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M Fulop

Publications and source records attributed to M Fulop.

At least 37 records · Page 2Linked to original sources
PubMed1993

Unusual calcified goiter associated with increased iodoprotein in serum.

For 30 years we have followed the case of a euthyroid patient who had a goiter diagnosed at age 15. It was originally diffuse and did not shrink during treatment, first with desiccated thyroid extract and then with triiodothyronine. After treatment was stopped, the goiter gradually became nodular and calcified when the patient was in her late teens or early 20s; it then shrank. She remains clinically and chemically euthyroid, with a calcified, multinodular goiter and persistent elevation of the serum PBI concentration which, early in the course of the disease was shown to include a substantial fraction of butanol-insoluble iodine. In a euthyroid patient, the association of an elevated serum PBI concentration (with an abnormally large butanol-insoluble iodine fraction) with a diffuse goiter that became nodular and calcified may be unique.

Adolescent↗
PubMed1993

Alcoholic ketoacidosis.

AKA is an acute metabolic disorder that occurs in ethanol abusers who have usually had a recent binge and who, because of gastritis or another intercurrent illness, stop eating and drinking and often vomit repeatedly. This causes dehydration and ketoacidosis which, unlike in diabetics, is usually associated with little or no hyperglycemia or glucosuria. Despite the ketoacidosis, blood pH findings are variable, depending on the severity of coexisting metabolic alkalosis (owing to vomiting) and respiratory alkalosis (owing to pain or delirium tremens). The metabolic disorders respond rapidly and gratifyingly to parenteral rehydration and administration of glucose, potassium salts, and thiamine. Insulin is usually not necessary, except in patients known or suspected to have diabetes. Because some patients have serious coexisting acute illnesses (which may even have precipitated the acute metabolic disorder), assiduous search for those and the appropriate treatment are essential. The prognosis for the acute metabolic disorder per se is excellent, that for coexisting illness depends on the illness, and that for the ethanol abuse is still often problematic.

Alcoholism↗
PubMed1993

Activation of the complement system by Francisella tularensis lipopolysaccharide.

We have shown by combining lipopolysaccharide (LPS) extracted and purified from Francisella tularensis live vaccine strain (LVS) with normal complement and back titrating with sensitised sheep red blood cells that the LPS activates complement. Deionising the LPS and converting it into the single salt forms of pyridine, ethanolamine and triethylamine altered the ability to activate complement according to the apparent molecular weight due to aggregation. Francisella tularensis LPS activated complement deficient in a component of the alternative pathway (factor B) but failed to activate complement deficient in a component of the classical pathway (C1q). In addition normal complement suspended in ethyleneglycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA) which inactivates the classic pathway was not activated by LPS, and we concluded that the LPS activates complement predominantly via the classical pathway. LPS bound to specific monoclonal antibodies activated complement more than LPS alone. An anti-core monoclonal antibody was approximately tenfold more potent when bound to LPS then an anti-O side chain monoclonal antibody in activating complement.

Antibodies, Bacterial↗
PubMed1991

Case report: extensive brain calcification in hypoparathyroidism.

It is well known that most patients with hypoparathyroidism have radiologically detectable basal ganglia calcification. Not as well known is that the brain calcinosis may be more extensive. We describe a 55-year-old woman with a 44-year history of symptomatic idiopathic hypoparathyroidism who has extensive calcification of her cerebrum and cerebellum as well as her basal ganglia, evident on computed tomography of the head. When first evaluated here 32 years ago, plain radiography of the skull demonstrated calcification of both caudate and lentiform nuclei (basal ganglia). Despite fair control of her serum calcium level, she has developed focal seizures, possibly related to the calcinosis of her brain.

Basal Ganglia↗
PubMed1990

Hyperkalemia in diabetic ketoacidosis.

Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients.

Adult↗
PubMed1990

Severe hypertriglyceridemia in diabetic ketosis.

In order to learn whether patients with diabetic ketosis who had very severe hypertriglyceridemia had underlying genetic hyperlipidemia, the authors measured plasma lipids in 211 episodes. They report the findings in the 15 patients who had initial plasma triglyceride concentrations above 11.3 mmol/L (1,000 mg/dL). These patients were detected during a prospective study of 155 episodes of ketoacidosis and 56 episodes of ketosis. Eleven of the 15 patients had definite or probable insulin-dependent diabetes mellitus (IDDM), but eight of the 15 were not acidemic despite their ketosis. Twelve of the 15 patients (80%) were men, a far higher percentage of men than the 53.6% in the base population of 211 episodes. Plasma triglyceride concentrations returned to normal levels either during the acute episode (seven cases) or well within a year (two more cases) in most of the patients. From that and other considerations, the authors infer that at least ten, and perhaps 12 of the 15 patients did not have an underlying genetic hyperlipidemia contributing to their original severe hypertriglyceridemia. That contrasts with the findings of others who reported that most patients with severe hypertriglyceridemia associated with noninsulin-dependent diabetes mellitus (NIDDM) (usually without ketosis) did have coexisting familial hypertriglyceridemia.

Adult↗
PubMed1989

Pouting sublinguals: enlarged salivary glands in myxoedema.

Enlarged salivary glands are common in patients with hypothyroidism but this finding is not widely appreciated. Although chronic painless enlargement of the salivary glands was reported in papers published 50-60 years ago, mainly in German, it is not mentioned in current textbooks on the thyroid. Along with the parotids, the submandibular and especially the sublingual glands may be quite enlarged, and the enlargement can be a useful clue to the diagnosis of hypothyroidism. The gland enlargement regresses at least partly after thyroid replacement therapy.

Female↗
PubMed1989

Alcoholism, ketoacidosis, and lactic acidosis.

Alcoholic ketoacidosis is a metabolic disorder that occurs in acute-on-chronic ethanol abusers who become acutely starved because of cessation of all caloric intake (including ethanol) owing to gastric intolerance or to an intercurrent acute illness. The precise pathogenesis, and especially the cause of the increased lipolysis, is not known, but several factors known or believed to promote ketogenesis are present in those patients. These are particularly starvation and recent ethanol ingestion. The metabolic disorder responds rapidly to rehydration and administration of glucose intravenously, which stops the ketogenesis. The prognosis in these patients depends on the presence and severity of any underlying illness and the adequacy and effectiveness of treatment for that illness. Patients rarely if ever die from either the ketoacidosis or the lactic acidosis associated with ethanol abuse, but they may succumb to other precipitating or coexisting illnesses.

Acidosis↗
PubMed1989

Comparison of the reactions of older and younger patients to intensive care.

To determine whether age affected the attitudes of patients to intensive care, we administered a questionnaire to 57 patients who had been hospitalized in our ICU or coronary care unit (CCU). The 28 men and 29 women ranged in age from 20 to 92 yr (mean 58.4). Nineteen patients were greater than or equal to 70 yr and nine were greater than or equal to 80 yr. The "intensity" and "severity" of the treatments were similar in the older and younger patients, both men and women, in the ICU and CCU. The great majority of the patients, both old and young, were satisfied with their treatment and outcome, and expressed willingness to undergo similar treatment(s) in the future, if needed. Only five patients were dissatisfied with their treatment: two were greater than 70 yr, the other three were 27, 62, and 65 yr. We did not interview a large number of patients and thus, cannot draw far-reaching conclusions without additional study. Nevertheless, although we expected that older patients would be particularly distressed about their treatments and hence, say they would decline them in the future, in this study both the older and the younger patients were highly accepting of the treatment they received.

Adult↗
PubMed1989

Plasma triglycerides and cholesterol in diabetic ketosis.

To better characterize the severity and course of hyperlipidemia in diabetic ketosis and ketoacidosis, we measured plasma triglyceride and cholesterol concentrations in 50 episodes in 46 adults hospitalized on a municipal hospital medical service. Moderate hypertriglyceridemia was common: 32 patients (64%) had triglyceride levels above the 95th percentile (adjusted for age and sex), and 18 patients (36%) had cholesterol levels above the 95th percentile. Severe hypertriglyceridemia (levels above 5.65 mmol/L) was found in 14 patients (28%). Plasma high-density lipoprotein (HDL) cholesterol and the HDL2 and HDL3 subclasses were measured in 22 episodes. The initial HDL cholesterol levels were usually subnormal in the patients who had not received insulin previously and normal in those who had. Treatment of the ketoacidosis was usually associated with a rapid decrease in plasma lipid levels. At late follow-up (between 1 1/2 and 14 1/2 months), only 2 of the 14 patients with initial plasma triglyceride levels above 5.65 mmol/L still had such high concentrations.

Adult↗
PubMed1987

Residency training.

Explore the source record for details and available documents.

Internal Medicine↗
PubMed1986

Plasma lactate and 3-hydroxybutyrate levels in patients with acute ethanol intoxication.

In order to assess the frequency and severity of lactic acidosis and 3-hydroxybutyric acidosis in ethanol abusers, 29 patients who presented to an emergency room with acute intoxication were tested. Most were also chronic ethanol abusers but were not otherwise seriously ill. Their serum ethanol concentrations averaged 226.5 +/- 94.8 mg/dl (range 98 to 426 mg/dl). In 20 patients, the plasma lactate level was elevated only mildly or not at all (1.1 to 3.0 mmol/liter). Seven patients had plasma lactate levels between 3.5 and 4.3 mmol/liter, and only two patients had moderately elevated levels, 5.1 and 8.7 mmol/liter. Thus, severe lactic acidosis was uncommon in these ethanol-intoxicated patients. Only two patients had even trivially elevated plasma levels of 3-hydroxybutyrate, 1.0 and 1.2 mmol/liter. Thus, these patients did not have unrecognized "alcoholic ketosis" manifested mainly as 3-hydroxybutyric acidosis. An unexpected and unexplained finding was the presence of hyperchloremia in 10 of the 29 patients, with serum chloride levels of more than 110 mmol/liter.

3-Hydroxybutyric Acid↗
PubMed1986

Alcoholic ketosis.

We prospectively studied 23 episodes of suspected alcoholic ketosis in order to learn whether there was objective evidence of the patients having stopped drinking ethanol a few days before admission, and of being starved. Eight patients had moderate ketosis (plasma 3-hydroxybutyrate 4.1-7.8 mmol/liter); seven patients had mild ketosis (2-4 mmol/liter); and eight had little or no ketosis (less than 2 mmol/liter). The latter eight patients had mainly lactic acidosis (plasma lactate 2.0-13.3 mmol/liter). Most of the ketotic patients did not have ethanol detected in their blood. The presence of starvation was supported by the finding of subnormal plasma triiodothyronine levels (less than 90 micrograms/dl) in six of seven ketotic patients (average 60 micrograms/dl for all seven). The ketotic patients usually had low-normal plasma insulin levels (3- 16 microU/ml), as is common in starvation. Our findings support the previously undocumented belief that most patients with alcoholic ketosis did stop drinking ethanol some time before admission, and that starvation is a major pathogenetic factor in the disorder.

Acidosis↗