[Anniversary decompensations. Decompensation predictions].
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Dysregulation of the serum and IgG N-glycome in decompensated cirrhosis and its association with Model for End-Stage Liver Disease-Sodium (MELD-Na).
BACKGROUND AND AIMS: N-glycans modulate glycoprotein structure and function and are altered during chronic inflammation. We sought to define the extent of serum and IgG N-glycan disruption in patients with decompensated liver cirrhosis from alcohol-related liver disease (ALD), primary sclerosing cholangitis (PSC), and ALD-related hepatocellular carcinoma (HCC). Finally, we aimed to examine whether serum and IgG glycosylation is associated with changes in Model for End-stage Liver Disease-Sodium (MELD-Na) scores, a clinical marker used to prioritise liver transplantation. METHODS: Serum samples were obtained from patients with ALD (n = 17), PSC (n = 7), ALD-related HCC (n = 4), and healthy controls (n = 10). N-glycans were released, fluorescently labelled, and profiled by hydrophilic interaction ultra performance liquid chromatography (HILIC-UPLC). Chromatograms were integrated into 46 and 23 glycan peaks for serum and IgG respectively. These peaks and their associated glycosylation traits were statistically compared with healthy controls using age- and sex-adjusted linear regression models. RESULTS: In serum, decompensated cirrhosis shows statistically significant shifts toward less complex, agalactosylated and asialylated biantennary glycans, accompanied by significant losses of highly branched, galactosylated and sialylated structures. IgG mirrored this pattern, which is characteristic of a pro-inflammatory signature, with increased agalactosylation and bisected glycan levels, along with reduced levels of digalactosylated and sialylated species. N-glycan profiles showed significant associations with MELD-Na scores, indicating that inflammatory processes in decompensated liver cirrhosis continue to reshape serum glycoproteins. CONCLUSION: Decompensated liver cirrhosis shows profound remodelling of serum and IgG N-glycans. These data establish a reference framework for terminal glycomic disruption in liver disease and highlight the potential value of incorporating glycosylation analysis into broader assessments of liver disease progression.
Humans↗
The decompensated back.
There is no single circumstance or combination of circumstances which precipitate all clinical instances of back discomfort. This simple statement should be so obvious that one must question the finality and accuracy of the diagnostic effort in those reports which relate to large series of patients treated by one method. There is no thought of impugning the basic honesty of the reporting physician in this statement, but rather of raising the fair question of whether the "slipped disc" (or whatever the etiological diagnosis) is all that happened to produce the symptoms, and whether its removal (or whatever) is all that occurred in accomplishing clinical cure improvement. If there is doubt that the answer to both questions is in the affirmative, then serious consideration must be given to those other factors, if the medical profession is ever to be a science instead of a trade. The back structures are different from comparable structures elsewhere in the body, principally in their neurological organization and controlmthere is the specific, discrete, segmental arrangement of both sensory and motor functions of muscular and nonmuscular structures via the posterior primary rami of the spinal nerves. Coupled with this is a different mechanism of segmental innervation of the vascular and nonmuscular structures which line the vertebral canal, via the sinu-vertebral nerves. Both are modulated by higher level influences. The sinu-vertebral nerves, through the sympathetic chain, may provide an additional avenue of response which may avoid or alter the influence of higher levels. The Melzack-Wall hypothesis would seem to provide an acceptable explanation for the need to modulate nociceptive afferent stimuli before they evoke pain perception and response. Since this modulation mechanism decompensates under numerous conditions, pain perception and responses do occur. Among those responses are the alterations in normal function of the low back structures, perhaps the disastrously effective one of which is decompensation of the muscular strength necessary to accomplish the demands of daily use. This problem is not so simply solved by a handout sheet of exercises. The primary consideration is to modify or relieve pain by a careful evaluation of its source and the employment in combination of those therapeutic efforts which a logical treatment plan indicates. If these be accomplished, the final and most important consideration, then, is the improvement of neuromuscular function to the level compatible with normal activities by a carefully guided activity program. There is no method for instant reversal of the status of the decompensated heart--nor the decompensated back.
Adult↗
[Excretion of uric acid in cardiac decompensation].
The role of hyperuricemia is confirmed, in literature, as a risk factor in ischemic heart disease and in the development of atherosclerotic complications. The problem of uric acid concentration in serum is still not elucidated as well as the role of the eventual hyperuricemia as a risk factor and its excretion from the kidneys of patients with heart diseases in a decompensation stage. Thirty five patients with different heart diseases in various decompensation stages were observed. In all patients, the uric acid concentration in serum were studied as well as the clearance of uric acid, reabsorption percentage in tubules and glomerular filtration according to the clearance of endogenous creatinine. The results obtained revealed that hyperuricemia (over 7 mg%) is found in a great number of the patients (40%) with heart decompensation. The hyperuricemia established resulted primarily from the reduced filtration of glomeruli. In some of the cases, an increased reabsorption of uric acid in tubules was found. In other, single cases, data exist about uric acid secretion in tubules. The problem of heart patients treatment in decompensation stage with the presence of hyperuricemia is discussed. In those cases, very likely, prophylactic measures should be undertaken due to the fact that hyperuricemia is a factor, secondarily leading to atherosclerotic heart alterations.
Adolescent↗
Self-catheterization for decompensated bladder: a review of 100 cases.
The non-neurogenic decompensated bladder is a poorly defined entity. In an attempt to elucidate this condition 100 consecutive patients with non-neurogenic decompensated bladders were studied, etiology was sought and treatment with intermittent self-catheterization was done. Of the patients 34 per cent were able to resume voiding. Bacteriuria and pyuria were decreased from 90 to 18 per cent. Complications were few and over-all acceptance was excellent. A definition of non-neurogenic decompensated bladder was established.
Adolescent↗
[Insulin treatment of decompensated diabetes mellitus with a new artificial endocrine pancreas (author's transl)].
During the past decades insulin has been given in relatively high doses when treating diabetic coma. Recently low-dose insulin treatment has been proposed by several groups. In the reported investigation insulin was initially given in moderate to high doses (12-200 U/h) with a steady reduction in dose during the course of treatment. Insulin infusion was regulated either manually with an adjustable infusion pump (7 patients) or automatically with an artificial endocrine pancreas (glucose-controlled insulin infusion system; 11 patients). Thus 18 patients with decompensated diabetes mellitus (coma or precoma) were treated. In 14 patients with ketoacidotic decompensation laboratory data on hospital admission were: blood glucose 7.35 +/- 0.61 g/l, serum potassium 4.7 +/- 0.4 mmol/l, pH 7.1 +/- 0.04, base excess - 19,7 +/- 2.2 mmol/l (x +/- SEM). The other patients had hyperglycaemic or hyperosmolar non-ketotic decompensation. In all patients controlled reduction of blood glucose levels was achieved within 2.3 to 18 hours. The amounts of insulin infused during this ranged from 17 to 320 units, but in one instance was 1950 units. There were no complications.
Adolescent↗
[Role of secondary hyperaldosteronism in the pathomecanism of hydropic decompensation in the cirrhotic patient (author's transl)].
Plasma aldosterone levels before and after walking were compared in a series of 10 controls and 41 patients with cirrhosis of the liver. The latter were distributed in the following way: 8 had compensated cirrhosis, the remaining 33 were in a situación of hydropic decompensation, 10 with associated renal insufficiency, and 23 without. Basal aldosterone levels in compensated cirrhotics were similar to those of the controls, but these values increased significantly more than the controls following postural stimulation. Decompensated cirrhotics without renal insufficiency had significantly higher values than the controls, both in basal conditions and after stimulation. The highest values corresponded to the decompensated cirrhotic patients with renal insufficiency who were in advanced stages of liver disease. On the basis of the present findings and those of other authors, it is suggested that a certain reduction in the metabolic clearance of aldosterone appears to exist in hepatic cirrhosis. However, hormonal hyperproduction is the dominant factor in the pathogenic mechanism of secondary hyperaldosteronism. The pathogenesis of the excessive production of hormone is discussed. In conclusion, it appears that the scant affluence of sodium to the macula densa may be the primary factor in explaining this common situation in patients with cirrhosis of the liver.
Adult↗
Value of the test of spontaneous reduction of nitroblue tetrazolium in diabetes decompensation.
Nitroblue tetrazolium (NBT) test was performed in forty-four diabetic patients of both sexes ranging in age from 15 to 64 years. Some of the patients were tested both before and after diabetes compensation. In cases of decompensated diabetes caused by dietary errors or by inadequate dosage of the antidiabetic drugs, NBT results were within normal range. Significantly higher values were observed in decompensation of diabetes caused by bacterial infection. This observation may be used to detect the real cause of diabetes decompensation.
Adolescent↗
Distribution of serum zinc between albumin and alpha2-macroglobulin in patients with decompensated hepatic cirrhosis.
Lower concentrations of total serum zinc (540 +/- 111 mug/1, mean +/- SEM), and of albumin-bound serum zinc (295 +/- 113 mug/1) and a higher concentration of alpha2-macroglobulin-bound zinc (245 +/- 69 mug/1) were found in 25 patients with decompensated hepatic cirrhosis, compared to 28 healthy subjects (835 +/- 91; 679 +/- 83; 156 +/- 27 mug/1 respectively). Levels of total and albumin-bound zinc were significantly and positively correlated with serum albumin levels. Higher levels of alpha2-macroglobulin-bound zinc were associated with higher levels of alpha2-macroglobulin in these patients (2.8 +/- 0.8 g/1) compared to normals (2.3 +/- 0.6). Hence, not only do decompensated cirrhotics exhibit a lower serum zinc level but a greater proportion of this zinc is associated with the tightly bound, and presumably metabolically more inert, serum fraction. This situation exaggerates the zinc deficiency state of the severe cirrhotic.
Humans↗
A method of estimating intracranial decompensation in man.
A new method of estimating intracranial decompensation in man is described. An on-line computer system is connected to an intracranial pressure (ICP) monitoring system to compute regression plots of mean ICP vs standard deviation; standard deviation is used as a measure of ICP instability. Two zones with distinctly different slopes are a characteristic feature of these plots. It is thought that the changes of slope signify intracranial decompensation.
Humans↗
Clinical recognition of early schizophrenic decompensation.
The early signs and symptoms of schizophrenic decompensation are subtle and variegated. Today's community patient often presents with vague complaints of brief duration making it imperative that today's diagnostician be able to recognize and appropriately treat early psychopathology. This paper collates a number of observations of developing psychotic phenomena -- self reports, clinical studies and controlled experiments -- and provides a useful format for organizing these complex and changing behaviors. Data are presented and discussed using our clinical schema for detailing the natural progression of developing psychotic phenomena into four distinct stages. Efficacy of early recognition and treatment in aborting or diminishing a major psychotic episode is discussed. The advantages of recognizing the early signs of psychotic decompensation are apparent. First, with adequate intervention and treatment, the overt psychotic state may be attenuated. Although the feasibility of reducing the incidence of schizophrenia through intervention in "high risk" groups, or those experiencing insidious symptoms remain speculative (further investigation in this area is urgently needed), nonetheless, early diagnosis and comprehensive rehabilitative care significantly improves social and occupational adjustment. A second advantage accrues from early diagnosis. It enables patient and family to better cope with the illness. We have previously outlined a schema detailing the natural progression of developing psychotic phenomena into four distinct stages. The phenomena, when identified, can be seen as a continuum. However, many clinicians fail to recognize the earlier phases and typically the diagnosis of psychosis is made relatively late at what we call stage three of the four stages we described.
Affective Symptoms↗
[State of the cardiovascular system in patients with decompensated mitral valve defect under conditions of high altitude].
A clinical study was conducted in 236 patients with decompensated mitral valve disease--permanent residents of the areas located at various altitudes in the Pamirs and Tien Shan (760 to 4,200 m above the sea level). The main parameters of haemodynamics were studied by means of the dye dilution method in 158 of them, as well as the indices of cardiodynamics by way of polycardiography. The data obtained in 120 normal individuals living in foothills (760 m) served as control. It was demonstrated that with the same stages of cardiac insufficiency, the most striking changes in the haemo- and cardiodynamics were noted among the residents of the high altitude areas. Among those living at medium altitudes (1,650 to 2,020 m), the cardiac output and the left ventricular function appeared to be reduced most distinctly. These patients also exhibited a clear relationship between the main variables of the cardiovascular functions and the severity of cardiac insufficiency. The revealed clinical and functional peculiarities of the decompensated mitral valve disease in mountaneers are atrributable to the effect of hypoxic hyposy upon the regulation of the respiration and the pulmonary circulation.
Adolescent↗
[Cerebral hemodynamic disorders in patients with chronic decompensated respiratory insufficiency. Physiopathogenetic considerations].
The present paper reports on 12 patients (8 males, 4 females) suffering from chronic decompensated respiratory failure, who presented concomitant transient haemodynamic disturbances in the carotid and vertebrobasilary systems, manifested by hemisphere or brain stem symptoms. Owing to the adaptive capacity of these patients there exists a certain tolerance threshold to hypercapnic hypoxemia, but following accentuated or rapid aggravation of acid-base hypercapnic hypoxemia, the biological balance is abruptly perturbed leading to cerebral haemodynamic disturbances. The pathophysiological mechanism of production appears to be the accumulation of acid ions caused by pH acidification of the cerebrospinal fluid. Increase in the cerebral arterial output with decrease in the rate of circulation and vascular resistance take place especially in the vessels with atheromatous or hyaline lesions. Under conditions of severe acidosic hypercapnic hypoxemia this, nevertheless, insures a minimum of 10--20% oxygen required by the metabolism of the nerve cell, sufficient for maintaining the structure of the cell (vita minima). These vasculometabolic mechanisms explain why with improvement of haematosis, following remission of the decompensated disease and fall in acidotic hypercapnic hypoxemia values, the cerebral haemodynamic disturbances also show a more or less evident remission because the nerve cells having maintained their structure are able to take up their function again.
Acidosis, Respiratory↗
Correlation between skeletal muscle vascular decompensation and survival: roles of tissue ischemia and innervation.
A constant-flow, cross-perfused, vascularly isolated gracilis muscle preparation was used to examine the hypothesis that locally produced and released products of ischemic muscle metabolism are responsible for the vascular decompensation (vasodilation) reported to occur in late oligemic hypotension. Well-oxygenated donor arterial blood perfused recipient gacilis muscles at a constant flow rate of 5.2 +/- 0.5 ml/100 gm/min while the recipient animals were subjected to a modified Wigger's hemorrhage protocol. Arterial and venous blood gases taken across the gracilis muscle at regular intervals during the experiments verified adequate tissue perfusion. Of the thirteen studies reported, only ten shocked recipient dogs progressed to irreversible shock postreinfusion. This series was identified as the "recipient-irreversibly shocked group." The remaining three shocked animals recovered from the shock protocol and were labeled "recipient-reversibly shocked series." The initial response to blood loss in both groups was intense vasconstriction, with the greatest initial constriction occurring in the irreversibly shocked series. The three animals that survived the protocol were able to sustain this compensatory effort, but the ten that ultimately progressed into irreversible shock postreinfusion invariably demonstrated a significant loss of vascular tone during late oligemia (conductance rose from 43% to 63% of control). Thus evidence is presented which indicates decompensation during adequate tissue perfusion, or absence of ischemia. A strong correlation was also shown to exist between sustained compensatory vasoconstriction in the gracilis muscle, and survival. The suggestion is made that part of the loss of vascular tone may be related to prejunctional inhibition of adrenergic transmission or alpha-receptor fatigue, with a minor role being played by the vasodepressor products of local tissue ischemia.
Animals↗
Abdominal pain in diabetic metabolic decompensation. Clinical significance.
Severe abdominal pain and tenderness occured in 46 of 211 episodes of severe diabetic metabolic decompensation. No association was found between abdominal pain and the degree of dehydration or the initial blood glucose level. In 17 instances, the abdominal pain could be attributed to the precipitating cause of the metabolic decompensation. The episodes of unexplained pain all occurred insulin-dependent patients less than 40 years of age; of these, only three had a plasma bicarbonate level greater than 10 mEq/liter, and in two patients, additional factors could account for the relative lack of ketoacidosis. Abdominal pain occurring in patients more than 40 years old, irrespective of the plasma bicarbonate level, and in patients of any age with a plasma bicarbonate level in excess of 10 mEq/liter, almost invariably indicates a specific underlying cause.
Abdomen↗
The study of calcium, phosphorus, hydroxyproline, and nitrogen in decompensated coxarthroses and gonarthroses.
A study was undertaken to find our the biological profile of bone symptomatology of decompensated coxarthrosis and gonarthrosis. In a group of 77 patients and in 48 individual patients the levels of calcium, phosphorus, hydroxyproline and nitrogen were studied for four successive days. Calcium was administered by the intravenous route on the third day (186 mg). The results were compared to 16 healthy controls. Analysis was made with reference to the differences in sex, age, stature and anabolic therapy. The products eliminated were referred in absolute amounts to the body surface and to the period of 1 minute. 91 patients and 17 healthy controls were subjected to a provoked hypercalciuria test. Five patients were followed up in a 47Ca kinetic study and its result was compared to the content of Ca/P and P/Ca in serum and urine found in the same patients and in 21 healthy controls. The biological profile was also compared to a group of patients with gonarthrosis and varose deformity and to 127 patients with inflammatory joint diseases. From the results it is assumed that in women with decompensated coxarthrosis and gonarthrosis the syndrome of disease is a bone manifestation which affects the mineral bone substrate and particularly its calcium level. Phosphorus and the organic products of bone (nitrogen and hydroxyproline) of these patients are susceptible to intravenous administration of calcium. In women the metabolism of collagen appears to be more active than that seen in controls, and tends to resemble that of phosphorus. With its lower activity calcium tends to relate to noncollagenic products, such as osseomucoid (glycoprotein, proteoglycan) and osseoalbumoid. In accord with the findings, the patients show a higher miscible pool of calcium (47Ca), and its lower elimination (in urine and stools) and lower accretion to bone. There are a number of factors (sex, stature, age, clinical compensation of disease) that must be taken into consideration when evaluating the results.
Adult↗
Correlation between skeletal muscle free fatty acid extraction and vascular decompensation during hemorrhagic hypotension.
The objective of this study was to determine whether or not a relationship exists between free fatty acid (FFA) extraction by skeletal muscle and onset of irreversible shock. Hind limb skeletal muscle vasculature of anesthetized dogs was surgically isolated from cutaneous tissue and subjected to a modified Wigger's hemorrhage shock protocol which was divided into five stages (I-V). Since the first signs of irreversibility began in stage II, this stage of hypovolemic hypotension was subdivided into IIa, IIb and IIc. Arterial and venous blood samples were taken during each stage for subsequent blood gas and FFA analysis. The data indicated that the onset of severe tissue ischemia and metabolic acidosis occurs concurrently with increased uptake of FFA and skeletal muscle vasodilation (decompensation). A possible physiological explanation for these observations could be related to an increased synthesis and release of PGE1. This agent has been shown by others to inhibit adrenergic neurotransmitter release causing loss of vascular tone.
Animals↗
Action of oral and parenteral bethanechol on decompensated bladder.
A double blind balanced Latin-square study was conducted on 20 adult patients with decompensated bladders to determine the relative effectiveness of oral and parenteral bethanechol chloride (Urecholine) on the stretch response of bladder muscle. Detrusor reaction was measured by modified cystometry. Five mg. of subcutaneous bethanechol chloride produced a significant increase in intravesical pressure which was more rapid in onset, of larger magnitude, and of shorter duration than oral doses of 100 and 200 mg.
Administration, Oral↗