Chronic diarrhoea in a human immunodeficiency virus/acquired immunodeficiency syndrome patient: A case report

Abstract

BACKGROUND

Chronic diarrhoea in people living with human immunodeficiency virus (PLHIV)/acquired immunodeficiency syndrome presents a diagnostic challenge, often resulting from opportunistic infections (OIs), malignancies, or disease progression itself. We present a case of an advanced human immunodeficiency virus (HIV) patient with chronic diarrhoea, significant weight loss, and antiretroviral therapy (ART) non-compliance, highlighting the diagnostic dilemma between HIV wasting syndrome, OIs, and malignancy.

CASE SUMMARY

A 36-year-old female, diagnosed with HIV five years ago on family screening, presented with three months of profuse watery diarrhoea, associated with crampy abdominal pain and weight loss (14 kg, 30% in 3 months). She was non-compliant with ART. There was no history of recent travel, food contamination, or tuberculosis contact. Fever episodes were mild and transient. Physical examination revealed pallor and bilateral pedal oedema without lymphadenopathy or organomegaly. Genital examination was unremarkable. Routine investigations revealed severe anaemia and confirmed PLHIV status. CD4 count was < 36 cells/µL. Empirical treatment with nitazoxanide was initiated for possible cryptosporidiosis. After ruling out OIs, ART was restarted. With treatment, her diarrhoea resolved, and she tolerated oral intake. Nutritional support was provided, and she was discharged in stable condition with ART, prophylactic antibiotics, and follow-up instructions for further evaluation.

CONCLUSION

In ART-noncompliant PLHIV with chronic diarrhoea, distinguishing between HIV wasting syndrome, OIs (Cryptosporidium, Mycobacterium avium complex, cytomegalovirus colitis) and malignancies (non-Hodgkin lymphoma and anal carcinoma) are critical. Gradual CD4 decline, systemic inflammation, and malnutrition favour progressive HIV/acquired immunodeficiency syndrome rather than an acute OI or malignancy. Early recognition and management, including ART reinitiation and nutritional support, are crucial for prognosis.

Key Words: Human immunodeficiency virus-associated wasting syndrome; CD4 decline; Systemic inflammation; Microbial translocation; Malnutrition in human immunodeficiency virus; Case report

Core Tip: This case highlights chronic diarrhoea and profound weight loss in a human immunodeficiency virus-positive patient as manifestations of progressive immunosuppression, systemic inflammation, and gut barrier dysfunction rather than an identifiable opportunistic infection. It underscores the importance of early antiretroviral therapy reinitiation, nutritional support, and hygiene interventions to improve prognosis in human immunodeficiency virus-associated wasting syndrome.

INTRODUCTION

Diarrhoea is a common manifestation in individuals with human immunodeficiency virus (HIV) infection and can result from opportunistic infections (OIs) and non-OIs, malignancies, or gastrointestinal inflammation[1]. Chronic diarrhoea, lasting more than four weeks, is associated with significant morbidity, particularly in resource-limited settings where delayed HIV diagnosis and limited access to antiretroviral therapy (ART) exacerbate complications[2]. The World Health Organization classifies persistent diarrhoea with weight loss as an acquired immunodeficiency syndrome (AIDS)-defining condition, emphasizing its prognostic significance in HIV progression.

HIV-associated wasting syndrome is characterized by progressive weight loss, malnutrition, and systemic inflammation, often occurring due to a combination of factors, including gastrointestinal malabsorption, metabolic dysregulation, and chronic inflammation. The interplay between immune dysregulation and enteric pathogens, particularly coccidian parasites such as Cryptosporidium and Isospora, is well-documented, with increasing prevalence observed in individuals with CD4 counts below 200 cells/μL[3]. Beyond infections, HIV-induced gut barrier dysfunction contributes to microbial translocation and systemic inflammation, further accelerating disease progression[4]. In this study, we present a case of chronic diarrhoea in a HIV-infected patient with progressive weight loss, malnutrition, and systemic inflammation.

CASE PRESENTATION

Chief complaints

A 36-year-old female from North India, working as a receptionist in a homoeopathic clinic, presented with diarrhoea, fever, and weight loss for three months.

History of present illness

There was profuse, watery, foul-smelling diarrhoea for three months, occurring 7-8 times per day and associated with crampy abdominal pain. The episodes were not linked to food intake, dairy consumption, or mucus in the stool. However, she reported two episodes of blood-streaked stool, each with 2-3 drops of blood, one week previously. She also had a low-grade fever reaching 100°F, associated with chills and relieved with medication. Over the past three months, she experienced significant unintentional weight loss from 50 kg to 35 kg (30% in 3 months). She denied urinary, respiratory, neurological, or constitutional symptoms.

History of past illness

There was no travel history, prior hospitalisation, contaminated food intake, passage of worms, or tuberculosis exposure. She was diagnosed with people living with HIV (PLHIV) in December 2018 during family screening after her husband tested HIV-reactive. She was initiated on ART on December 11, 2018. Her CD4 count was 387 cells/mm³ at the time of diagnosis, and she was started on the tenofovir, lamivudine and efavirenz regimen. She remained on ART until June 2021, with an estimated 85%-90% adherence rate. A viral load of 3325 copies/mL was documented in December 2021. Subsequently, she discontinued treatment on her own due to medication intolerance, reporting symptoms of fatigue and nasal bleeding; since then, she has not been on any medication until now (January 2025).

Personal and family history

She lived a hygienic life, and her family history was inconclusive except that her husband was PLHIV.

Physical examination

On examination, she appeared pale with bilateral pitting pedal oedema extending up to the ankle. Severe muscle wasting was present with a body mass index (BMI) of 14.9 kg/m². There was no icterus, cyanosis, clubbing, or lymphadenopathy. Oral and genital examination was unremarkable. Her abdomen was non-distended and non-tender, with shifting dullness, suggesting mild ascites. No hepatosplenomegaly was noted, and the rest of the systemic examination was unremarkable.

Laboratory examinations

Laboratory investigations revealed severe anaemia (hemoglobin = 5.6 g/dL), thrombocytopenia, and leukopenia, showing relative lymphocytosis (Table 1). Direct Coombs test was positive, suggesting possible immune-mediated haemolysis. Peripheral smear revealed normocytic normochromic anaemia with a mildly increased reticulocyte count. Liver function tests were largely normal, except for hypoalbuminemia and elevated alkaline phosphatase levels. Kidney function tests were within normal limits, although mild hyponatremia and hypokalemia were observed. Metabolic workup revealed subclinical hypothyroidism/sick euthyroid syndrome [free triiodothyronine (2.30-4.20 pg/mL): 0.97; free thyroxine (0.89-1.76 pg/mL): 0.25; thyroid stimulating hormone (0.35-5.5 mcIU/mL): 5.023], vitamin D deficiency [vitamin D (47-190 pmol/L): 23.2] and dyslipidemia with low high-density lipoprotein were also noted [total cholesterol (< 200 mg/dL): 179.2; triglyceride (< 150 mg/dL): 98.8; high-density lipoprotein (> 50 mg/dL): 41.7; low-density lipoprotein (< 100 mg/dL): 117.74]. Routine stool examination and microscopy revealed no ova, cysts, or parasites. Stool culture showed no growth, and modified Ziehl-Neelsen staining did not detect any acid-fast structures. Additionally, the stool occult blood test was negative. Infectious workup confirmed HIV seropositivity, while hepatitis B surface antigen, hepatitis C virus, rapid plasma reagin, toxoplasmosis-rubella-cytomegalovirus-herpes simplex virus panel, and typhoid immunoglobulin M/immunoglobulin G were negative. Tuberculosis workup, including a tuberculin skin test, was negative.

Table 1 Basic and advanced investigations at and after hospitalization of the patient.

Investigation	Unit	Reference range	Day 1	Day 5	Day 10	Follow up at 1 month
Hb	g/dL	13-17	5.6	6	7.8	7
TLC	× 103 cells/mm3	4-11	3.09	3.54	4.31	2.2
DLC (N/L/M)	%	40-70/20-40/2-8	70/21/6.8	76/18/4.1	81/13/12	56.8/28.9/8
Platelet	× 103 cells/mm3	150-400	100	53	56	136
Total bilirubin	mg/dL	0.3-1.2	0.54	0.2	0.29
Direct bilirubin	mg/dL	0-0.2	0.32	0.12	0.2
ALT	U/L	0-50	32	30	38
AST	U/L	0-50	34	35	25
ALP	U/L	30-120	213	220	183
GGT	U/L	0-55	100	112	96
Albumin	g/dL	3.5-5.2	1.17	1.1	1.1
Globulin	g/dL	2.5-3.2		4.8	4.8
Urea	mg/dL	17-43	25		10
Creatinine	mg/dL	0.72-1.18	1.03		0.88
Sodium	mmol/L	136-146	135		138
Potassium	mmol/L	3.5-5.1	3.2		3.4
Uric acid	mg/dL	3.5-7.2	7.22		6.7
INR		0.8-1.1	1.4
Ferritin	ng/mL	22-322	211.4

Hb: Hemoglobin; TLC: Total leukocyte count; DLC: Differential leukocyte count; N: Neutrophil; L: Lymphocyte; M: Monocyte; ALT: Alanine transaminase; AST: Aspartate transaminase; ALP: Alkaline phosphate; GGT: Gamma-glutamyl transferase; INR: International normalized ratio.

Imaging examinations

Chest X-ray was normal. Abdominal ultrasound was largely unremarkable except for mild ascites and hepatomegaly with fatty infiltration. Contrast-enhanced computed tomography imaging of the chest showed patchy ground-glass opacities in both lungs, suggesting a possible fluid overload (due to hypoalbuminemia). In contrast, abdominal imaging revealed dilated small bowel loops with sluggish peristalsis, primarily due to chronic diarrhoea. No significant lymphadenopathy, mass lesions, or biliary abnormalities were detected.

MULTIDISCIPLINARY EXPERT CONSULTATION

Considering her clinical presentation, an infectious disease consultation was obtained, which included differential diagnosis of HIV wasting syndrome, HIV enteropathy, OIs such as Cryptosporidium, Mycobacterium avium complex, or cytomegalovirus colitis, and HIV-associated malignancies like non-Hodgkin lymphoma or anal carcinoma.

FINAL DIAGNOSIS

At discharge, the patient was diagnosed with PLHIV and wasting syndrome.

TREATMENT

Empirical treatment was initiated with nitazoxanide targeting suspected cryptosporidiosis. Supportive management included packed red blood cell transfusion for anaemia, prophylactic antibiotics with azithromycin and trimethoprim-sulfamethoxazole (Septran DS), and antifungal coverage with fluconazole. After ruling out OIs, she was restarted on ART (tenofovir, lamivudine and dolutegravir regimen) on February 7, 2025 as per government of India National Acquired Immunodeficiency Syndrome Control Organization guideline. Since then, she has been adherent to treatment. Nutritional supplementation was provided, including multivitamins, folic acid, vitamin D3, and protein powder. Symptomatic management included pantoprazole for gastric protection, ondansetron for nausea as needed, and paracetamol for fever control.

OUTCOME AND FOLLOW-UP

On follow-up at one month, she presented to the outpatient department in an ambulatory state, with static haemoglobin levels and weight gain from 35 kg in February (BMI: 14 kg/m²) to 38 kg in March (BMI: 15.2 kg/m²). Her diarrhoea had resolved, and she was compliant with ART and other prescribed medications. Further outpatient monitoring was advised for continued immune recovery and nutritional rehabilitation.

DISCUSSION

The patient’s history of progressive weight loss and chronic diarrhoea despite prior ART initiation suggests a state of systemic immune activation and progressive CD4 depletion. Studies indicate that even in the absence of acute OIs, chronic low-grade inflammation, driven by microbial translocation and cytokine dysregulation, accelerates HIV disease progression[5]. Elevated levels of inflammatory markers such as interleukin-6 and C-reactive protein correlate with poor clinical outcomes, reinforcing the need for early ART reinitiation[6].

Although OIs are well-recognised causes of chronic diarrhoea, their role in our patient appears secondary to underlying HIV-induced gut dysfunction. In individuals with advanced immunosuppression (CD4 < 200 cells/μL), coccidian parasites such as Cryptosporidium and Isospora are commonly implicated in chronic diarrhoea[7]. However, in our case, multiple stool examinations did not reveal an identifiable parasitic aetiology, supporting the hypothesis that gut inflammation rather than active infection was the primary driver of symptoms.

HIV disrupts intestinal epithelial integrity, leading to increased permeability, microbial translocation, and immune activation[8]. This mechanism, rather than an isolated infectious aetiology, may explain the patient’s persistent symptoms. Gut microbial dysbiosis, characterised by reduced beneficial bacterial species and increased pathogenic flora, further exacerbates malabsorption and inflammatory responses[9]. Emerging evidence supports the role of gut microbiota modulation in improving gastrointestinal and systemic health in PLHIV[10].

HIV-associated wasting syndrome is strongly correlated with poor nutritional status, independent of viral load suppression[11]. In 1987, the Centers for Disease Control and Prevention included HIV-associated wasting syndrome as an end-of-life AIDS-defining illness. They defined it as profound, involuntary weight loss of > 10% of baseline body weight plus diarrhoea or weakness with documented fever for ≥ 30 days without a concurrent illness[12]. In our patient, progressive weight loss without ART adherence suggests a combination of malnutrition-related catabolism and immune activation. Nutritional interventions, including protein-calorie supplementation and micronutrient support, are crucial adjuncts to ART in preventing further decline in BMI and functional status[13]. Effective ART restores immune function, reduces systemic inflammation, and improves gastrointestinal health. Studies have shown that early ART initiation is associated with decreased gut permeability and lower rates of chronic diarrhoea[14]. In this case, prompt ART reinitiation and supportive nutritional therapy are expected to improve the patient’s long-term prognosis.

Good personal and environmental hygiene is crucial in preventing OIs, particularly in individuals with advanced HIV/AIDS. Proper sanitation, clean water access, and food safety measures significantly reduce gastrointestinal diseases, which can exacerbate wasting syndrome and systemic inflammation[15]. Hand hygiene and infection control strategies in healthcare settings further limit exposure to potential pathogens. Incorporating hygiene education into HIV care programs can play a vital role in reducing morbidity associated with recurrent infections.

CONCLUSION

Chronic diarrhoea in HIV is often multifactorial, involving immune dysregulation, gut barrier dysfunction, and malnutrition rather than isolated OIs. Systemic inflammation and progressive CD4 decline play a central role in disease progression and should be prioritised in therapeutic strategies. Nutritional support is a crucial adjunct to ART and can significantly impact morbidity and mortality in patients with HIV-associated wasting syndrome. ART reinitiation at the earliest stage of immune decline is essential for reducing gut inflammation and improving long-term outcomes. Maintaining proper personal and environmental hygiene helps restrict OIs and mitigate gastrointestinal complications in progressive HIV disease.

ACKNOWLEDGEMENTS

Thanks to a patient who maintains personal hygiene in a developing country, and is now convinced to continue antiretroviral therapy.