subjects showed a 2.5-fold higher incidence of a positive family history of hypertension (p less than 0.01), and a significantly higher blood pressure and lower salivary sodium concentration during the usual high sodium diet. Although there were no differences in Na,K-ATPase activity and in Na-K cotransport of erythrocytes, the pressor response to infused norepinephrine in salt-sensitive subjects was double that of salt-resistant subjects independent of the diet and this was linked to indirect evidence for enhanced proximal tubular sodium reabsorption. On the usual high sodium diet, 40% of the normal population may be salt-sensitive and prone to develop hypertension. Hypersensitivity to catecholamines (genetically determined?) may be the cause of salt sensitivity. A low sodium concentration in saliva deserves further study as a simple screening test to identify salt-sensitive subjects.

Adult↗