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Biomedical subjects

A H Teeuw

Publications and source records attributed to A H Teeuw.

9 recordsLinked to original sources
PubMed2004

[Unnatural and unexplained death in a paediatric intensive-care unit, 1993-2002].

OBJECTIVE: To analyse the causes of unnatural death in a general paediatric intensive-care unit. DESIGN: Retrospective and descriptive. METHODS: The cause of death was reviewed for all deceased children who were admitted to the paediatric intensive-care unit of the Emma Children's Hospital/Academic Medical Centre in Amsterdam, the Netherlands from 1993 through 2002. Three investigators independently categorised the cause of death as 'natural' or 'unnatural'. Unnatural death was defined as death by external cause, such as drowning, suffocation or violence, whether intentional or not. For all patients who died an unnatural death the cause of death and (if available) results of autopsy were analysed. RESULTS: During the study period, 5523 patients were admitted to the ICU, of whom 360 (6.5%) died during the period of admission. In 45 (12.5%) of these this was an unnatural death. In 7 (16%) patients there was a suspicion of death by deliberately caused injury. In 4 of these patients forensic autopsy was performed. The results of autopsy confirmed the suspicion of child battery in 3 patients, whereas in 1 case the diagnosis was refuted. CONCLUSION: In 16% of the children who died of unnatural causes there was a suspicion of child battery. A forensic autopsy was useful in all cases to confirm or refute the suspicion of child battery, but was not carried out in all cases.

Autopsy↗
PubMed1997

Chronic bullous disease of childhood and a paecilomyces lung infection in chronic granulomatous disease.

A 12 year old boy suffering from p67-phox deficient chronic granulomatous disease presented with a bullous skin disease and a lung infection with paecilomyces species. The histopathology of a bullous lesion showed subepidermal blister formation and microabcesses containing eosinophils in the dermal papillae. By direct immunofluorescence, linear staining of IgA at the dermal-epidermal junction was detected which confirmed the clinical diagnosis of chronic bullous disease of childhood (linear IgA dermatosis).

Amphotericin B↗
PubMed1993

[3 examples of fetal genetic neuromuscular disorders which lead to hydramnion].

Causes of polyhydramnios include foetal neuromuscular disorders which cause inability of the foetus to swallow amniotic fluid. Three examples of such disorders are presented: X-linked myotubular myopathy, congenital myotonic dystrophy, and congenital nemaline myopathy. It is concluded that in case of polyhydramnios a search for foetal neuromuscular disease should be carried out. This implies ultrasound evaluation of the foetal movements, especially swallowing movements, neurological examination of the mother for myotonic dystrophy and examination of the newborn, which in selected cases includes muscle biopsy. Foetal neuromuscular disorders are usually genetic in origin. This adds to the need for accurate diagnosis and proper genetic counseling.

Genetic Linkage↗
PubMed1993

[Cholestasis associated with total parenteral feeding in premature infants].

TPN-associated cholestasis in premature and low-birth weight infants is a specific entity for which no single etiologic factor is found. The introduction deals with the different theories concerning the etiology. In the following section results of a retrospective study in 20 patients with TPN-associated cholestasis are shown. Two case histories illustrate the different clinical views in dealing with the problem. In our institute we assume an attitude of expectation.

Cholestasis↗
PubMed1992

[Complete situs inversus in one half of a monozygotic twin].

The history of a monochorial monoamniotic twin, born at 27 weeks of gestation, in which a situs inversus was present in one of the twin is given. The incidence of a situs inversus in twins and the etiologic factors as described in literature are given.

Autopsy↗
PubMed1979

The value of a sensitive assay of carcino-placental alkaline phosphatase (CPAP) in the follow-up of gynecological cancers.

Using a sensitive enzyme immunoassay, carcinoplacental alkaline phosphatase (CPAP) was determined in sera of 1266 patients with gyneocological cancers. All these patients were referred after initial surgical treatment elsewhere. There were 95 patients with evidence of disease at the time of the study and 1171 without evidence of disease. Of the 95 patients with active disease, 47 were treated for ovarian carcinoma, 36 for carcinoma of the cervix and 12 for endometrial carcinoma. Raised levels of CPAP were seen in 40% of patients with ovarian carcinoma, in 22% with carcinoma of the cervix and in 41% in the small group with endometrial carcinoma. In patients without evidence of disease, raised levels of CPAP were seen in 12% of patients with carcinoma of the cervix, in 6% of endometrial carcinoma and only in 2% of patients with carcinoma of the ovary. Therefore it was considered that in the latter group CPAP studies would prove of some value. In the group of patients with carcinoma of the ovary and evidence of disease, raised levels of CPAP were seen almost exclusively in patients with epithelial tumors. It is considered that CPAP may be of value as a tumor marker in this group of patients. When compared with CEA, CPAP tends to give fewer false positives and correlates better with the presence of disease.

Adult↗
PubMed1979

Atenolol and chlorthalidone on blood pressure, heart rate, and plasma renin activity in hypertension.

The antihypertensive effect of atenolol, with and without chlorthalidone, on hypertension was assessed in an outpatient as well as in an inpatient study. In the outpatient study atenolol alone induced decreases in systolic and diastolic BP amounting to 20 and 15 mm Hg. Maximal response of BP and HR developed within a week at the lowest dose used (100 mg twice daily). Combined atenolol-chlorthalidone treatment decreased lying and standing systolic BP by 7 and 14 mm Hg more than atenolol alone, but diastolic BP was decreased little more. In the inpatient study the addition of atenolol to chlorthalidone therapy in a dose of 100 mg twice daily resulted in a maximal decrease in BP within 3 days. At this dose PRA was lowered only slightly. Larger doses did not lead to any significant further decrease in BP, whereas PRA fell progressively. Our results indicate that, in contrast to nonselective blockade, specific beta-1-adrenoceptor blockade by atenolol is capable of inducing a distinct antihypertensive effect, unrelated to suppression of PRA. The decrease in PRA after larger doses of atenolol was not accompanied by a further decrease in BP. Because diuretic-induced renin release plays a role in the maintenance of the BP, our findings suggest that at higher dosages a hypertensive effect of the beta blocker compensated for the hypotensive effect of the decrease in PRA.

Adult↗