Aphakic hydrogel contact lens fitting on a monocular canine: a case report.

BACKGROUND: Though plano bandage contact lenses used for therapeutic purposes are not uncommon for dogs, no literature regarding contact lenses to correct aphakic canines currently exists. CASE REPORT: Oliver, a 7-year-old terrier mix, was aphakic in his left eye and essentially blind in his right eye as the result of a large retinal detachment. Surgical complications and endothelium damage contraindicated an intraocular lens implant in his left eye. While co-managed with his veterinary ophthalmologist, Oliver was prescribed an aphakic hydrogel contact lens to improve his monocular vision. CONCLUSION: Oliver was successful (by clinical criteria) with his contact lens. Although it is difficult to quantify his vision without a visual evoked potential, Oliver appeared more attentive and confident with the contact lens. This case report demonstrates a successful canine aphakic contact lens fit through the efforts of his owners, co-managing veterinary ophthalmologist, and optometrist.

A comparison of Fluoracaine and Fluorox on corneal epithelial cell desquamation after Goldmann Applanation Tonometry.

BACKGROUND: The purpose of this study was to quality the frequency and amount of corneal desquamation from a sodium fluorescein/proparacaine combination (Fluoracaine) as compared with sodium fluorescein/benoxinate combination ophthalmic solution (Fluorox) after Goldmann Applanation Tonometry. METHODS: One drop of Fluoracaine was randomly instilled into one eye and one drop of Fluorox was instilled into the opposite eye of the same patient. Intraocular pressures (IOPs) by GAT and tear break-up times (TBUTs) were taken. Corneal stinging was compared. Corneal integrity by Cornea and Contact Lens Research Unit (CCLRU) standards was evaluated at 0, 3, 7, 10, 15, and 20 minutes after instillation of the ophthalmic solutions. RESULTS: Sixty eyes of 30 patients were observed Forty-seven percent of the patients reported Fluorox to string more than Fluoracaine; 23% of the patients reported that Fluoracaine stings more than Fluorox; and 30% the patients reported no difference. Average TBUTs were 6.87 and 7.17 seconds with Fluoracaine and Fluorox, respectively. Fluoracaine produced micro- and macropunctate keratitis of the superficial epithelium in 31% to 45% of the cornea. Fluorox caused superficial micropunctate keratitis in about 16% to 30% of the cornea. At 20 minutes, all eyes with Fluoracaine and all eyes but one with Fluorox had corneal desquamation. CONCLUSIONS: Fluoracaine causes marginally less stinging--however, clinically and statistically more corneal desquamation--than Fluorox after GAT. Corneal integrity after use of Fluoracaine should be evaluated even 20 minutes after GAT procedures for corneal disruption.

Chronic treatment with angiotensin II type 1 receptor antagonist suppresses glomerular activator protein-1 activity in salt-sensitive hypertensive rats.

We examined the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor antagonist (AT1a) on the action of protooncogene c-fos in salt-sensitive hypertensive rats. Seven-week old Dahl salt-sensitive rats fed a high (8%)-salt diet were treated with ACEI, cilazapril (10 mg/kg) or AT1a, TCV-116 (1mg/ kg) every day for 6 weeks. The control animals were fed a low (0. 3%)-salt diet. Systolic blood pressure gradually increased in high-salt-loaded rats and was higher than low-salt-treated rats throughout the study. However, both medications had no significant antihypertensive effect. After 6 weeks of therapy, glomerular mRNA and nuclear protein were extracted from the resected kidneys. Competitive reverse transcription-polymerase chain reaction showed a high level of glomerular c-fos mRNA in high-salt-loaded rats and that ACEI or AT1a treatment did not significantly change its level. Electrophoretic mobility shift assay demonstrated that treatment with AT1a significantly decreased the activator protein-1 (AP-1) binding activity in the glomerular nuclear extract compared to ACEI. Our findings suggest that, compared with ACEI treatment, long-term treatment with AT1a may contribute to attenuation of the glomerular injury in salt-sensitive hypertension by inhibiting AP-1 transcription activity independent of its antihypertensive effect.

Pharmacologically stimulated portal flow measurement by magnetic resonance imaging for assessment of liver function.

PURPOSE: To evaluate pharmacologically stimulated portal flow measured by magnetic resonance (MR) imaging for assessment of liver function. MATERIALS AND METHODS: Pharmacologically stimulated portal flow was measured by phase contrast MR imaging in 27 patients when they were undergoing abdominal angiography for liver tumors or gall bladder cancer. The patients included 11 cases of liver cirrhosis and eight of chronic hepatitis. Pharmacological stimulation was done by infusion of 10 microg/Kg of nicardipine hydrochloride into the superior mesenteric artery through an angiographic catheter. We examined the correlation between stimulated or non-stimulated portal flow and biochemical liver function tests. RESULTS: Correlation coefficients and their corresponding p values between non-stimulated portal flow and the indocyanine green residual rate at 15 min after injection (ICG R15), serum albumin (ALB), total bilirubin (TB), cholinesterase (CHE), and hepaplastin test (HP) were--0.414 (0.056), 0.296 (0.134), -0.570 (0.002), 0.289 (0.153), and 0.321 (0.126), respectively, whereas those between stimulated portal flow and ICG R15, ALB, TB, CHE, and HP were--0.561 (0.007), 0.411 (0.033), -0.509 (0.007), 0.445 (0.023), and 0.494 (0.014), respectively. CONCLUSION: Stimulated portal flow showed better correlations with biochemical liver function tests than non-stimulated portal flow. It is suggested that stimulated portal flow measurement is more useful for the evaluation of liver function than non-stimulated portal flow measurement.

Long-term administration of adrenocorticotropin modulates the expression of IGF-I and TGF-beta 1 mRNAs in the rat adrenal cortex.

The effects of long-term adrenocorticotropin (ACTH) therapy on the expression of IGF-I and TGF-beta 1 on rat adrenal cortex was investigated. ACTH (0.1 mg/kg/day) or saline as control was injected intraperitoneally in 5-week-old Wistar rats every day for 4 weeks. ACTH significantly increased adrenal weight (P < 0.05) and serum corticosterone (P < 0.05). Competitive RT-PCR analysis on the adrenocortical mRNA showed increased IGF-I (P < 0.01) at 4 weeks of ACTH and increased TGF-beta 1 (P < 0.01) at 1 week of ACTH compared the control group. ACTH also significantly increased proliferating cell nuclear antigen mRNA level (P < 0.01), at 4 weeks of treatment, which correlated with IGF-I level (P < 0.01), but correlated negatively with ACTH-stimulated TGF-beta 1 level (P < 0.05). There was a weak correlation between IGF-I and serum corticosterone (P < 0.05), and between TGF-beta 1 mRNA levels and serum corticosterone concentration (P < 0.05). Histologically, ACTH induced hypertrophy in the zona fasciculata cells and increased the clear cells containing lipid deposits. Immunohistochemistry showed that IGF-I peptide was mainly expressed in the periphery of the zona fasciculata at 4 weeks of ACTH therapy, while the same therapy caused a slight increase in TGF-beta 1 expression in the same area. Our results show that an increase in adrenocortical growth resulting from ACTH treatment is associated with an increase in IGF-I mRNA expression but only a transient increase in TGF-beta 1 mRNA expression.

Renal c-fos expression induced by angiotensin II is enhanced in spontaneously hypertensive rats.

We compared the effect of a bolus injection of angiotensin II (Ang II) on the expression of protooncogene c-fos in the renal cortex and medulla of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Intravenous infusion of 5 ng/kg body weight of Ang II resulted in an immediate rise in systolic blood pressure (SBP) in both SHR and WKY rats. The percent rise in SBP was similar in both strains. Pretreatment with Ang II type 1 (AT1)-receptor antagonist, L-158,809 (1 mg/kg) abolished the pressor response in both strains. Competitive reverse transcription-polymerase chain reaction (RT-PCR) showed that administration of Ang II increased the expression of c-fos mRNA within 10 min in both the renal cortex and medulla of SHR significantly higher than WKY rats. Moreover, the enhanced c-fos mRNA expression due to Ang II was significantly suppressed by the pretreatment of L-158,809 in both strains. These findings indicate that c-fos expression in the kidney is mediated by AT1-receptors and that the renal c-fos response to exogenous Ang II was significantly augmented in SHR compared with WKY rats, suggesting that this hyperresponsiveness on renal AT1-action may partly contribute to the progression of renal injury in SHR.

[MRI phase contrast flow measurement of portal vein: influence and compensation of respiratory motion and propriety of phase correction using background].

The purposes of this study were to (1) determine which condition, breath holding (BH) or quiet breathing (QB), is better for phase contrast (PC) measurement of the portal flow (PF); (2) assess the usefulness of respiratory compensation (RC), a technique that diminishes motion artifacts due to breathing, on PC flow measurement; and (3) evaluate the propriety of phase correction (PhC) using background for PC flow measurement. For purposes (1) and (2) respiratory simulation phantom (RSP) was measured, and PF measurements were performed in 6 healthy subjects (HS) and 53 patients. Thirty of the patients had liver cirrhosis (LC) and 23 did not. For purpose (3), flow measurements were carried out in the phantom and 6 HS. (1) In 6 HS, intra-subjective coefficients of variation (CV) were smaller under QB than under BH (p < 0.05). And PF in patients with LC was less than in those not under QB (p < 0.01). This difference was not statistically significant under BH. (2) In the RSP study PC flow measurement with high sort RC showed good reliability. (3) Intraobserver variation was smaller without PhC than with PhC (p < 0.05) in the HS study. It may be more useful to perform portal flow measurements under QB with RC and without PhC than with PhC or under BH.

Reversible hypothyroidism in empty sella syndrome: a case report.

A 33 year-old Japanese woman complained of generalized fatigue, recurrent infections and gradual weight loss 1 year after her first delivery. During delivery, no excessive bleeding or change in blood pressure was noted. On endocrinologic examination 2 years after delivery, she was found to have severe adrenal insufficiency and hypothyroidism. Pituitary function tests revealed impaired responses of ACTH, PRL and gonadotropins, and normal response of GH. TSH response to TRH was delayed but not exaggerated. Cranial magnetic resonance imaging showed an empty sella. The adrenal glands were responsive to extrinsic ACTH, and adequately accumulated 123I-aldosterol. Antipituitary and antithyroid autoantibodies were detected in her serum. She was diagnosed with partial hypopituitarism associated with empty sella syndrome. Approximately 2 months after administration of cortisone acetate 25 mg/ day her general condition was noticeably improved, with normalization of thyroid function and improvement of gonadotropin responses to GnRH. This case suggests that a physiologic dose of glucocorticoid is necessary to maintain not only thyroid function but also some of the remaining pituitary functions in patients with empty sella syndrome manifesting hypopituitarism.

Pituitary apoplexy induced by a combined anterior pituitary test: case report and literature review.

We report the case of a 31-year-old woman with a pituitary adenoma who suffered symptomatic pituitary apoplexy. The patient developed a severe headache 2 min after undergoing a combined anterior pituitary function (CAP) test. Emergent computed tomography revealed a hemorrhagic pituitary tumor with evidence of a small subarachnoid hemorrhage. The headache improved spontaneously within half a day. Transsphenoidal surgery was performed 4 days later. Histologic examination demonstrated that the tumor was an eosinophilic adenoma with areas of diffuse hemorrhage. Although pituitary apoplexy caused by endocrinological testing has been reported in only 28 patients, apoplexy caused by a CAP test has been reported in only 1 patient. All of the previous cases had pituitary macroadenomas, 69% of which were involved in suprasellar extension. Non-functioning adenomas (24%) and prolactinomas (24%) were the most often affected by endocrine stimulation tests. With respect to the stimulants of pituitary adenomas, gonadotropin-releasing hormone (76%), TSH-releasing hormone (69%), and insulin (34%) were primarily responsible for the apoplexy. This case report with the literature review suggests that routine testing on pituitary function should be ordered cautiously given the risk of possible apoplexy.

Sheehan's syndrome of more than 30 years' duration: an endocrine and MRI study of 6 cases.

The endocrine function and pituitary imaging in Sheehan's syndrome more than 30 years after causative events were evaluated. Magnetic resonance imaging (MRI), a combined anterior pituitary test, plasma vasopressin-to-osmolality adaptation study, and antithyroid and antipituitary cell antibody measurement were performed in 6 women with Sheehan's syndrome. The interval from delivery to the onset of symptoms of hormonal deficiency ranged from 3 to 32 years. Since clinical onset, all had received glucocorticoid and thyroid replacement therapy. Cranial MRI examination showed an "empty sella" in 5 cases. Among these, 2 of 5 (40%) demonstrated panhypopituitarism and the other 3 (60%) maintained gonadotropin response. The pituitary gland was normally discernible but with a low-intensity lesion on T1-weighted images in a patient who maintained PRL and gonadotropin responses. Posterior pituitary function was abnormal in 3 of 6 (50%) despite the absence of polyuria. No antipituitary antibodies were detected in any of the cases. Thyroid peroxidase antibody was negative in all cases, but antithyroglobulin antibody was detected in 2 of 6 (33%). Thyroid-stimulating antibody was not detected, but one case had an anti-TSH antibody. Thirty years after the initial events, most patients with Sheehan's syndrome showed signs of an empty sella on MRI, all having noticeable suppression of anterior and/or posterior pituitary hormones with no related autoimmunity.

IDDM accompanied by a growth hormone-producing pituitary adenoma. A case report.

CASE HISTORY: A 30-year-old Japanese man who presented with recurrent ketoacidosis caused by IDDM was found to have increased secretion of growth hormone (GH). On initial cranial magnetic resonance imaging (MRI), no pituitary lesion was detected; however, a pituitary microadenoma was found 2 years later during a repeat MRI. In spite of the hypersecretion of GH, serum IGF-I was dramatically suppressed. Transsphenoidal surgery was performed to resect the pituitary tumor that was histologically an acidophilic pituitary adenoma. Although the GH excess rapidly improved postoperatively, the IGF-I level remained low. Subsequent insulin therapy initiated 1 year after the operation elevated the serum IGF-I level to within the normal range. DISCUSSION: The first case of coexistent IDDM and a GH-producing pituitary adenoma suggests that patients with uncontrolled IDDM may develop GH hypersecretion. Furthermore, the low IGF-I levels may be closely associated with the GH excess and with the development or progression of GH-secreting pituitary adenomas.

A case of primary hyperparathyroidism accompanying multiple myeloma.

We report a case of 77-year-old woman who presented with lumbago and hypercalcemia. Multiple myeloma (MM) was first diagnosed by serum protein electrophoresis and bone marrow aspiration, but intact parathyroid hormone (intactPTH) was also found to be high in the presence of persistent hypercalcemia with anorexia and nausea. After lowering serum calcium with bisphosphonate administration, parathyroidectomy was performed. Upon histologic examination, the tumor was determined to be parathyroidal chief-cell hyperplasia and the patient was treated with melphalan and prednisolone. The relationship between MM and primary hyperparathyroidism (I degree HPT) remains unknown. Although the co-existence of MM and I degree HPT was reported in 12 reports from various parts of the world, there was only 1 report in Japan. The present case is an example of successful treatment for a complicated disorder, and suggests that patients suffering from bone pain or hypercalcemia need to be examined both endocrinologically and hematologically.

Manifestation of primary hyperthyroidism after pituitary adenomectomy: a case report.

We report a 47-year-old Japanese man who presented with visual disturbance due to a pituitary tumor with suprasellar extension. The patient had mild secondary hypothyroidism preoperatively, and was started on administration of levothyroxine sodium immediately before transsphenoidal surgery. After the operation, levothyroxine sodium was continued for several months. Pathological examination of the surgical specimen, together with endocrinological investigation revealed that the suprasellar tumor was a FSH-producing pituitary adenoma. Since 3 months after the operation, he has developed muscle weakness and finger tremor. He was found to be thyrotoxicosis, and levothyroxine sodium was discontinued. Seven weeks after levothyroxine sodium was discontinued, thyrotoxicosis continued, with a positive thyrotropin binding inhibitory immunoglobulin (TBII) and a high diffuse 123I-uptake by the thyroid. He was started on thiamazole 30 mg/day. Although his thyroid dysfunction improved within 2 months, hyperthyroidism worsened repeatedly on attempts to discontinue thiamazole, and he required continuous treatment at 2.5 mg/day. Patients with occult autoimmune thyroiditis rarely progress to thyrotoxicosis after operations on other endocrine organs such as the adrenal or parathyroid gland. In patients with pituitary adenoma, thyroid function and thyroid-associated autoantibodies should be investigated pre- and post-operatively.

A case of Schmidt syndrome accompanied by a pituitary adenoma.

Schmidt syndrome consists of adrenal insufficiency and Hashimoto's thyroiditis, which are probably caused by an autoimmune process. We encountered a patient who manifested severe generalized fatigue due to Schmidt syndrome recurrently. The endocrinological examination tests on the patient showed that the increase in thyroid stimulating hormone (TSH) and ACTH concentrations were not remarkable, despite hypo-function of the peripheral glands. Subsequent cranial magnetic resonance imaging (MRI) exhibited the existence of a pituitary tumor. The pathological findings on the resected tumor and endocrinological stimulation tests proved that the tumor was a FSH-producing adenoma. Although involvement of the pituitary region in Schmidt syndrome on rare occasions presents as hypophysitis, no pituitary adenoma has previously been reported in association with this syndrome. We present a patient with Schmidt syndrome and an accompanying FSH-producing pituitary adenoma. The coexistence of these disorders suggests that the functioning pituitary tumor might be considered as a pituitary lesion in Schmidt syndrome.

A patient with sarcoidosis associated with recurrent urolithiasis and tubular injury caused by calcium deposition.

A 38-year-old woman was hospitalized in January 1994 with renal dysfunction and hypercalcemia. Before admission, she was diagnosed as having urolithiasis, and had been treated twice with extracorporeal shock wave lithotripsy (ESWL). Ophthalmologically, she exhibited iritis and secondary glaucoma. Hypercalcemia, an extremely low titer of parathyroid hormone (PTH), and elevation of angiotensin-converting enzyme (ACE) and lysozyme activity were noted. These findings suggested sarcoidosis, although the chest X-ray showed only fibrotic changes. Hypercalcemia was suspected of having been caused secondarily by sarcoidosis. Since her laboratory data also showed renal dysfunction and abnormal urinalysis, a renal biopsy was performed. The histological findings indicated a tubular and interstitial disorder without glomerular abnormality; calcium deposition, which was detected by X-ray energy dispersive analysis, was observed in the tubular cytoplasm. Administration of prednisolone alleviated the renal dysfunction and decreased the elevation of ACE activity and lysozyme level of the blood. Sarcoidosis is sometimes associated with hypercalcemia, but rarely with renal dysfunction. These findings suggested that sarcoidosis may be associated with renal dysfunction due to tubular injury caused by calcium deposition in the tubules, and that glucocorticoid therapy was effective for these disorders.

Developmental change of kidney dopamine receptors in spontaneously hypertensive rats.

To elucidate the role of the kidney dopamine system on blood pressure regulation, we investigated the developmental change of kidney dopamine receptors in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The autoradiogram of [3H]-SCH23390, a specific DA1 receptor antagonist, showed that DA1 receptors were localized mainly in the rat renal cortex. The radiolabeled receptor assay (RRA) of [3H]-spiperone was performed on 3-, 7-, and 18-week-old SHR using the homogenate of renal cortex. Neither dissociation constant (Kd) nor maximum binding capacity (Bmax) were different between SHR and WKY rats at the age of 3 and 7 weeks. Nevertheless, Kd and Bmax were significantly low in 18-week-old SHR. The systolic blood pressure of 7-, and 18-week-old SHR was significantly higher than that of age matched WKY rats. The urinary dopamine excretion in 16-week-old SHR was significantly higher than that in age-matched WKY rats, although urine volume and urinary sodium excretion were the same as those in the control in both sodium-loaded and -restricted state. In summary, although renal dopamine production was enhanced in SHR in the hypertensive state, dopamine was found not to contribute to natriuresis since the number of dopamine receptors was reduced in these rats. We also found that enhanced dopamine production in response to a salt load was lacking in these rats. These two pathological phenomena noted in the renal dopamine system play a role in the progression of hypertension in SHR.