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Biomedical subjects

J Havrankova

Publications and source records attributed to J Havrankova.

At least 19 recordsLinked to original sources
PubMed1993

Long-term use of intramuscular insulin therapy in a type I diabetic patient with subcutaneous insulin resistance.

We studied a 26-year-old Type 1 diabetic patient who experienced recurrent episodes of ketoacidosis and who was unresponsive to subcutaneous insulin, but normally responsive to intravenous insulin as demonstrated by insulin challenge test. Attempts at intravenous and intraperitoneal insulin administration were complicated by recurrent septicaemia. We therefore investigated the hypoglycaemic effect of intramuscular insulin administration in this patient. After intramuscular injection of NPH and Ultralente human insulin (0.1 U kg-1), the lowest plasma glucose levels occurred 1 and 7 h later, respectively; the hypoglycaemic effect lasted approximately 2 and 12 h, respectively. We based insulin therapy on intramuscular NPH as a fast-acting insulin and Ultralente as an intermediate-acting insulin using four injections a day. During the next 24 months, the patient was hospitalized for 4 weeks versus 56 weeks in the 20 months preceding intramuscular insulin administration, and was able to resume full-time work. HbAlC decreased from 11.7% to 8.7% (normal range: 4.2-5.9%). Thus, long-term intramuscular insulin therapy is a feasible alternative to intravenous or intraperitoneal insulin in patients with well-demonstrated resistance to subcutaneous insulin.

Adult↗
PubMed1993

Calcium is essential in normalizing intolerance to glucose that accompanies vitamin D depletion in vivo.

Vitamin D is essential for normal insulin secretion in vivo and in vitro. The differential effect of calcium and of the vitamin D endocrine system in the insulin response to secretagogues is still a subject of debate. To study the roles of calcium and the vitamin D system in the in vivo insulin response, GTT and insulin sensitivity tests were conducted in rats presenting vitamin D depletion and hypocalcemia or vitamin D depletion supplemented with calcium alone for 3, 7, or 14 days, vitamin D3 (6.5 nmol/day x 7 days), or 1,25(OH)2D3 (28 pmol/day x 7 days). Serum calcium was 1.28 +/- 0.04 mM in hypocalcemic vitamin D-depleted rats, 1.47 +/- 0.06 (NS), 1.8 +/- 0.2 (P < 0.0002), and 2.04 +/- 0.07 (P < 0.0001) mM after 3, 7, or 14 days, respectively, of calcium supplementation; vitamin D3- or 1,25(OH)2D3-supplemented animals had serum calcium of 2.61 +/- 0.04 or 2.48 +/- 0.05 mM (P < 0.0001 vs. hypocalcemic vitamin D-depleted rats). Rats with hypocalcemia and vitamin D depletion had significantly higher glucose concentrations (P < 0.0005) and lower insulin response during GTT than all other groups (P < 0.001). Differences in insulin sensitivity could not account for differences in response because exogenous insulin administration led to a similar drop in glucose concentrations in all groups, with the nadir averaging 51.7 +/- 2.6% of initial values. To distinguish between calcium and the vitamin D system in the GTT response, rats were treated with a nonhypercalcemic analogue of 1,25(OH)2D3, OCT (28 pmol/day x 4-7 days) with or without dietary calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1990

Vitamin D depletion retards the normal regeneration process after partial hepatectomy in the rat.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3], the hormone of the vitamin D3 (D3) endocrine system, has been shown to influence malignant and normal cell proliferation/differentiation, while insulin (I) is known to be essential for liver growth. To investigate the influence of D3 on liver regeneration, the effect of the D status was studied in D-depleted rats (D-) pretreated with: G1, placebo (D-, hypocalcemic); G2, oral calcium only (D-, normocalcemic); G3, D3; and G4, 1,25-(OH)2D3. Two thirds hepatectomy (HX) or sham operation was performed, and regeneration was studied for 3 weeks. I response to glucose challenge and the hepatic I receptor were also studied. Cell volume, DNA, and RNA were not affected by pretreatment. After HX, the pattern of [3H]thymidine incorporation into DNA (P less than 0.003) and the cell labeling index (P less than 0.0001) were highly influenced by pretreatment and suggestive of an earlier appearance of the S phase of the cell cycle in the 1,25-(OH)2D3-treated compared to the D- hypocalcemic group. Furthermore, the mitotic index revealed a significant effect of pretreatment (P less than 0.01), with peak mitosis 24 h after HX in D3-treated and 1,25-(OH)2D3-treated rats compared to 30-36 h after HX in the D- groups. Liver weight restitution was impaired in D- rats (P less than 0.009) and is illustrated by the estimated time required to achieve 70% recovery of the resected liver mass, which was found to be 186 and 300 h in G1 and G2, and 154 and 107 h in G3 and G4. G1 rats had significantly higher glucose concentrations (fasting as well as after glucose injection) and reduced I secretion when challenged with glucose (P less than 0.001); they also had an upregulation in hepatic I receptor number (P less than 0.005) compared to calcium or D3-treated rats, while 1,25-(OH)2D3 led to a liver I receptor number similar to that found in hypocalcemic D- rats; the affinity of the I receptor was, however, only slightly changed by pretreatment (P less than 0.08). Our data indicate that in D depletion, hypocalcemia retards DNA synthesis and liver mass recovery, while normocalcemia contributes to DNA synthesis, but fails to sustain mitosis and compensatory liver growth to a level comparable to that found after D3 and/or 1,25-(OH)2D3 repletion. The observation that both D3 and 1,25-(OH)2D3 significantly promoted normal liver recovery after partial HX illustrates the role of the D endocrine system in normal cell physiology in vivo.

Animals↗
PubMed1989

Blood glucose measurements during symptomatic episodes in patients with suspected postprandial hypoglycemia.

Postprandial (reactive) hypoglycemia is a controversial disorder because its symptoms are not specific, the presence of symptoms often correlates weakly with blood glucose concentrations measured after oral glucose administration, and glucose levels have rarely been measured when symptoms have developed spontaneously. In this study, we measured blood glucose in 28 patients with suspected postprandial hypoglycemia while they were experiencing their typical symptoms, in capillary blood collected on filter paper. Five patients (18 percent) had symptoms of "hypoglycemia" that were associated with blood glucose levels of 2.8 mmol per liter (50 mg per deciliter) or less, and eight other patients (29 percent) had symptoms associated with glucose levels of 2.9 to 3.3 mmol per liter on at least one occasion. Six (5 percent) of 132 reported symptomatic episodes that were associated with blood glucose levels of 2.8 mmol per liter or less, and 16 (12 percent) with levels of 2.9 to 3.3 mmol per liter. In 140 measurements made in 17 normal subjects, blood glucose levels were never found to be less than 2.8 mmol per liter, and levels of 2.9 to 3.3 mmol per liter were found only twice. No specific symptom was associated with low glucose levels in the patients with suspected hypoglycemia. The relief of symptoms by ingesting food was more often associated with low than with normal blood glucose levels: 86 percent of episodes in which blood glucose values were less than or equal to 3.3 mmol per liter were relieved by eating, as compared with 53 percent of episodes in which values were more than 3.3 mmol per liter (P less than 0.007). No correlation was found between plasma glucose levels measured after oral glucose administration and blood glucose levels measured during symptoms. We conclude that postprandial hypoglycemia is infrequent, even in a referral population, and that recording blood glucose measurements during spontaneously occurring symptomatic episodes is necessary to establish the diagnosis since symptoms are not specific and oral glucose-tolerance testing is not helpful.

Adult↗
PubMed1989

Suppression of T4 secretion in a metastatic follicular carcinoma.

Despite total thyroidectomy, a patient with metastatic follicular carcinoma of the thyroid remained biologically euthyroid three months after stopping thyroxine (T4) therapy. Thyroid hormone production was investigated by means of a modified tri-iodothyronine (T3) suppression test, in which serum T4 was used as a suppression marker. After three weeks of oral T3 (Cytomel) therapy (50 micrograms/day), the serum T4 decreased from normal (108 nmol/L) to undetectable values. However, even though suppressive therapy was effective in preventing TSH dependent hormone secretion by the tumor, it did not prevent tumor growth and the eventual death of the patient.

Adenocarcinoma↗
PubMed1986

Late increase in serum 1,25-dihydroxyvitamin D one month after surgery for adenomatous hyperparathyroidism.

This study was designed to follow the evolution of serum 1,25(OH)2D after surgery for primary hyperparathyroidism. Ten patients were studied before and for up to 85 d after removal of a single parathyroid adenoma. Blood and 24 h urine were obtained at various time points, for the measurement of serum or urinary phosphate and calcium indices. Before surgery, serum calcium (2.91 +/- 0.06 mmol/l; mean +/- SEM), parathyroid hormone (354 +/- 47 pg/ml) and 1,25(OH)2D (61.2 +/- 7.8 pg/ml) were elevated while serum phosphate (1.01 +/- 0.07 mmol/l) tended to be low. Relative hypoparathyroidism was evident for up to 5 d after surgery with the lowest value for serum parathyroid hormone (41 +/- 16 pg/ml) on day 1, serum calcium (2.12 +/- 0.06 mmol/l) on day 3 and highest value for serum phosphate (1.41 +/- 0.13 mmol/l) on day 5. As expected, serum 1,25(OH)2D levels decreased to 35.9 +/- 4.2 pg/ml 24 h after surgery. Stabilization of serum and urinary parameters to normal values was seen between day 5 and day 27; the only exception was serum 1,25(OH)2D, which increased again at day 27 to 57.6 +/- 5.0 pg/ml, a value as high as that before surgery. It was still elevated at day 50 (58.3 +/- 4.3 pg/ml), but returned towards normal values in three out of four patients (44 +/- 3.9 pg/ml) by day 80. No variation in 25(OH)D or 24,25(OH)2D was seen throughout the study. 1,25(OH)2D values could be related to serum parathyroid hormone values before surgery (r = 0.659, P less than 0.05) but not after. The secondary increase in serum 1,25(OH)2D could not be related to variations in serum calcium, phosphate, parathyroid hormone or diet. Further studies will be required to explain this phenomenon.

Adenoma↗
PubMed1986

Characteristics of patients with normal T3 and T4 and a low TSH response to TRH.

The nature of the thyroid disorder presented by patients with normal T4 and T3 but blunted TSH response to TRH has not been clarified. In this study, we compared thyroid function tests in 16 such patients with those of 14 controls and 10 hyperthyroid patients. Basal total T4, free T4, total T3, iodine uptake and cholesterol of the study group were similar to controls but significantly (P less than 0.001) lower than in hyperthyroid patients, except for cholesterol which was higher. In contrast, the basal TSH, increase in TSH after TRH stimulation, and decrease of T4 during T3 suppression tests were similar to data obtained in hyperthyroid patients but significantly (P less than 0.001) lower than in controls. Pulse rate was mid-way between the control and the hyperthyroid group. Thyroid stimulating antibody (TSAb) was measured with human thyroid cells in culture; the assay was positive in four subjects in the 16-patient group and in all hyperthyroid patients tested. TSH stimulation test showed a hyporesponse in iodine uptake in the four patients with positive TSAb (26 +/- 29%), as well as in hyperthyroid patients (6 + 5%). However, there was a hyper-response to TSH (213 +/- 52%) in the remaining 12 patients in the group, none of whom had TSAb. Thus TSAb is not seen as responsible for the thyroid disorder in the majority of patients with normal T3 and T4 and absent or blunted TSH response to TRH; surprisingly, most of these patients have thyroid hypersensitivity to TSH. These two characteristics, absence of TSAb and hypersensitivity to TSH, delineate a thyroid disorder clearly different from Graves' disease.

Adult↗
PubMed1986

Effect of trimebutine on intestinal motility and plasma motilin in the dog.

In a previous report, trimebutine was shown to induce premature periods of phase III activity in fasting dogs, and its action was blocked by naloxone. In this study, we observed that trimebutine (5 mg X kg-1 iv) could induce premature phase IIIs in canine small intestine during interdigestive and digestive periods; trimebutine-induced phase IIIs were migrating along the small intestine faster than spontaneous activity fronts and; trimebutine-induced phase IIIs were accompanied by sharp rises in concentrations of plasma motilin. To further elucidate the trimebutine-stimulatory mechanism, we verified its effects on the release of various circulating peptides that influence intestinal motility: short-interval blood sampling during trimebutine infusion revealed that plasma motilin increases induced by trimebutine preceded the beginning of phase III in proximal duodenum; and gastrin and insulin postprandial releases were abolished by trimebutine. Therefore, trimebutine, by its simultaneous but opposite effects on various peptides that individually carry positive (e.g., motilin) or negative (e.g., gastrin and insulin) influences on the generation of activity fronts, could alter the equilibrium between stimulatory and inhibitory forces in such a way that, in some circumstances (e.g., postprandial period), stimulatory mechanisms become predominant.

Animals↗
PubMed1984

Simple method for development of sensitive and specific antiinsulin antisera for laboratory use.

Commercial sources provide good, though expensive antiinsulin antisera. We describe here a simple, fast and inexpensive method for the production of antiinsulin antisera. Purified pork insulin (Lente) was injected subcutaneously in oil/water/complete Freund adjuvant mixture. Three guinea pigs received 0.25 mg of insulin and three received 0.5 mg of insulin. Subsequent injections of the same dose were done 40 and 60 days later. Five animals developed antisera with titers superior to 1:10,000 40 days after the primary inoculation. Four out of five guinea pigs improved further their antibody titer after the 2nd and 3rd injection (p less than 0.0005). Good sensitivity was associated with titers superior to 1:50,000 and appeared only after the 2nd injection to improve further after the 3rd. Thus, four out of six animals developed antiinsulin antisera suitable for the radioimmunoassay (RIA). The antisera bound proinsulin on an equimolar basis with insulin while glucagon was not bound up to 100 ng/ml. The minimum detectable insulin concentration was about 12 pg (0.3 microU) at the optimum antiserum dilution. Six animals given a small dose of insulin (0.06 mg) developed antisera of a low titer and sensitivity, unsuitable for the RIA.

Animals↗
PubMed1983

The thyroid nodule: evaluation of fine-needle biopsy.

Sixty-three consecutive unselected patients with a solitary cold nodule of the thyroid were submitted to surgery. Prior to surgery they all had clinical evaluation and a fine-needle aspiration (FNA) biopsy of the nodule. Results of this study show that the FNA biopsy was correct in predicting cancer in 12 of 13 cancers for a sensitivity of 92%. When the nodule was benign, the FNA biopsy was right in 42 of the 50 benign nodules for a specificity of 84%. In comparison the clinical criteria alone were correct in suspecting only eight of the 13 cancers for a sensitivity of 62%, while correctly identifying 39 of the 50 benign nodules for a specificity of 72%. An association of the clinical criteria with the results of the FNA biopsy would have identified all the cancers in our group.

Adult↗