[Aim] This study evaluated the nutritional status of older patients who expired during long-term hospital stays of five or fewer years to investigate the appropriate nutritional management. [Methods] We analyzed the data of 573 older patients who expired during a long-term hospital stay, including their diagnosis, bedridden degree, malnutrition level, and nutritional administration methods. Nutritional evaluation was done with the Controlling Nutritional Status variant score, calculated using the serum albumin level, lymphocyte count, and hemoglobin level within one month of admission and at discharge. Malnutrition levels were categorized into normal, mild, moderate or severe, and oral, enteral, and venous feeding were assessed by survival period. [Results] The mean ages of men (n = 293) and women (n = 280) were 85.2 ± 7.2 and 88.4 ± 7.6 years, with the mean length of hospital stay being 10.6 ± 1.7 and 13.5 ± 2.1 months, respectively. Of the patients, 66.5% were unable to turn over in bed on admission, and 73.8% were moderately to severely malnourished. The survival times by nutrient administration method were 12.4 ± 3.2 months for oral intake (n = 117), 16.0 ± 3.6 for nasogastric tube feeding (n = 159), 24.9 ± 7.2 for gastrostomy (n = 94), 2.5 ± 0.6 for peripheral venous nutrition (n = 75), and 6.8 ± 1.9 for central venous nutrition (n = 128). [Conclusions] Patients with gastrostomy tend to have longer lifespans.

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Cystinuria is a hereditary disorder characterized by a defective reabsorption of amino acids that leads to the formation of cystine stones: clinical presentations of this disorder include renal colic, hematuria, and staghorn calculi. Herein, we report the cases of two asymptomatic sisters who were incidentally diagnosed with cystinuria following the results of the elder sister’s urinalysis. Patient 1 was the elder sister aged 9 years. She was referred to our hospital due to detection of cystine crystals by urinalysis following group A streptococcal infection. Her urinary amino acid analysis revealed a cystine concentration of 3,868.9 μmol/g·Cr, and computed tomography revealed renal calculi in the bilateral kidneys. Patient 2 was the younger sister, aged 6 years. Urinalysis was performed for Patient 2 following Patient 1’s diagnosis of cystinuria. Cystine crystals were detected in urinary sediment, and a urinary cystine concentration of 2,087.6 μmol/g·Cr was identified. Urolithiasis is a risk factor of hypertension and chronic kidney disease; hence, it is generally managed by urologists. However, cystinuria is a hereditary disorder that can be detected in childhood, even in asymptomatic patients. Pediatricians and general practitioners should consider cystinuria in their daily clinical practice.

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A 43-year-old woman with Sjögren’s syndrome had developed hypophosphatemia six years previously. The patient had been diagnosed with Fanconi syndrome induced by Sjögren’s syndrome and was treated with oral phosphate and active vitamin D. Despite supplementation, severe hypophosphatemia continued. The serum fibroblast growth factor 23 (FGF23) level was 32.7 pg/ml three years previously, above the 30 pg/ml diagnostic cut-off for FGF23-related disease. However, the result was interpreted as a deviation rather than a diagnosis. The patient needed higher doses of oral phosphate, and she experienced bilateral ankle pain and difficulty walking. One year previously, the FGF23 level was 53.7 pg/ml, which confirmed the diagnosis of FGF23-related disease. Although tumor-induced osteomalacia was strongly suspected due to its acquired onset, a causative tumor had not been found. The measurement of FGF23 level is crucial for the evaluation of musculoskeletal symptoms and phosphaturic hypophosphatemia. FGF23-related disease, such as tumor-induced osteomalacia, presents several inherent challenges for accurate diagnosis.

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We report the case of a 46-year-old man who had persistently high thyroid hormone and low TSH levels for approximately 3 years. Although his thyroid gland was enlarged, with an estimated weight of 52 g, TRAb, TSAb, TgAb, and TPOAb were all negative. The I-123 thyroidal uptake rate was high, and scintigraphy showed diffuse enlargement of the thyroid gland. A study of the TSHR (TSH receptor) gene identified a heterozygous variant in codon 523 of Exon 10. This variant resulted in an amino acid substitution from ATC (Ile) to TTC (Phe). His mother and older sister also had hyperthyroidism and were negative for TRAb, TSAb, and TPOAb. Although the TSHR genes of the mother and sister have not been identified due to lack of consent from the family, familial non-autoimmune hyperthyroidism was suspected in this case. The patient’s thyroid function is currently well controlled with thiamazole. However, we will continue to monitor the patient closely as antithyroid medication cannot induce remission in non- autoimmune hyperthyroidism.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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